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NEUR3905 > Weeks 10 to 11 > Flashcards

Weeks 10 to 11 Flashcards

1
Q

What are the two types of arousal?

A

• Two types of arousal
o Wakefulness: responsive to external environment
 Alert
• Focused
 Non-alert
• Daydreaming
o Sleep: lowered response to external environment (readily reversible)

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2
Q

What is wakefulness?

A
  • Wakefulness- active brain in a moveable body
  • Can interact with external environment
  • State of active consciousness
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3
Q

Describe the EEG of wakefulness?

A 
•	EEG of wakefulness-
o	Low voltage/amplitude
o	Fast 
	Alpha waves (9-10Hz)
	Beta waves (14-15 Hz)
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4
Q

Describe sensation in wakefulness

A

• Sensation
o Vivid
o Externally generated

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5
Q

Describe movement in wakefulness

A

• Movement (Measured by EMG (muscles) and EOG(eyes))
o Continuous
o Voluntary control

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6
Q

Describe the autonomic nervous system in wakefulness

A

• Autonomic nervous system

o Continuous, but involuntary

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7
Q

Describe the thought process in wakefulness

A

• Thought
o Logical
o Progressive

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8
Q

Describe the neural centres and their function in wakefulness

A

• Neural centres
o Brainstem controls and is the epicentre of the state of wakefulness (trigger)
 Increased activity in the brainstem reticular formation (acetylcholine)
• Main cause for wakefulness ability
 Increased activity in the raphe nucleus (serotonergic)
• Mood and gives the cortex a sense of reality
• Dampens down overtly aggressive behaviour
 Increased activity in the locus coeruleus (Noradrenergic neurons)
• Mood and global attention
o Cortex is required to make sense of environment

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9
Q

What are the two forms of sleep?

A
  • Progressive changes over minutes: regular/predictable cycle
  • Two forms: REM (rapid eye movement) sleep, non-REM sleep
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10
Q

What is non-REM sleep?

A

o Non-REM sleep/ slow-wave sleep
 An idle brain in a movable body
 Designed for a state of rest

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11
Q

Describe the EEG in non-REM sleep

A 
•	EGG:
o	High voltage/amplitude
o	Slow (low Hz)
	θ wave
	δ wave
•	Bit slower than θ wave
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12
Q

Describe sensation in non-REM sleep

A

• Sensation:
o Dull/absent
o Not very responsive to outside world

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13
Q

Describe movement in non-REM sleep

A

• Movement (EMG, EOG)
o Lowered movements
o Stage where there can be sleep walking/talking

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14
Q

Describe the autonomic nervous system in non-REM sleep

A 
•	Autonomic nervous system
o	Lowered body temperature
o	Lowered energy use
o	Lowered oxygen use (brain)
o	Lowered heart rate 
o	Lowered respiration 
o	Lowered kidney
o	Heightened gastrointestinal activity
o	Heighted parasympathetic activity
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15
Q

What are thought processes in non-REM sleep

A

• Thought

o Unknown- no memory of thought in non-rem sleep

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16
Q

What are the 4 stages of non-REM sleep and their EEG waves?

A

o As progress through the stages, voltage gets higher and frequency gets lower-> start to get into a deeper type of sleep
• Stage 1: lightest and transitional stage (pheta waves)
• Stage 2: slightly deeper sleep (spindle/K complex waves generated by the thalamus)
o Thalamus sets the pace for the sleep cycles
• Stage 3 and 4: deep sleep (delta waves)

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17
Q

What is the behaviour of neural neurotransmitter centres in non-REM sleep?

A

• Neural centres:
o Lowered noradrenergic system activity
o Lowered serotonergic system activity
o Lowered cholinergic system activity

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18
Q

What is REM sleep?

A

 Active brain in an immovable body- no rest

• Where dreams occur

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19
Q

What is the EEG of REM sleep?

A

 EGG-looks like state of wakefulness
• Low voltage/amplitude
• Fast
• β waves

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20
Q

What is sensation in REM sleep?

A

 Sensation
• Vivid
• Internally generated

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21
Q

Describe movement in REM sleep

A 
	Movement (EMG, EOG)
•	Paralysis 
o	Flat EMG wave
•	Except eye-ear (respiratory muscles)
o	High EOG waves
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22
Q

Describe the autonomic nervous system in REM sleep

A 
	Autonomic nervous system
•	Increased heart rate
•	Increased respiration 
•	Increased oxygen use (brain)
•	Increased sympathetic system 
•	Decreased body temperature 
o	Paradoxical to sympathetic control
•	Increased erectile tissue activation
o	Paradoxical to the increased sympathetic control
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23
Q

Describe thought in REM sleep

A

 Thought

• Vivid, bizarre, illogical

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24
Q

Describe the amount of REM sleep during the sleep cycle

A

 Amount of REM sleep during the sleep cycle
• Around 20% in adults but changes with age
o Dream more when humans are younger

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25
Q

Describe the behaviour of neurotransmitters during REM sleep and the purposes of this

A

 Neural centres
• Increased cholinergic cells in the pons
o Triggers dreams
o Cortex gives content for the dream
• Increased cholinergic input to the spinal cord inhibits spinal cord and prevents movement

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26
Q

Describe the cycle of REM vs non-REM sleep during sleep

A

o Brain cycles through these two stages four to five times a night
 First 3 hours of sleep- get best and deepest non-REM sleep
 After 3 hours, don’t reach deepest non-REM sleep often
 non-REM decreases as night progresses whilst REM increases as night progresses

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27
Q

Describe the amount of sleep required in mammals, and what influences this amount

A

• Sleep amount required
o Amount of sleep needed varies
 Some people only need 2-3 hours of sleep whilst some need 18 hours of sleep
 Normally, 8 hours of sleep is needed
o With age, we spend less time sleeping
 We sleep more as we grow
o All mammals sleep-some more than others
 Bats and cats sleep a lot
 Prey animals sleep less than predator animals

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28
Q

How do dolphins sleep?

A

 Dolphins sleep with half a brain at a time (only one side of the brain is sleeping and the other is in a state of wakefulness)
• Dolphins sleep by swimming in circles

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29
Q

What is the function of sleep?

A

• Not definitely known, but sleep is essential or death will occur

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30
Q

Describe theories on the function of non-REM sleep

A

o nonREM
 Time of restoration (recover/renew) and/or protection (safety)
• Restoration: recover the body and giving autonomic nervous system to do repairs
• Adaptation: protection- a way to get out of the way of predators in safety

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31
Q

Describe theories on the function of REM sleep

A

o REM: go to REM sleep a lot quicker if we’re interrupted during it and are allowed to subsequently go back to sleep (REM rebound)
 Ancient view: window into another spiritual world trying to guide us
 Freudian view: dream for wish fulfillment- everything in our dreams is related to sexual frustration
 Activation-synthesis hypothesis:
• Random cholinergic discharges during REM releases a memory/image, and cortex builds story around memory/image to make sense of it (makes dream about situation)
 Memory formation hypothesis:
• Important for memory forming and learning through hippocampal activation
o In the process of consolidation, dreams are created

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32
Q

What are examples of common sleeping disorders?

A
  • Insomnia
  • Sleep apnea
  • Narcolepsy
  • Talking and walking
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33
Q

Describe insomnia and its possible causes

A

o Inability to sleep/deprived of sleep
o Feel tired
o Due to stress, alcohol, coffee, disease

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34
Q

Describe sleep apnea and its possible causes

A

o Blocked airways
o Sleep is interrupted
o Lack/reduced amount of oxygen for 10 seconds-60 seconds: snorts
 Brain hypoxia-> brain realises it’s running out of oxygen-> pharyngeal muscles contract-> passage is opened up
o Get headaches or if there is intense hypoxia, patients might get reduced brain function
o Due to age, obesity, alcohol, tobacco and sedatives

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35
Q

Describe narcolepsy and its possible causes

A

o Uncontrollable sleep at anytime (may last from 1 min-30 mins)
o Mayhem of sleep and wake cycle
o Abnormal sleep pattern- enter in REM sleep prematurely
o Due to genetics, stress, disease/damage

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36
Q

Describe sleep talking/walking and the best way to handle it

A 
o	Happens in non-REM sleep (stage 3,4)
o	Patients are not aware of it and have no memory of the incident (early teens is where most people sleep walk)
o	Sleep walkers are difficult to wake 
	Best is to guide them back to bed
o	Sleep talkers mostly garble
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37
Q

Describe the border landmarks of the hypothalamus

A
  • Base of the forebrain
  • Optic chiasm rostrally
  • Midbrain tegmentum caudally
  • Floor and lateral walls of the third ventricle
  • Continuous with the posterior pituitary
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38
Q

What is the main function of the hypothalamus?

A

• Function:
o Integrates information from the spinal cord, brainstem, forebrain and various endocrine systems
o Important in the central control of visceral motor functions and generating specific behavioural outputs and motivational states

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39
Q

Describe how the hypothalamus is divided into different sections and their locations

A

• Three longitudinal regions (medial to lateral)
o Periventricular zone
 Near the wall of the 3rd ventricle
o Medial zone
 Between periventricular and lateral regions
o Lateral zone
 Far laterally

•	Anterior-posterior regions
o	Anterior (or pre-optic)
	Above the optic chiasm 
o	Tuberal
	Above the infundibulum 
o	Posterior
	Posterior to the infundibulum
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40
Q

Describe the nuclei in the anterior hypothalamus and their longitudinal location

A

 Nuclei:
• Periventricular zone- suprachiasmatic nucleus
• Medial zone-medial preoptic nucleus
• Lateral zone- lateral preoptic nucleus (containing median forebrain bundle)

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41
Q

Describe the nuclei in the tuberal anterior hypothalamus and their longitudinal location

A

o Periventricular zone- periventricular nucleus
o Medial zone- paraventricular nucleus, supraoptic nucleus and anterior nucleus
o Lateral zone- lateral nucleus (containing median forebrain bundle)

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42
Q

What is the function of the suprachiasmatic nucleus?

A

o Important in regulating circadian rhythms

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43
Q

What is the function of the paraventricular nucleus and the supraoptic nucleus?

A

 Paraventricular nucleus and supraoptic nucleus play important roles in endocrine regulation (HPA axis and pituitary function)

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44
Q

Describe the nuclei in the tuberal posterior hypothalamus and their longitudinal location

A

o Periventricular zone- periventricular nucleus and arcuate nucleus
o Medial zone- dorsal, dorsomedial and ventromedial nuclei
o Lateral zone- lateral nucleus (containing median forebrain bundle)

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45
Q

Describe the nuclei in the posterior hypothalamus and their longitudinal location

A

 Nuclei:
• Medial zone- posterior nucleus, mamillary bodies
• Lateral zone- lateral nucleus (containing median forebrain bundle)

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46
Q

Describe Cannon’s 1920s agression experiment, what he discovered and what was so important about this discovery

A

• Cannon 1920s
o If you removed the forebrain in a cat, could produce sham rage
 Cannon termed aggressive rage, sham rage in decorticate cats, as there was no appropriate precipitating stimulus
• Decorticate cats would spontaneously be angry with no or minor triggering stimulus
o Led Cannon to propose that the critical circuitry for producing aggressive behaviours were contained in the brainstem region

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47
Q

Describe how Bard in the 1940s elaborated on Cannon’s research and what new discoveries he made

A

• Phillip Bard 1940s
o Bard and colleagues removed neocortex and cats were totally placid
o Started to systematically remove parts of the cortex
 Produce sham rage behaviours when he removed the cingulate gyrus, the anterior limbic regions, the piriform, the amygdala and the hippocampus
o Precipitating areas for sham rage were the removal of specific regions of the forebrain (limbic cortex)
 Limbic cortex is important for regulation of behaviours
o Posterior hypothalamus was critical for producing aggressive behaviours

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48
Q

Describe how Hess (1940s) elaborated on the field of aggression research and where aggression was localised, as well as what new discoveries he made

A

• Electric stimulation
o Introduced an electrode into certain areas of the cat brain and electrically stimulated the brain with an electrical current to produce a behaviour that looked like a normal aggressive/defensive behaviour in the cat
• Started to delineate the neuroanatomical substrates for aggressive behaviours
• Defined areas of the hypothalamus and periaqueductal grey regions of the midbrain for producing aggressive behaviours

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49
Q

Describe Hunsperger (1950s) discoveries in the aggression localisation field of research and how he did so

A

Hunsperger (1950s)
• Electrical stimulation of brain with an electrode
• Describe affective behaviours produced by specific regions of the hypothalamus
o Defence
o Attack
o Flight
• Starting to separate out components of aggressive behaviours and the hypothalamic regions responsible for these subtypes of behaviour
o First report that growling and hissing could be produced
o Described site dependent sequences of behaviour
• They suggested a hierarchical organisation of behaviour, with environmental modulation
o In response to a dummy cat and when subject cat had some stimulated brain areas, some stimulation sites evoked attack, and some stimulation sites evoked flight
o Richness of behaviours became much greater in more social contexts
 The way in which the cat responded when stimulated in isolation was different from the way in which the cat responded when stimulated in a social context
o Context of stimulation and location of stimulation is additive towards output

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50
Q

Describe what affects the behavioural output of the hypothalamus in aggression

A

-Regulation by limbic cortex
-Stimulation duration
—–Behaviours are time locked to a stimulus: start when stimulation starts and stop when stimulation stops
-Environmental modulation: hypothalamus is very sensitive to context
• Hypothalamus alters its responsivity dependent on the context in which the hypothalamus is stimulated

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51
Q

Describe Flynn’s (1970s) research and how it progressed the field of aggression research

A

• When stimulating hypothalamus directly, if stimulate a particular side of the hypothalamus and on the ipsilateral side provide a stimulus to the cat face, can trigger defensive behaviours but if the contralateral side of the cat face is stimulated, then don’t get the behaviour
o Can shape the behaviour by adding external forces
o Hypothalamus is very sensitive to context
• Hypothalamus is constructing motivation towards aggression and driving the circuitry for aggressive behaviours
• Showed sub-neuronal specificity for the behaviours (the specific nuclei for aggression)
• Found that behaviours were time locked to a stimulus
o When hypothalamic areas were stimulated, behaviour was triggered but when stimulation was stopped, the behaviour stops as well
 Mood state isn’t retained after stimulation ends

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52
Q

Describe Flynn 1970s differentiation between affective attack and quiet biting attack in cats, as well as the different areas responsible for these behaviours

A

Affective attack:

  • Similar to rage behaviour seen in decorticate cats
  • Sympathetic arousal, pupillary dilation and piloerection
  • Hisses and snarls, back arched and attacks
  • Electric stimulation of the ventromedial hypothalamic nucleus

Quiet biting attack

  • Different quality of emotionality
  • Cat stalks prey, pounces and bites the neck
  • No vocalisation
  • Electrical stimulation of the lateral hypothalamic nucleus
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53
Q

Describe how Hilton’s (1980) research progressed the aggression/defensive behaviours field

A
  • Showed that the regions of the hypothalamus that produced aggressive behaviours produced the cardiovascular, respiratory, endocrine responses required to support the fight behaviour
  • Targets of hypothalamus were referred to as the fight and flight pathways
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54
Q

Name the current contemporary scientist leading the aggression field

A

• Main contemporary scientist working in the aggression field- Dayu Lin (2010s)

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55
Q

What is the main hypothalamic nucleus responsible for aggressive behaviour? What are the main neurons.genes in the ventromedial hypothalamus responsible for this aggressive behaviour?

A

Ventromedial nucleus of the hypothalamus

Oestrogen receptor alpha neurons/genes

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56
Q

Describe how Dayu Lin (2010s) confirm that ventromedial hypothalamic cells and oestrogen receptor alpha neurons were vital for aggression in male rats

A

o Chemogenetic approaches
 Inhibition of ventromedial hypothalamic cells by:
• Reversible inactivation of neurons
• Estrogen receptor alpha knockdown
o Estrogen receptor alpha genes critical for producing aggressive behaviours
• Selective ablation of ventromedial hypothalamus neurons containing the progesterone receptor
• Optogenetic inhibition of ventromedial hypothalamus oestrogen receptor alpha cells
o Used optogenetic techniques to stimulate ventromedial hypothalamus neurons and evoke attack behaviours in animals

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57
Q

How does the optogenic technique work?

A

 Optogenetic technique: involves the use of light to control neurons that have been genetically modified to express light-sensitive ion channels
• Turn on neurons by shining light of particular wavelength

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58
Q

Describe how Lin (2010s) found that fluctuations in behaviours were produced by fluctuations in oestrogen-receptor alpha neuron activation

A

o Used optogenetic techniques to selectively target the oestrogen receptor-alpha cells which evokes male attack behaviours towards castrated males, females and males
 Low intensity stimulus (light) to activate oestrogen-receptor cells will produce mounting behaviours (reproductive behaviours)
 High intensity stimulus (light) to activate oestrogen-receptor cells will produce attack behaviours (aggression)

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59
Q

Describe how differential stimulation of oestrogen-receptor alpha cells produces differential aggressive/reproductive behaviours

A

• Low levels of oestrogen-receptor cell activation produce reproductive behaviours
• High levels of oestrogen-receptor cell activation produces aggressive behaviours
 Intensity of activation selects one behaviour over the other
• Reproductive behaviours could modulate defensive behaviours

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60
Q

Describe how Dayu Lin (2010s) discovered whether the same or different populations of ventromedial hypothalamus neurons regulate reproductive and/or defensive behaviours

A

o In-situ hybridization experiment used to identify whether the same or different populations of ventromedial hypothalamus neurons regulate reproductive and/or defensive behaviours
 Location of mRNA intermediate early gene (cFos)
• Switched on when a neuron is depolarised
o Neurons are depolarised in the ventromedial hypothalamic nucleus when animals fight and when animals mate
• Investigated if cells responded to either reproductive behaviour or fighting behaviour by looking at Fos expression in the cellular compartments which is distinctly different depending on the timing of behaviour
o The first behaviour will make Fos switch on in the cytoplasm, while the second behaviour will lead to Fos switching on in the nucleus
• By looking at relative proportions of nuclear vs cytoplasmic Fos expression in animals that have done specific behavioural patterns, can determine whether cells are mate specific, fight specific or responsible for both types of behaviour
o Specific behavioural patterns
 A mate early and a mate late
 A fight early and a fight late
 A fight early and a mate late
 A mate early and a fight late
• Determined that populations of neurons reproducing reproductive behaviours and defensive behaviours are largely segregated

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61
Q

Do the same populations of neurons reproduce reproductive behaviours and defensive behaviours?

A

• Determined that populations of neurons reproducing reproductive behaviours and defensive behaviours are largely segregated

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62
Q

For defensive behaviours, when do ventromedial hypothalamic neurons increase firing? What will this firing predict?

A

o Ventromedial hypothalamic neurons increase firing when investigating and attacking
 Fire most when subject is an appropriate subject to direct that behaviour towards
 Activity level at investigation predicts attack
 Activity level prior to investigation predicts attack duration
 Inter-attack interval inversely correlates with activity at onset of next attack

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63
Q

What is the relationship between length of attack preparation and length of attack response? Why?

A

 The longer you wait to attack, the larger the attack response
• Ventromedial hypothalamic neurons fire during the execution of the behavioural repertoire, but code for the motivation to fight and the acceleration of motivation in the individual

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64
Q

Describe where the hypothalamic nuclei responsible for reproductive and defensive behaviours are found

A

• Found in the medial zone

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65
Q

What are the hypothalamic nuclei responsible for reproductive and defensive behaviours? Describe their functions

A 
•	Include:
o	Medial preoptic nuclei
	Reproductive purposes
o	Anterior hypothalamic nuclei
	Defensive purposes
o	Ventromedial nuclei
	Reproductive and defensive purposes
o	Premamillary nuclei
	Reproductive and defensive purposes 
•	Important for integrating behaviours that occur between individuals of the same species (inter-specific behavioural nuclei)
o	Social behaviours
o	Common nuclei with a small amount different between these behaviours is probably to allow for seamless switching
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66
Q

Describe the factors that the hypothalamus takes into account when producing behaviour

A

• Hypothalamus is doing the addition of context, the current status of the individual and the needs of the individual

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67
Q

When can fight (or flight) be evoked?

A
  • Fight (or flight) can be evoked in the absence of hypothalamus, although the evoking thresholds are higher
  • Fight (or flight) can be evoked in the absence of limbic cortex and amygdala
  • Stimulation of PAG and ventral tegmental area can evoke fight and flight
  • Lesions of the PAG abolish fight and flight behaviours
  • Early observations led Hunsperger to conclude that these behaviours are hierarchically controlled, this conclusion has not been challenged
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68
Q

What region of the periaqueductual grey can produce attack/defense behaviours and what inputs allows it to do this

A

• When stimulated cells in periaqueductal grey, can produce attack/defense behaviours in region lateral to aqueduct
o The medial wall of the prefrontal cortex projects to the medial hypothalamus and dorsolateral column of the PAG
o There are interconnections between the medial hypothalamus and the dlPAG
 dlPAG also gets strong input from anterior hypothalamus (area in which ventromedial hypothalamic neurons projected to regulate expression of defensive and reproductive behaviours)
 Projections from the ventromedial nucleus via the anterior hypothalamus to the PAG is the critical output pathway for producing aggressive/defensive motor outputs

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69
Q

How do outputs of the periaqueductal grey produce attack/defense behaviours?

A

o The dlPAG can trigger cardiovascular changes via its descending pathways through the cuneiform nucleus
o This PAG area is activated during exposure to a cat, where flight (at distance) or fight (in close proximity) would be adaptive behavioural responses
• PAG projects to all of the brainstem motor neuronal pools and projects to spinal cord via the reticulospinal pathways
o Strong projections into pontine and medullary-reticular formation and is the projection of those areas into the spinal cord that drive the behavioural repertoires
 PAG projects to the premotor parasympathetic and sympathetic areas, and projects to premotor reticulospinal pathways that will regulate motor outflow
• Affects balance pathways

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70
Q

Describe the neural pathway of fight or flight responses

A

• Cerebral cortex-> amygdala-> hypothalamus-> periaqueductal grey, ventral tegmental area-> aggressive behaviour

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71
Q

What is homeostasis?

A

• Maintenance of the internal environment of the body within a narrow physiological range

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72
Q

What are the three components of neuronal response coordinated to work towards feeding?

A

• Three components of neuronal response coordinated to work towards feeding
o Endocrine (humoral) response
o Autonomic (visceromotor) response
o Somatic motor response

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73
Q

What is the main energy supply for neurons?

A

Glucose

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74
Q

What happens if there is a disruption of glucose supply to the brain?

A

o If have disruption of glucose supply to the brain, become unconscious very quickly: homeostatisis of glucose important to keep brain active

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75
Q

What is the prandial state and what type of chemical reaction characterises it?

A

• Prandial state- fed state (anabolism)

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76
Q

Describe what occurs during the prandial state

A

o Full intestines
o Nutrients are absorbed into the blood
o Majority of energy is stored in glycogen in liver and skeletal muscles
o Excess energy stored in adipose (fat) tissue
o Some glucose is given to neurons

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77
Q

What is the postabsorptive state and what type of chemical reaction characterises it?

A

• Postabsorptive state- hungry state (catabolism)

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78
Q

Describe what occurs during the postabsorptive state?

A

o Empty intestines
o Glycogen is released from liver and triglycerides are broken down to provide nutrients for energy
o Glucose is given to neurons

79
Q

What is the body weight of a mouse whose energy intake= energy expenditure

A

• If energy intake= energy expenditure, normal body fat will ensue

80
Q

What is the body weight of a mouse whose energy intake is higher than energy expenditure

A

• If energy intake> energy expenditure, obesity will ensue as fat is not used in postabsorptive state

81
Q

What is the body weight of a mouse whose energy intake is lower than energy expenditure

A

• If energy intake< energy expenditure, starvation will ensue as no regeneration of adipose tissue occurs

82
Q

What type of behaviour does low leptin drive?

A

• Low leptin drives feeding behaviour

83
Q

What type of behaviour does increased leptin drive?

A

• Increased leptin decreases feeding behaviour and increases energy expenditure

84
Q

What is the dual-centre hypothesis of the hypothalamus and feeding? Is it still used?

A

• The lateral hypothalamus is the feeding centre
o Activation drives eating
o Inhibition results in starvation
• The ventromedial hypothalamus is the satiety centre
o Activation drives satiety
o Inhibition results in obesity
• The dual-centre hypothesis is now considered to be overly simplistic

85
Q

What is the role of the arcuate nucleus in feeding?

A

• Arcuate nucleus can detect levels of leptin in the blood and inform the hypothalamus about the level of leptin in the body

86
Q

Describe the location and structure of the arcuate nucleus

A

o Located at the base of the third ventricle (median eminence)
o Contains specialised layer of ependymal cells that are able to sample substances in the CSF and the blood called tanycytes

87
Q

What are tanycytes?

A

 Tanycytes- long winding processes which allows substances to be sampled and passed through to neurons in the arcuate nucleus

88
Q

What are circumventricular organs?

A

• Circumventricular organs- areas within the brain where the blood brain barrier is able to sample substances in the circulation and transmit the signals to the brain

89
Q

Describe the effect of increased leptin on the arcuate nucleus and what, in turn, the arcuate nucleus activates to inhibit feeding behaviour in a coordinated manner

A

• Leptin increases activate arcuate neurons that release alpha-MSH and CART peptides
o Project to regions that orchestrate coordinated response of endocrine, autonomic and somatic motor responses
 Paraventricular nucleus of the hypothalamus (endocrine response)
 Brainstem and intermediolateral gray matter of lateral horn of spinal cord (autonomic responses)
 Lateral hypothalamus (somatic motor responses)
• Inhibits lateral hypothalamus-> inhibits feeding behaviour

90
Q

Describe the response of the paraventricular nucleus of the hypothalamus in response to innervation by the arcuate nucleus after detection of increased leptin levels

A

 Paraventricular nucleus of the hypothalamus (endocrine response)
• Activate brainstem neurons and preganglionic neurons of sympathetic autonomic nervous system
• Parvocellular neurosecretory cells transport hormones in axons-> trigger the release of hypophysiotropic hormones into hypothalamic-putuitary portal system (a series of blood vessels sitting in infindibulum)-> Stimulate release of ACTH and thyrotropin from anterior pituitary in circulation of the HP portal system-> acts on thyroid gland to increase metabolism (HPT axis) and the adrenal gland to release cortisol that alters carbohydrate metabolism (HPA axis)

91
Q

Describe the response of the brainstem and intermediolateral gray matter of lateral horn of spinal cord in response to innervation by the arcuate nucleus after detection of increased leptin levels

A

 Brainstem and intermediolateral gray matter of lateral horn of spinal cord (autonomic responses)
• Increase in activation of the sympathetic nervous system-> increase heart rate, increase in blood pressure, increase of energy usage
• Increase body temperature through brown adipose tissue thermogenesis

92
Q

What kind of peptides are a-MSH and CART?

A

o Anorectic peptides- diminish appetite

93
Q

What is the hypophysiotropic hormone of the HPA axis relevant to feeding?

A

CRH (corticotropin-releasing hormone)

94
Q

What is the anterior pituitary hormone of the HPA axis relevant to feeding?

A

ACTH (adrenocorticotropic hormone)

95
Q

What is the hormone released by the adrenal gland in the HPA axis relevant to feeding?

A

Cortisol

96
Q

What is the HPA’s axis effect on metabolism?

A
  • Increase in gluconeogenesis in liver

- Increase in carbohydrate metabolism

97
Q

What is the hypopohysiotropic hormone of the HPT axis relevant to feeding?

A

TRH (thyrotropin-releasing hormone)

98
Q

What is the anteriopituitary hormone of the HPT axis relevant to feeding?

A

TSH (thyroid stimulating hormone)

99
Q

What is the hormone released by the thyroid gland in the HPT axis relevant to feeding?

A

Thyroxine (T4) and triiodothyronine (T3)

100
Q

What is the HPT’s axis effect on metabolism?

A

-Increase in basal metabolic rate

101
Q

Describe the effect of decreased leptin on the arcuate nucleus and what, in turn, the arcuate nucleus activates to activate feeding behaviour in a coordinated manner

A

• Effects of decreased leptin levels on the hypothalamus
o Activation of arcuate neurons that release NPY and AgRP
 The arcuate neurons activated during decreased leptin levels are completely different populations with no overlap to those activated during elevated leptin levels
 Opposite to the effects of alpha-MSH and CART
 Inhibits paraventricular nucleus
• Inhibit secretion of TRH and CRH hypophysiotropic hormones
o Reduce TSH and ACTH from anterior pituitary
o Switch off HPA/HPT axes and reduce metabolic rats
 Activates parasympathetic division of ANS
• Lower temperature
• Reduce energy expenditure
 Stimulate feeding behaviour by stimulating lateral hypothalamic area

102
Q

What is the mechanism behind AgRP stimulating feeding behaviour through hypothalamic stimulation in comparison to alpha-MSH?

A

 Stimulate feeding behaviour by stimulating lateral hypothalamic area
• AgRP is an antagonist of the MC4 receptor within the lateral hypothalamus of which alpha-MSH is the agonist
o Alpha-MSH activates MC4 receptor
 When MC4 receptor is activated, get inhibition of feeding behaviour
o AgRP disinhibits MC4 receptor by competing with alpha-MSH
 When MC4 receptor is disinhibited, feeding behaviour is activated

103
Q

What does overall activation of the hypothalamus stimulate?

A

• Overall activation of the lateral hypothalamus results to activation of both neurons intrinsic to the lateral hypothalamus and axons of median forebrain bundle passing through the lateral hypothalamus

104
Q

What neurotransmitters relevant to feeding do neurons intrinsic to the lateral hypothalamus contain and how are they relevant to feeding?

A

o Neurons intrinsic to lateral hypothalamus
 Contain peptide neurotransmitters:
• Melanin concentrating hormone (MCH)
o Projects to motor cortical areas, brainstem (chewing behaviour)
o Tightly linked to feeding behaivours
• Orexin: peptide neurotransmitters
o Projects to cortical regions and brainstem (chewing behaviours)
o Also related to sleep and wakefulness cycles-> may be indirectly linked to feeding behaviour

105
Q

What is the role of neurons intrinsic to the lateral hypothalamus in feeding?

A

 Informs cortex about leptin levels

 Engage somatic motor systems to search for food

106
Q

How does a rise in leptin levels result in inhibition of feeding behaviours and increases of metabolism?

A

• Rise in leptin levels

o Increases alpha-MSH and CART in arcuate neurons-> inhibits feeding behaviour and increases metabolism

107
Q

How does a fall in leptin levels result in stimulation of feeding behaviours and decreases in metabolism?

A

• A fall in leptin levels
o Increases NPY and AgRP in arcuate and MCH and orexin neurons in lateral hypothalamus-> stimulates feeding behaviour and decreases metabolism

108
Q

Is leptin a short-term or long-term regulator of feeding behaviour?

A

• Leptin is more of a long-term regulator of feeding behaviour (time scale= weeks)

109
Q

What does appetite depend on?

A

• Appetite: motivation to eat depends on:
o Time and quantity of last meal
o Satiety signals which peak just after a meal and diminish over period of time
o Orexigenic signals decrease after a meal and and build up as we get hungrier- drives feeding
o Low satiety signal and high orexigenic signal will drive feeding

110
Q

List three satiety signals

A
  • Gastric distension
  • Cholecystokinin
  • Insulin
111
Q

How does gastric distension work as a satiety signal?

A

o Stretched out stomach detected by mechanosensitive fibres in the stomach and are carried to CNS via vagus nerve afferents and terminate in nucleus of the solitary tract

112
Q

How does chloecystokinin work as a satiety signal?

A

• Cholecystokinin
o Neuropeptide in enteric nervous system and walls of the intestine is CCK
o Released when intestine becomes full
o Activates nerve terminals of vagus nerve
o Signals back to nucleus of the solitary tract

113
Q

How does insulin work as a satiety signal?

A 
•	Insulin 
o	Released in 3 phases
	Cephalic phase
•	Food presented
•	Small spike
	Gastric phase
•	Food eaten
•	Small spike
	Substrate phase 
•	Food digesting
•	Huge spike 
o	Acts on hypothalamus the same way as leptin does
	High insulin levels will activate CART and alpha-MSH neurons and decrease feeding behaviour
	On a shorter time-scale than leptin
114
Q

What is a common orexigenic signal? Describe

A

o Grehlin- released when stomach is empty (minutes to hours)
 Orexigenic signal
 Acts directly on hypothalamus and has the opposite effect of leptin

115
Q

What are areas for reinforcement and reward in the brain

A 
•	Areas for reinforcement and reward include:
o	Ventral tegmental area
o	Basal forebrain area
	Nucleus accumbens
o	Medial prefrontal cortex
116
Q

Describe the role of dopamine in feeding

A

• Dopamine and motivation
o Dopamine is responsible for the motivation for reward: dopamine drives motivation
o Actual hedonic part of the reward is not dopamine-depedent
 Dopamine-depleted animals like food but do not want food-> lack motivation to seek food, but enjoy it when available
 Stimulation of dopamine axons-> craving for food without increasing hedonic impact
o Dopamine system drives motivation which can allow organisms to overcome satiety systems

117
Q

Describe the impact of Kennedy 1952’s experiment on the understanding of how feeding is regulated, his procedure and what he hypothesised

A

• Kennedy 1952
o Results:
 If give rats access to unlimited supply, they don’t become obese but maintain their body weight at a normal level
 If starve rats, body weight will increase, but when they are once again given access to free food they will increase their body weight back up to original baseline
 If forcefeed rats to increase body weight above the baseline, when period of forcefeeding is ended the rat will regulate its body weight back to the original level
o Lipostatic hypothesis- the body has a mechanism to regulate the amount of adiposity at a particular set point and it will defend any pertubations away from the set point
 Homeostatic mechanisms maintain a set point
o Proposed that there was a circulating factor in the bloodstream produced by adipose cells which is proportional to fat deposit amount which communicates with the brain

118
Q

Describe the impact of Coleman 1973’s experiment on the understanding of how feeding is regulated, his procedure and what he hypothesised

A

• Coleman (1973)
o Done in a strain of mice which are genetically obese (ob/ob)
o Surgically joined the obese mouse with a normal mouse (parabiosis)
 Share a common blood suuply
o When joined these two mice, obese mouse returned to normal body weight
o Circulating factor in the normal mouse was able to pass to the obese mouse through blood supply
 Regulate feeding in the obese mouse
o Confirmed Kennedy’s lipostatic hypothesis

119
Q

Describe the impact of Jeffrey 1994’s experiment on the understanding of how feeding is regulated, his procedure and his findings

A

• Jeffrey (1994)
o Genotyped ob/ob mouse and found that OB gene product served an endocrine function to regulate body fat stores
 Did leptin replacement experiment in ob/ob mouse and found that leptin therapy decreased body weight
 Was also effective for normal weight mouse- overexpression of leptin led to decrease in body fat so that normal mice were underweight afterwards
o Identified circulating factor which regulates feeding behaviour- leptin
o Released from adipocytes proportionally to amount of adipose tissue
 Leads to reduced appetite and higher energy expenditure
 The more leptin is reduced, the more feeding behaviours are inhibited
o Leptin depletion incites adaptive responses to fight starvation

120
Q

Describe Gibson 2004’s experiment on leptin therapy and the impact of leptin therapy on the wider obese community

A

• Gibson 2004
o Five year old girl with mutation in OB gene was given leptin over four years
o At nine years of age, girl’s body weight was approximately normal
o However, leptin treatment only works for the group of people who have obesity due to an abnormal copy of leptin (mutation in OB gene)
 Very small proportion of people who have obesity (less than 0.5% of cases)
 This is because of leptin resistance- some people who are obese have very high levels of leptin but the brain no longer responds to the leptin

121
Q

Describe the impact of Coleman and Hummel 1969’s experiment on the understanding of why leptin therapy does not work on the general obese population, his procedure and his findings

A

o Implication of study: Leptin treatment only works on people with ob mutation
o Findings
 When surgically joining an ob mouse with a normal mouse, the ob mouse will fluctuate back to normal weight
 When surgically joining a diabetic (db) obese mouse with a normal mouse, the db mouse stayed a constant weight but the normal mouse lost weight to the point of starvation
• db mouse has a very high level of leptin- when join with normal mouse, the normal mouse will reduce its feeding
• However, leptin in db mice do not have desired effect on the brain to reduce feeding in these animals
o Animals are leptin-resistant
 This could be due to downregulation of leptin receptor within the hypothalamus
 When surgically join an ob mouse and a db mouse, the ob mouse loses weight but the db mouse stays constant

122
Q

Describe the impact of Hetherington and Ranson 1940’s experiment on the neuroanatomy of feeding, his procedure and his findings

A

• Hetherington and Ranson 1940-
o Hypothalamus and regions around the pituitary gland is essential for regulating feeding behaviour
o Lesioned areas of the hypothalamus in the rat
 Bilateral regions of the hypothalamus led to adiposity in the rat

123
Q

Describe the impact of Brugger 1943, Anand 1955’s experiment on the neuroanatomy of feeding, his procedure and his findings

A

• Brugger 1943, Anand 1955
o Hyperphagia/obesity
 Activation of the lateral hypothalamus in cats resulted in intense eating of edible and incredible objects

124
Q

Describe the impact of Anand and Brobeck 1951, Anand 1955’s experiment on the neuroanatomy of feeding, his procedure and his findings

A

• Anand and Brobeck 1951; Anand 1955
o Aphagia/starvatioon
 Bilateral lesions of the lateral hypothalamus in rats and cats cause them to stop eating; they refuse to eat even when food is placed in their mouths

125
Q

Describe Olds and Milner’s (1950s) experiment on the neuroanatomy of reinforcement and reward, his procedure and his findings

A

• Olds and Milner (1950s)
o Put animals in cage and when animal pressed lever, they would get electrical stimulation to part of their brain
o Reposition electrodes in the brain in numerous locations to identify which regions in the brain would encourage the animal to press the lever
o Map out regions which were critical in driving behaviour
o Showed that effective sites to encourage behaviour were located in trajectory of dopaminergic axons in the ventral tegmental area projecting via median forebrain bundle to the forebrain
o Drugs that block dopamine receptors reduce self-stimulation
o Animals will lever press for drugs that release dopamine
 Dopamine release in the brain will reinforce the behaviour that causes it

126
Q

What is hypovolemia and what is it caused by?

A

• Hypovolemia-> volumetric thirst

o Decrease in blood volume

127
Q

What is hypertonicity and what is it caused by?

A

• Hypertonicity-> osmotic thirst

o Increase in the concentration of dissolved substances in the blood

128
Q

What two mechanisms is drinking behaviour triggered by?

A

• Results in coordinated endocrine, autonomic and somatic behavioural response by hypothalamus

129
Q

Describe how volumetric thirst is detected and how drinking behaviour is promoted after detection

A

• Subfornical organ (type of circumventricular organ) detects increased angiotensin II
o Subfornical organ detects volumetric thirst, which is thirst due to a reduction of blood volume
 Subfornical organ sits just below the fornix
o Bloodborne angiotensin II signals reduced blood flow to kidneys
• Mechanoreceptors in walls of major blood vessels and heart detect decreased blood pressure
o Activates nucleus of the solitary tract
o Vasopressin (ADH) released
 Acts on kidneys to increase water retention
• Promotes drinking behaviour via activation of lateral hypothalamus

130
Q

Describe how osmotic thirst is detected and how drinking behaviour is promoted after detection

A

• Osmotic thirst- driven by increase in salt within the blood
• Specialised OVLT (vascular organ of lamina terminalis) neurons detect blood hypertonicity
o OVLT is in lamina terminalis
o Water leaves cells by osmosis generating action potentials
• Vasopressin (ADH) release via magnocellular neurosecretory cells targeting the posterior lobe of the pituitary
• Promotes drinking behaviour via lateral hypothalamus

131
Q

Describe the body’s response to decreased leptin in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: Arcuate nucleus
  • Humoral response: Lowered ACTH and lowered TSH
  • Viscermotor response: Increase in parasympathetic activity
  • Somatic motor response: Feeding
132
Q

Describe the body’s response to decreased insulin in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: Arcuate nucleus
  • Humoral response: Lowered ACTH and lowered TSH
  • Viscermotor response: Increase in parasympathetic activity
  • Somatic motor response: Feeding
133
Q

Describe the body’s response to increased angiotensin II in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: Subfornical organ
  • Humoral response: Increased vasopressin
  • Viscermotor response: Increased sympathetic activity
  • Somatic motor response: drinking
134
Q

Describe the body’s response to increased blood tonicity in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: OVLT
  • Humoral response: Increased vasopressin
  • Viscermotor response: Increased sympathetic activity
  • Somatic motor response: drinking
135
Q

Describe the body’s response to increased temperature in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: medial preoptic area
  • Humoral response: lowered TSH
  • Viscermotor response: Increased parasympathetic activity
  • Somatic motor response: panting-seeking cold
136
Q

Describe the body’s response to decreased temperature in terms of:

  • Site of transduction
  • Humoral response
  • Viscermotor response
  • Somatic motor response
A
  • Site of transduction: medial preoptic area
  • Humoral response: increased TSH
  • Viscermotor response: increased sympathetic activity
  • Somatic motor response: shivering-seeking warmth
137
Q

How similar is the neural machinery underlying sexual behaviours, reproductive behaviours and mating behaviours to those regulating eating, drinking and aggression?

A

• The neural machinery underlying sexual behaviours, reproductive behaviours and mating behaviours are similar to those of eating, drinking and aggression
o Regulated by sub-cortical structures
 Ensures success in environment
o Some degree of conscious control by the cerebral cortex

138
Q

Are sexual and reproductive mating behaviours different or similar between males and females? What does this imply?

A

• Sexual and reproductive mating behaviours are different between males and females
o Implies a male brain and a female brain

139
Q

Is the axis between the endocrine system and the CNS unidirectional or bidirectional?

A

• The brain affects the endocrine system and the endocrine hormones affect the brain

140
Q

List the steps in Masters & Johnson 1966’s sexual response cycle

A

o Arousal
o Plateau
o Orgasm
o Resolution

141
Q

Describe the physiological responses of the arousal phase of the sexual response cycle

A

 Increased muscle tone
 HR increase/cutaneous vasodilation
 Vasodilation in clitoris/labia minora
 Breast tissue engorges/vaginal walls swell
 Vasodilation in penis
 Testicles swell/scrotum tightens/lubrication

142
Q

Describe the physiological responses of the plateau phase of the sexual response cycle

A

 Arousal intensifies
 Vagina wells, clitoris hypersensitises and retracts under clitoral hood
 Testicles retract in scrotum
 Respiration, arterial blood pressure and heart rate all increase
 Muscle tension increases and muscle spasm may be triggered

143
Q

Describe the physiological responses of the orgasm phase of the sexual response cycle

A

 Involuntary muscle contractions
 Vagina and uterus have rhythmic contractions
 Muscles in penis base have rhythmic contractions and ejaculate semen
 Respiration, arterial blood pressure and heart rate at maximum increase
 Muscle spasm in feet

144
Q

Describe the physiological responses of the resolution phase of the sexual response cycle

A

 Restoration of normal levels of functioning
 Feeling of fatigue
 Feeling of intimacy
 Rewarding feelings

145
Q

What does the overall hypothalamus regulate in sexual reproduction?

A

• Hypothalamus- regulates the expression of the response cycle
o When it’s expressed
o The contextual cues that lead it to be expressed
o Coordination

146
Q

What does the spinal cord regulate in sexual reproduction?

A

• Spinal cord- mediates sexual response of genitals

o Motor cues

147
Q

What does the cerebral cortex regulate in sexual reproduction?

A

• Cerebral cortex- modulates the hypothalamic regulation of the expression of the response cycle
o This regulation differs between species

148
Q

How many chromosomes do humans have and where do they come from?

A

• 46 chromosomes
o 23 male
o 23 female

149
Q

Describe the genotype that commonly determines males

A

XY

150
Q

Describe the genotype that commonly determines females

A

XX

151
Q

How many genes does the X chromosome contain?

A

 X contains 1500 genes

152
Q

How many genes does the Y chromosome contain?

A

 Y contains 50 genes

153
Q

Is the Y chromosome bigger than the X chromosome?

A

o X chromosome larger than Y

154
Q

What does the SRY encode and where is this gene located? What is it important for?

A

• SRY: gene on Y chromsome, encodes Testis Determining Factor
o Location of SRY on Y chromosome is on the short tail (Yp)
o It is the testes determining factors
o Important in defining phenotypically male characteristics

155
Q

When and by whom was the location of the SRY located and how?

A

o Location of gene discovered by Goodfelllow, Lovell-Badge and colleagues (1990)
 Used transgenic mouse model-> deleting the gene and showing that animals with the Y chromosome did not develop into phenotypically characteristic male body plans

156
Q

Does sex genotype (XX or XY) always predict the corresponding sex phenotype? Give examples

A

• However, the genotype doesn’t always predict the sex phenotype
o Sometimes SRY gene is found on the short tail of the X chromosome, which leads to testes in individuals that are genetically female, leading to a male phenotype
 External genitalia produced by testosterone metabolite DHT would also be a consequence of this genotype
o Sometimes SRY is not present on Y chromosome, so genetically male individuals would have a female phenotype

157
Q

Describe how the SRY determines gonad differentiation

A

• Critical for transition from undifferentiated gonads to adult male/adult female gonads
o Structures in the gonad:
 Mullerian duct
 Wolffian duct
o SRY presence leads to testes determining factor production which leads to:
 Mullerian duct inhibiting factor
• Inhibits vaginal production
 Testosterone
o If don’t have SRY, Wolffian duct degenerates and Mullerian duct develops-> adopts adult female genitals

158
Q

What is hermaphroditism and when does it occur?

A

o Hermaphroditism
 External genitals develop from undifferentiated urogenital structures
 If SRY gene is disfunctional

159
Q

Describe the role of the hypothalamus and its pathway in regulating sex hormone synthesis and release

A

• Hypothalamus regulates anterior pituitary gland via Gonadotropin-releasing hormone (GnRH)
• Anterior pituitary regulates sex hormone release via the gonadotropins LH (luteinizing hormone) and Follicle-stimulating hormone (FSH)
o In males, LH produces testosterone and FSH aids maturation of sperm cells
o In females, LH and FSH cause eostrogen secretion and regulates progesterone

160
Q

What affects the function of sex hormones?

A

• Alteration to cholsterol structure affects function of hormones
o Sex hormones are based on cholesterol structure

161
Q

What is the sex organ of males and what hormones does it release?

A

• Males
o Testes- release androgen
 Testosterone- sudden increase at puberty leads to development of secondary sex characteristics

162
Q

What is the sex organ of females and what hormones does it release?

A

• Females

o Ovaries- secrete estradiol (oestrogen) and progesterone (progestin)

163
Q

Are blood concentrations of sex hormones constant in both males and females? Describe.

A

• Blood concentrations of sex hormones vary
o Male levels fluctuate daily
o Female levels fluctuate in a 28-day cycle

164
Q

When are there high releases of testosterone in males and what is the effect of these releases?

A

• Testosterone
o Early release of testosterone as the testes develop is critical for brain development, and there is an important phase during development prior to birth in which the exposure to testosterone is critical for structural development of the brain
o Period after birth in which exposure of testorone is critical for masculinisation of the brain
o Testosterone increase at puberty also acts on the CNS to activate circuits that have their origin in the hypothalamus

165
Q

When are there high releases of oestrogen in individuals and what is the effect of these releases?

A

• Oestrogen
o Oestrogen release impacts brain development pre-natally and during a critical period after birth
o Impacts masculinisation and feminisation of the brain
 In females, important for feminisation
 In males, important for masculinisation

166
Q

What is the impact of testosterone and oestrogen?

A

• Both act on the hypothalamus to trigger the endocrine system and to shape behaviour that would be appropriate around sexual reproductive behaviours

167
Q

What are the two ingredients for making oestrogen?

A

o Testosterone (androgen) + aromatase-> estradiol (oestrogen)

168
Q

Are androgen and oestrogen receptor concentrations constant in brain regions between males and females? Why/why not?

A

• Men- high concentration of androgens
• Women- high concetration of oestrogens
• Androgen and oestrogen receptor concentrations vary in different brain regions between males and females
o However, brain regions in which you find sex steroid receptors are about the same

169
Q

Where are sex steroid receptors found in the brain?

A

 High concentration of sex steroid receptors in the pituitary gland, the hypothalamus, the periaqueductal grey region and the basal forebrain (nucleus accumbens and septal regions)

170
Q

What does sexual dimorphism in the brain depend on?

A

• Differentiation or dimorphism of brain depends on gonadal hormones and temporal processes

171
Q

Contrast activational versus organisational effects of sex hormone on the brain and how do they happen?

A

o Transient (activational)
 Short-term effects due to puberty cycles
• Hormone is released-> binds to a receptor-> cell responds to the short-term-> cell goes back to its normal activity
o Permanent (organisational)
 Long-term effects that tend to be irreversible
• Characteristically pre-natal, during critical period (around 7-10 days after birth) and during puberty

172
Q

Describe Amateau & McCarthy’s study displaying an organisational effect of sex hormone

A

o Amateau & McCarthy- developmental changes that persist into adulthood
 During the sensitive period, eostregen receptor activation in the preoptic area of the hypothalamus increases prostaglandin E2
 The increase occurs via a COX-2 mechanism and triggers increased dendritic spine numbers
 Administering prostaglandin E2 to females, masculinises their sexual behaviours.
 COX inhibitors (which inhibit an increase of prostaglandin E2 and triggers decreased dendritic spine numbers) administered to males, triggers female sexual behaviours
 These effects persist into adulthood

173
Q

Describe the pathway of steroid influence on neurons

A

o Pathway
 The steroid hormone diffuses through the plasma membrane and binds to an intracellular receptor found in the cytoplasm or on the nucleus membrane
 The receptor-hormone complex enters the nucleus
 The receptor-hormone complex binds a hormone response element (a specific DNA sequence)
 Binding initiates transcription of the gene to mRNA
 The mRNA directs protein synthesis
 Changes can be permanent or transient depending on the timing of their release

174
Q

What is the function of steroid influence on neurons?

A

o Function
 Alter membrane excitability, sensitivity to neurotransmitters, neurotransmitter release
 Modulates functions of various enzymes, channels and transmitter receptors

175
Q

Describe how the sympathetic supply from the spinal cord controls sexual behaviours

A

• Sympathetic supply is critical for orgasm phase of the sexual response cycle
o Intermideal cell column of the upper lumbar ssegment (L1-3) mediates sexual response of external genitalia
 Males- penis
 Females- labia and clitoris

176
Q

Describe how the parasympathetic supply from the spinal cord controls sexual behaviours

A

• Parasympethic supply comes from sacral spinal cord- critical for arousal and preparation of sexual behaviour
o Pelvic splanchnic nerves to reproductive organs

177
Q

What neurotransmitters are vital in controlling sexual behaviours in the spinal cord and what do they do?

A

• Neurotransmitters which all act to relax smooth muscle (parasympathetic) to produce muscular contractions (both males and females) and ejaculations (males) (sympathetic)
o Acetylcholine
o Vassoactive intestinal polypeptide (VIP)
o Nitric oxide

178
Q

Are sexual dimorphisms in the CNS obvious?

A

• Difficult to show sexual dimorphisms in the CNS (between sex differences)
o More differences within males or within females

179
Q

List the sexually dimorphic structures in brains and spinal cords between males and females

A

-Onuf’s nucleus
-Ejaculation centre in the spinal cord
-Ventral premamillary area
-Sexually dimorphic nucleus of the preoptic area
-Interstitial nucleus of the anterior
hypothalamus
-Medial preoptic area: neuronal morphology sex steroid dependent
-Ventromedial nucleus: neuronal morphology sex steroid dependent
-Premamillary region: neuronal morphology sex steroid dependent. Has a relationship to LHRH secretion and sexual responsiveness

180
Q

Describe how Onuf’s nucleus is sexually dymorphic, what it is and where it can be found

A

o Onuf’s nucleus: controls motor neuron pools projecting to genitalia and found in the medial part of the ventral horn of the sacral spinal cord
 Number of motor neurons in males is denser at this section than females due to higher volume of external genital

181
Q

Describe the ejaculation centre in the spinal cord, what gender it’s present in, its location,its composition and what occurs when it is lesioned

A

o Ejaculation centre in the spinal cord- male specific
 Specific groups of L3-L4 cells activated by ejaculation in laminae VII and X of the lumbar spinal cord (specifically in L3-L4)
 Cells have neurokinin 1 receptor for substance P and are galanin positive
 Selective lesions of cell groups abolishes ejaculation, but leaves sexual behaviours intact

182
Q

What are the hypothalamic regions that are structurally and functionally different between males and females

A

• Hypothalamic regions that show structural differences between sexes which also lead to functional differences:
o Medial preoptic area: neuronal morphology sex steroid dependent
o Ventromedial nucleus: neuronal morphology sex steroid dependent
o Premamillary region: neuronal morphology sex steroid dependent. Has a relationship to LHRH secretion and sexual responsiveness

183
Q

What are the hypothalamic nuclei responsible for sexual behaviours?

A

o MPNI- median preoptic nucleus
o VMHvl-ventrolateral part of the ventromedial nucleus of the hypothalamus
o PMv-ventrall premammillary nucleus

184
Q

What are the two reproductive behaviours typical of females and how are they timed?

A

o Proceptive- attract attention of a male for reproduction
 Tightly linked to estrogen cycle and timing
 Only expressed when female can produce offspring- otherwise female will become aggressive to male attention
o Receptive- giving the male physical permission for penetration
o Proceptive and receptive behaviours are timed so damage free sexual reproduction can occur

185
Q

Describe the effect of stimulation of the ventromedial nucleus in females and the role of this ventromedial nucleus in regulating female sexual behaviours

A

• Ventromedial nucleus-
o Activation of estrogen receptors in ventromedial hypothalamic nucleus induce receptivity (lordosis behaviours)
o Proceptive behaviours suppressed by inactivation of the estrogen receptors in the ventromedial hypothalamic nucleus
o Stimulation of the ventromedial hypothalamic nucleus triggered responses in presence of male, but not without (incentive salience)
 Reproductive behaviours will not occur without males
 Motivational state (incentive salience) is captured in the ventromedial hypothalamus
o Direct stimulation and hormonal action of the ventromedial hypothalamic nucleus have similar effects when done under the right cues and context
o Responsible for lordosis and proceptive behaviours in response to tactile stimuli- proximal response system

186
Q

Describewhat happens when there is a lesion of the medial preoptic nucleus in females and how this is different in primates vs rodents

A

o Lesions of the medial preoptic nucleus reduce the threshold for activation of the ventromedial hypothalamus, suggesting it has inhibitory control over receptivity (lordosis) and might be setting the threshold for proceptivity
 Effects on proceptivity are not clear
• Clear demonstration on proceptivity in primates, but no have strong evidence for rodents
o Hence, organisation of proceptivity in primates may be different to that in rodents
 Primates are very responsive to males at a distance (distant incentive salience)-> longer term planning for sexual encounter
• Medial preoptic nucleus may release the ventromedial hypothalamic nucleus at that time to start driving these proceptive/receptive behaviours

187
Q

What is the role of the medial preoptic nucleus in females and what does stimulation of it result in?

A

o Stimulation of medial preoptic nucleus can inhibit proceptive and receptive behaviours in primates
 Planning and getting ready because the cues are appropriate
o Responsible for proceptive/approach behaviours- distal response system

188
Q

Describe the function of the medial preoptic nucleus in males

A

o Essential for male sexual behaviours (evidence lesions and stimulation studies)
 If stimulate medial preoptic nucleus, get stereotyped male specific behaviours
• Can drive motor and motivational components of male response
o Thus, medial preoptic nucleus inhibits female sexual behaviours in males and promote male specific behaviours

189
Q

Describe what happens when you lesion the medial preoptic nucleus vs when you lesion the ventromedial hypothalamic nucleus in males and what this suggests

A 
o	Lordosis (a female-specific behaviour) shown in males, enhanced by medial preoptic nucleus lesions, abolished by ventromedial hypothalamic ventrolateral side lesions 
o	Lesions of the ventromedial hypothalamic nucleus decrease the latency to mount and intromission in rats. They also increase the number of mounts, intromissions and ejaculations
	Suggests that males have some coding of female specific sexual behaviours in the ventromedial hypothalamic nucleus
190
Q

Describe the function of the ventromedial nucleus in males

A

o Essential for female sexual behaviours seen in males

o Thus, lesions of the ventromedial hypothalamic nucleus facilitates male sexual behaviours in males.

191
Q

Describe the role of the prefrontal cortex in male sexual behaviour and what happens when there is a lesion in this area

A

o Prefrontal cortex strongly regulates the ventromedial nucleus of the hypothalamus (vl) and the median preoptic area
o Lesions of the medial and dorsomedial prefrontal cortex result in lengthy delays in the initation of sexual behaviours in the presence of a female
o However, once sexual behaviour has begun, lesioned rats show no differences in the numbers of mounts, intromissions and ejaculations to controls
o Prefrontal cortex changes the incentive salience of the female
 Cortical inputs influence motivation of male for female
 Sets the likelihood of the system working

192
Q

Describe the composition of the ventral premamillary area, when its activated, its role and how it achieves this role, its feminisation and its inputs

A

• Ventral premamillary area
o Contains many LH-RH secreting cells, it is also selectively activated during sexual behaviour
o We know that during development there are sex dependent organisational differences in this region. Estradiol feminises the nucleus.
o It receives significant olfactory/ vomeronasal inputs, so may be a pheromone modulated nucleus
 Vomeronasal- takes information about pheromones and inputs to the hypothalamus to drive reproductive behaviours
 Pheromones are sex-specific
o There is a strong topographic representation of sex specific odour in the premamillary area
 Males and female brain respond differentially in this area to male/female odorants
 Sexually differentiated behaviours can be driven by olfactory cues due to this area

193
Q

Describe how and why the sexually dimorphic nucleus of the preoptic area is different between males and females, its location and its role

A

• Sexually dimorphic nucleus of the preoptic area
o Within the medial preoptic area
o It is 5x larger in males
o Preinatal exposure to testosterone or DSB masculinises the nucleus
o This nucleus is critical for organising male sexual behaviours

194
Q

Describe the location of interstitial nucleus of the anterior hypothalamus, and how it is dimorphic between males and women, as well as its possible role and evidence for this role

A

• Interstitial nucleus of the anterior hypothalamus
o A sexually dimorphic nucleus in the preoptic-anterior hypothalamic region of human brain
o INAH-3: twice as large in men
o INAH-3 in gay men is similar to that in women in humans
 However, there are the same number of neurons in males, it is packing density that differs between gay and straight men
 Could have a role in sexual orientation

NEUR3905 (5 decks)

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