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Psychology Stage 2 > Biological Psychology > Flashcards

Biological Psychology Flashcards

1
Q

Electro-encephalogram (EEG)

A

measures brain activity
many electrodes placed on the scalp
signals are a summation of the activity of many neurons close to the electrode
synchronised activity = large deflections

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2
Q

Hertz (Hz)

A

measure of how many times something happens in 1 second

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3
Q

Why is there EEG wave classification?

A

Exact frequencies of the waves are not consistent so they are grouped into different classes which represent the different states in sleep

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4
Q

beta waves classification

A

13-30 Hz

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5
Q

alpha waves frequency

A

8-13 Hz

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6
Q

theta waves frequency

A

3.5-7.5 Hz

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7
Q

delta waves frequency

A

<4 Hz

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8
Q

REM sleep

A

brain is very active - theta and beta activity
Rapid Eye Movements
loss of muscle tone: paralysis
clear, narrative dreams
(also called paradoxical sleep)

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9
Q

what are the effects of sleep deprivation?

A

compensate by more sleep later (mostly slow wave sleep and REM sleep)
no effect on ability to exercise
clear effect on concentration and cognitive abilities
clear effect on emotional control

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10
Q

evolutionary theory of sleep

A

sleep to conserve energy during the least productive parts of the day
for example humans sleep at night
some species like ducks can sleep one hemisphere at a time to keep a look out for predators

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11
Q

brain recovery theory of sleep

A

which is specifically to explain slow wave sleep
the idea that metabolic breakdown products are cleared during slow wave sleep
so it is the resting and recovery of the brain

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12
Q

memory consolidation theory sleep

A

the idea that the brain needs to do two mutually-exclusive functions so sleep is needed to be able to store memories for the longer term
this is not possible during wakefulness as the brain needs to be aware of its environment at all times so can’t also process memories

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13
Q

REM on brain area

A

Sublaterodorsal Nucleus (SLD) in dorsal pons

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14
Q

REM off brain area

A

Ventrolateral Peri-aqueductal Gray matter (vlPAG) in midbrain

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15
Q

what is the fastest classification of brain waves?

A

beta

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16
Q

what is the slowest classification of brain waves?

A

delta

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17
Q

which stages of sleep are delta waves seen most in?

A

stage 3 and 4 (slow wave sleep)

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18
Q

which brain waves are seen in REM sleep?

A

theta and beta

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19
Q

what type of brain waves are seen in stage 1 sleep?

A

theta

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20
Q

what brain waves are most associated with being awake?

A

alpha and beta

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21
Q

what is a sleep spindle on an EEG?

A

is a distinctive pattern of brain activity that is observed on an electroencephalogram (EEG) during stage 2 of non-rapid eye movement (NREM) sleep. Sleep spindles are characterized by a burst of high-frequency (12-15 Hz) oscillations that last for a brief period of time (usually around 0.5-2 seconds)

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22
Q

what have sleep spindles been said to define?

A

being asleep

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23
Q

is there obvious large deflections on an EEG during REM sleep?

A

NO

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24
Q

what stage of sleep has obvious frequent deflections (where neurons are firing synchronously)?

A

stage 4

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25
Q

how does increase in temperature effect slow wave sleep?

A

it increases slow wave sleep that night if the brain temperature has been higher
- heat increases metabolism in the brain
- study with hair dryer showed more SWS after participants had had head warmed with hair dryer

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26
Q

is the brain affected by ‘mental exercise’?

A

yes, it increases slow wave sleep

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27
Q

what is a study that supports the brain recovery theory of sleep?

A

study in mice found during slow wave sleep the space between cells in the brain increases which helps the brain to metabolise things

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28
Q

according to the memory consolidation theory of sleep why is sleep needed?

A

in order to block out external stimuli so that the brain can focus on storing memories into LTM

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29
Q

what is REM sleep required for according to the memory consolidation theory of sleep?

A

the consolidation of procedural memories and/or emotional memories

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30
Q

what is slow wave sleep required for according to the memory consolidation theory of sleep?

A

consolidation of explicit (consciously recalled - factual and experience based) memories

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31
Q

support for the memory consolidation theory of sleep

A
  • there is more REM sleep during early development (when infants are learning how to do a new of things)
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32
Q

study example that supports the purpose of REM according to the memory consolidation theory?

A

people performed a visual discrimination task (procedural) and then they found:
- people that did not sleep got worse
- people that slept but no REM sleep stayed the same
- people that got REM sleep improved

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33
Q

study example that supports the purpose of slow wave sleep according to the memory consolidation theory?

A

They let some people go to sleep and half of the people stayed awake, none got to REM sleep, they found:
- people got better in the word pair task after having SWS (semantic memory)
- but that they did not get better in the mirror drawing task (supports it is not needed for procedural memory)

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34
Q

what is the activation-synthesis hypothesis (Hobson)?

A

suggests that dreams are a by-product of REM sleep as they brain is replaying things that have happened so it is your consciousness interpreting them

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35
Q

why do we forget dreams?

A

some parts of the brain are suppressed during REM sleep
for example the inferior frontal cortex which is involved in memory
people who have damage in this area of the brain have reported life feeling like a dream

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36
Q

if you see glutamate what should be assumed?

A

excitation

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37
Q

if you see GABA what should be assumed?

A

inhibition

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38
Q

what neurotransmitters are in the monoamine category?

A
  • dopamine
  • epinephrine
  • norepinephrine
  • serotonin
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39
Q

what class of neurotransmitter are glutamate, aspartate, glycine and GABA?

A

amino acids

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40
Q

how do hormones travel in the body?

A

through the bloodstream

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41
Q

how do neurotransmitters travel?

A

from one neuron to the next

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42
Q

can individual neurons fire spontaneously?

A

yes

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43
Q

dorsal

A

top

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44
Q

ventral

A

bottom

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45
Q

rostral

A

front

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46
Q

caudal

A

back

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47
Q

telencephalon

A

all of the cortex

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48
Q

mesencephalon

A

tectum and tegmentum

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49
Q

metencephalon

A

cerebellum and pons

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50
Q

diencephalon

A

thalamus and hypothalamus

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51
Q

myelencephalon

A

medulla

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52
Q

what is the brainstem reticular formation

A

dozens of nuclei running through the medulla, pons and tegmentum with lots of different groups of neurons

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53
Q

where is the Reticular Activating System (RAS)?

A

in the Brainstem Reticular Formation

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54
Q

what is the Reticular Activating System?

A

part of the brain that keeps us awake and alert

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55
Q

what are the 5 different neurotransmitter systems in the brain involved in the sleep-wake cycle?

A

acetylcholinergic
noradrenergic
serotonergic
histaminergic
hypocretinergic

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56
Q

levels of acetylcholine during sleep and waking?

A
  • high in the neocortex during waking
  • high during REM
  • low during slow-wave sleep
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57
Q

what neurotransmitters are in high levels in the brain during REM sleep?

A

acetylcholine

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58
Q

are noradrenaline and norepinephrine the same thing?

A

yes

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59
Q

where is noradrenaline released from?

A

locus coeruleus
(in RAS in Pons)

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60
Q

why is noradrenaline released?

A

usually due to external stimuli, makes us pay attention
(cocaine, amphetamines)

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61
Q

where is serotonin released from?

A

Raphe Nucleus
(RAS in Pons and Medulla)

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62
Q

is serotonin sensitive to external stimuli?

A

no

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63
Q

how to the levels of serotonin fluctuate in the sleep-wake cycle?

A
  • high when awake
  • decreases until very low in REM sleep
  • spikes as soon as you come out of REM sleep
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64
Q

what does serotonin do?

A

influences locomotion and cortical arousal

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65
Q

which two neurotransmitters are incompatible with REM sleep?

A

noradrenaline and serotonin
both must be very low

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66
Q

where is histamine released from?

A

in the tuberomammillary nucleus (in the hypothalamus)

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67
Q

how to the levels of histamine fluctuate in the sleep-wake cycle?

A

-high during waking
-low during sleep

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68
Q

why do anti-histamines put you to sleep?

A

if these drugs get into the brain it will interfere with the histamine from the tuberomammillary nucleus (TMN) which keeps you awake

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69
Q

what is another name for hypocretin?

A

orexin

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70
Q

what does hypocretin do?

A

responds strongly to whether you are hungry or not
used by many excitatory neurons as their neurotransmitter
all things that are only active when we are awake

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71
Q

how do the levels of hypocretin fluctuate in the sleep-wake cycle?

A
  • active during active waking and exploration
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72
Q

where is hypocretin released from?

A

group of neurons in the lateral hypothalamus and has a lot of other excitatory hypocretinergic connections

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73
Q

which brain areas are involved in arousal/ keeping us awake?

A
  • reticular formation
  • locus coeruleus (noradrenaline)
  • raphe nucleus (serotonin)
  • pons (acetylcholine; serotonin)
  • hypothalamus (histamine; hypocretin)
  • basal forebrain (acetylcholine)
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74
Q

which area of the brain actively controls sleep?

A

ventrolateral preoptic area (vlPOA)

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75
Q

where is the vlPOA ?

A

hypothalamus

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76
Q

what is the vlPOA crucial for?

A

sleep induction

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77
Q

what does the vlPOA connect to?

A
  • different brain areas that keep us awake and alert
  • through GABA-ergic (inhibitory) synapses
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78
Q

What is the flip flop for sleep induction?

A
  • when the flip flop is on the vlPOA is actively inhibited
  • because the brain stem and forebrain arousal systems are active (awake)
  • when the flip flop is off the brain stem and forebrain arousal systems are inhibited so
  • the vlPOA is active (sleep)
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79
Q

What 3 things is the sleep-wake flip flop influenced by?

A
  • homeostatic control
  • allosteric control
  • circadian control
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80
Q

What is an example of homeostatic control of sleep?

A

Adenosine

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81
Q

What is adenosine (in relation to sleep)?

A

Adenosine is produced by astrocytes (provide energy to neurons) when they use up their glycogen stores
- increased levels of adenosine cause more delta activity during slow wave sleep
- adenosine has inhibitory effects on neurons

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82
Q

explanations for why adenosine induces sleep?

A
  1. adenosine accumulation inhibits the basal forebrain neurons so when they stop firing it takes away the inhibition from the vlPOA, so the flip-flop will eventually flip
  2. the adenosine directly inhibits the lateral hypothalamus, then if the lateral hypothalamus is inhibited a lot of the other wakeful brain areas will be inhibited
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83
Q

how does a G/A genotype differ to a G/G genotype?

A

G/A genotype individuals clear adenosine more slowly
- so they need around 30 minutes more slow wave sleep

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84
Q

how does a G/A genotype differ to a G/G genotype?

A

G/A genotype individuals clear adenosine more slowly
- so they need around 30 minutes more slow wave sleep

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85
Q

what does the allostatic control of sleep refer to?

A

response to threats to promote wakefulness

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86
Q

hypocretin

A

responds to hunger - a lot released when hungry

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87
Q

how does hunger influence sleep? (allostatic control of sleep):

A

hypocretinergic neurons are inhibited by leptin, a hormone which signals full fat reserves
- so more fat reserves = less sleep-wake cycle will try to keep you awake as you are not in danger of starving
hypocretinergic neurons are stimulated by ghrelin, a hormone signalling an empty stomach
- if you an empty stomach, more likely to stay awake
- wakeful areas are stimulated, vlPOA is inhibited, making it harder to fall asleep

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88
Q

which areas of the stress response stimulate parts of the arousal system?

A
  • sensory stimulation activates hypocretinergic and noradrenergic neurons
  • medial prefrontal cortex has excitatory synapses on these neurons, this brain area is more active when we’re stressed
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89
Q

describe what is meant by the circadian control of sleep

A
  • we sleep better at night than during the day
  • sleep-wake cycles continue without access to day-night information
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90
Q

what does the endogenous clock do?

A

responsible for the sleep-wake cycle

91
Q

what is the most important brain area in the endogenous clock?

A

the suprachiasmatic nucleus (SCN) in the hypothalamus

92
Q

where is the SCN?

A

the hypothalamus
- sits just above the chiasm of the optic nerves

93
Q

when is the SCN most active?

A

during the day
- not as active in the night
- does not necessarily relate to sleep because this is the same in nocturnal animals

94
Q

evidence for the role of the SCN in sleep:

A

the hamster study:
they had mutated hamsters with 25 hour circadian cycles and they transplanted the SCN from these hamsters into hamsters with normal cycles and then their cycles changed to 25 hours with this SCN

95
Q

what does the molecular mechanism of the endogenous clock consist of?

A

2 feedback loops of proteins inside the SCN neuron
-3 period genes (Per1-3)
- 2 cryptochrome genes (Cry1-2)
- Clock and Bmal1 genes (proteins form heterodimer)

96
Q

when does SCN activity peak?

A

at the middle of the subjective day

97
Q

which area of the brain does the SCN excite?

A

the Ventral Subparaventricular zone (vSPZ)

98
Q

which area of the brain does the vSPZ excite?

A

the Dorsomedial nucleus of the hypothalamus (DMH)

99
Q

what does the DMH do (in relation to sleep)?

A

inhibits the vlPOA (inhibits the sleep side)
excites the lateral hypothalamus (excites the wake side)

100
Q

how does the SCN influence the sleep flip-flop?

A
  • SCN excites the vSPZ through synapses and chemical signals
  • the vSPZ then excites the DMH
  • the DMH inhibits the vlPOA and excites the lateral hypothalamus
  • this is the circadian control of sleep-wake
101
Q

what does homeostatic control of sleep refer to? and give an example

A

keeping the body at a stable condition
- adenosine

102
Q

describe the allosteric control of sleep and give an example:

A

response to threats promote wakefulness
- hunger
- stress

103
Q

what does the Cry + Per1 + Per3 protein complex do?

A

inhibit the production of Clock and Bmal1 protein complex

104
Q

what does the Cry + Per2 protein complex do?

A

transcription factor to produce Bmal1

105
Q

what does the inhibition of the Clock and Bmal1 protein complex do?

A
  • inhibits the transcription of the Cry and Per genes
  • is a negative feedback loop
  • as the more Cry and Per is being transcribed and translated then it will be inhibit itself by the high levels inhibiting Clock and Bmal1 complex
106
Q

which gene is constantly being transcribed in the sleep-wake cycle?

A

Clock

107
Q

what is the brain like during REM sleep?

A

very active
theta and beta brain waves
pontine-geniculate -occipital (PGO) waves

108
Q

what does the Sublaterodorsal Nucleus (SLD) do?

A

when neurons in this brain area fire it triggers REM sleep (REM ON)

109
Q

what does the Ventrolateral Peri-Aqueductal grey matter (vlPAG) do?

A

inhibits the SLD so prevents REM sleep (REM OFF)

110
Q

what can the Sublaterodorsal Nucleus also be called?

A

Subcoeruleus Nucleus

111
Q

which brain areas actively inhibit the SLD?

A

Raphe Nucleus and Locus Coeruleus
- when these two are inactive enough then can go into REM sleep
- this is related to the fact that noradrenaline and serotonin need to be low enough for REM sleep

112
Q

how does a cortical EEG look during REM sleep?

A

similar to being awake, very active

113
Q

why does a REM EEG look so active?

A

because REM ON neurons in the SLD activate the acetylcholinergic basal forebrain which makes the EEG have small and fast deflections

114
Q

how does rapid eye movement occur in REM sleep?

A
  • SLD neurons activate the acetylcholinergic pons
  • this activates the Lateral Geniculate Nucleus (thalamus)
  • which then activates neurons in the Tectum (mesencephalon)
115
Q

what brain area is responsible for muscle paralysis during REM sleep?

A

magnocellular nucleus in the medulla

116
Q

how does muscle paralysis during REM sleep occur?

A
  • SLD activates the Magnocellular Nucleus (medial medulla)
  • the long cells go all down the spinal cord and inhibit spinal motor neurons
  • have inhibitory synapses on motor neurons
117
Q

what is insomnia?

A

the inability to fall asleep
- when they do fall asleep it may not be good sleep

118
Q

what is sleep apnea?

A

stopping breathing while you’re asleep
- if CO2 levels in the blood get too high then the body will wake the person up

119
Q

what is narcolepsy?

A

suddenly falling asleep

120
Q

what is cataplexy?

A

a form of narcolepsy
- people may go straight into REM sleep
- can have muscle paralysis whilst fully awake

121
Q

evidence for hypocretinergic system being responsible for narcolepsy?

A
  • study in dogs found they had a specific mutation in a hypocretin receptor
  • in humans usually due to damage in the hypocretinergic system
122
Q

what is likely the cause of narcolepsy?

A

a problem with the hypocretinergic system

123
Q

what is REM sleep behaviour disorder?

A
  • also called REM without Atonia
  • no paralysis during REM sleep
  • acting out dreams
124
Q

what can REM sleep behaviour disorder be due to?

A
  • genetics
  • or damage to brain stem (magnocellular nucleus, neurons aren’t being inhibited)
125
Q

what are symptoms of narcolepsy?

A

cataplexy
sleep attacks
sleep paralysis
hypnagogic hallucinations

126
Q

What hormone signals an empty stomach?

A

Ghrelin

127
Q

What hormone signals full fat reserves (a full stomach)?

A

Leptin

128
Q

female sex chromosomes

A

XX

129
Q

male sex chromosomes

A

XY

130
Q

what is the SRY gene?

A
  • located on the Y chromosome
  • turns the fetal gonads into testes (Testes-Determining Factor)
  • in its absence, gonads will become ovaries
131
Q

which 2 hormones do early testes produce?

A
  • anti-mullerian hormone (defeminising)
  • androgens (masculating)
132
Q

what happens in the absence of anti-mullerian hormone?

A

female internal sex organs develop

133
Q

what occurs in people who have the SRY gene but have issues with the anti-mullerian hormone?

A

they will develop both internal sexual organs

134
Q

what happens when the anti-mullerian hormone is present?

A

male sex organs will develop

135
Q

what is the Wolfian system?

A

male internal sex organs

136
Q

what is the Mullerian system?

A

female internal sex organs

137
Q

which hormone is required to result in male external sex organs?

A

DHT - dihydrotestosterone

138
Q

organisational action of hormones

A

effect remains after the hormone has been removed, often occurs during a sensitive period

139
Q

activational action of hormones

A

effect is reversible, depends on the presence or absence of hormone

140
Q

when do secondary sexual characteristics develop

A

puberty

141
Q

what does androstenedione do?

A

causes hair growth in males and females (in puberty)

142
Q

which neurons are responsible for the onset of puberty and regulation of sex hormones throughout life?

A

GnRH neurons
- Gonadotropin Releasing Hormone neurons

143
Q

why are GnRH neurons inactive before puberty?

A

because GABA/NPY neurons are inhibiting KNDy neurons
and it is these KNDy neurons that stimulate the neurons to release GnRH

144
Q

which neurons are shut down during puberty?

A

GABA/NPY neurons

145
Q

how often is GnRH released?

A
  • GnRH neurons stimulate the release of GnRH on a 2 hour pulse pattern
146
Q

where is the GnRH released from?

A

the hypothalamus

147
Q

what does the release of GnRH do in the posterior pituitary gland?

A
  • causes the release of oxytocin and vasopressin from the posterior pituitary
148
Q

what does the release of GnRH do in the anterior pituitary gland?

A
  • secretory cells in the anterior pituitary release FSH and LH when they detect GnRH
149
Q

what does FSH stand for?

A

follicle stimulating hormone

150
Q

what does LH stand for?

A

luteinising hormone

151
Q

what are gonadotropins?

A

hormones aimed at the gonads
- LH
-FSH

152
Q

what is FSH involved in in males?

A

sperm production

153
Q

what is FSH involved in in females?

A

causes follicles to ripen

154
Q

what is LH involved in in males?

A

the testosterone production feedback system

155
Q

what is LH involved in in females?

A

inducing ovulation and formation of corpus luteum

156
Q

what is aneuploidy?

A

when there is a different number of chromosomes in a haploid cell

157
Q

Turner syndrome sex chromosomes

A
  • only have one sex chromosome, only an X
158
Q

Turner syndrome symptoms

A
  • ovaries don’t develop properly
  • don’t have a period until late
  • short
159
Q

Klinefelter Syndrome sex chromosomes

A

XXY or XXXY

160
Q

Klinefelter Syndrome symptoms

A
  • male genitalia but small testes
  • some female external characteristics
  • tall (3 copies of SHOX gene)
161
Q

what is androgen insensitivity syndrome?

A
  • androgen receptors do not work
  • develop testes because they have the SRY gene
  • so will develop external female genitalia but no internal genitalia apart from testes somewhere
162
Q

5alpha-reductase deficiency

A

causes XY children to be born with female genitalia, but male internal genitalia
- then at puberty they develop male genitalia

163
Q

what does 5alpha-reductase do?

A

turns testosterone into DHT

164
Q

what is DHT crucial for?

A

male prenatal external genital development

165
Q

congenital adrenal hyperplasia (CAH)

A
  • have a non-functioning version of 21-hydroxylase enzyme so can’t make cortisol
  • means that more androgens are being made
  • can have serious health complications
  • causes high levels of prenatal testosterone in girls which can result in ambiguous external genitalia
166
Q

what does 21-hydroxylase do?

A

catalyses the production of cortisol in the adrenal cortex

167
Q

what may happen to CAH girls at birth?

A

they may be assigned male at birth

168
Q

which condition may result in someone being genetically female but assigned male at birth?

A

Congenital Adrenal Hyperplasia (CAH)

169
Q

which condition may result in someone that is genetically male presenting as a typical female?

A

Complete Androgen Insensitivity

170
Q

how does CAH possibly affect toy preference?

A

genetic females show more of a preference for typically male toys

171
Q

what affect does higher prenatal testosterone have on play in children?

A

more stereotypically masculine play behaviours

172
Q

are male brains around 10% larger than females?

A

yes

173
Q

is the female cortex generally thicker than males?

A

yes, means more grey matter

174
Q

gynophile

A

attracted to women

175
Q

androphile

A

attracted to men

176
Q

which area of the brain has been found to be smaller in androphillic men?

A

the sexually dimorphic nucleus (SLD)
- is influenced by prenatal T

177
Q

what is the fraternal birth order effect?

A

if you are male, the more older brothers you have (from the same mother) the more likely you will be to be gay

178
Q

what does the fraternal birth order effect indicate about sexual orientation?

A

that there is likely some genes involved

179
Q

Appetitive sexual behaviour

A

Behaviour aimed at finding and obtaining a sexual partner

180
Q

Consummatory sexual behaviour

A

Behaviour of the sexual act

181
Q

In mammals what detects pheromones?

A

The vomeronasal organ

182
Q

What is androstadienone?

A

It is in men’s sweat triggers alertness, good mood and sexual arousal in women (but poor mood in men)

183
Q

internal motivations of sexual motivation

A
  • hormones
  • brain mechanisms
184
Q

Role of hormones in sexual interest

A
  • Suppression of testosterone (T) reduces sexual interest
  • Studies showing that higher estradiol may increase sexual motivation in women (women more likely to initiate sex during ovulation and before it)
185
Q

What happens to testosterone with the anticipation of sex?

A

It increases

186
Q

Which brain area is important for sexual behaviour in all mammals?

A

Medial Amygdala
- it integrates stimuli and evaluates their sexual salience

187
Q

Why do we lose sexual inhibition when we are drunk?

A

Alcohol affects the prefrontal cortex which is involved in sexual inhibition

188
Q

Which neurotransmitter in the hypothalamus can decrease sexual motivation?

A

Serotonin
- why people on SSRIs report being less interested in sex because these drugs increase serotonin levels

189
Q

Which neurotransmitter do pre-ganglionic and post-ganglionic neurons use in the parasympathetic NS?

A

Acetylcholine

190
Q

Which receptors are found at the pre-ganglionic neurons?

A

Nicotinic

191
Q

Which receptors are found at the post-ganglionic neurons?

A

Muscarinic

192
Q

Which nervous system is involved in excitement during sexual activity?

A

Parasympathetic nervous system

193
Q

What does the parasympathetic NS do during sexual activity?

A
  • excitement (erection etc.)
  • relaxes smooth muscle so that more flood can flow in to these areas
194
Q

Which brain areas are involved in the control of sexual arousal?

A
  • Medial Amygdala
  • ACC
  • Insula activate hypothalamus

Both excitatory and inhibitory inputs to the sacral spinal cord

195
Q

Which nervous system is involved in orgasm?

A

Sympathetic nervous system

196
Q

How is the sympathetic NS involved in sexual activity?

A
  • need the sympathetic nervous system to be active for orgasm
197
Q

Which neurotransmitter is used by the pre-ganglionic neurons in the sympathetic NS?

A

Acetylcholine
On nicotinic receptors

198
Q

Which neurotransmitter is used by the post-ganglionic neurons in the sympathetic NS?

A

Noradrenaline

199
Q

How is an orgasm triggered?

A

By both local stimulation and central input
- the posterior pituitary gland that releases oxytocin

200
Q

How is the sympathetic nervous system involved in orgasm?

A

The action of the sympathetic NS along with the release of oxytocin results in a series of smooth muscle contractions in the pelvic floor

201
Q

How is an orgasm inhibited under normal conditions?

A

Nucleus paragigantocellularis (nPGi) in medulla inhibits orgasm circuitry in lumbar spinal cord (neurotransmitter: serotonin)

202
Q

What happens during sex to disinhibited orgasm?

A

During intercourse, hypothalamus inhibits the peri-aqueductal gray (PAG), which normally stimulates nPGi

203
Q

Which hormones are released during orgasm?

A

Oxytocin and prolactin

204
Q

What does prolactin do after orgasm?

A

Suppresses sexual motivation after orgasm

205
Q

How is oxytocin involved in sexual activity?

A

Oxytocin is involved in pair-bond formation

206
Q

Agonist at the synapse level

A

mimics action of the neurotransmitter

207
Q

Antagonist at the synapse level?

A

blocks action of the neurotransmitter

208
Q

Agonist at the receptor level?
(Effect on the receptor)

A

When an agonist binds to the receptor it does the same thing that the neurotransmitter would do

209
Q

Antagonist at the receptor level?
(Effect on the receptor)

A

When an antagonist binds to the receptor it blocks the neurotransmitter from binding or would stop the receptor from responding

210
Q

What is the fastest method to get a drug into the bloodstream

A

Intravenous- injecting

211
Q

Which method of drug intake is almost as quick as injecting?

A

Smoking

212
Q

What is the slowest method of getting a drug into the blood stream?

A

Ingesting - through the digestive tract

213
Q

What do drugs have to be to be able to pass through the blood-brain barrier?

A

Lipid soluble

214
Q

Water soluble molecules in the blood

A

can be directly dissolved in the blood, but do not pass through cell membranes

215
Q

Lipid soluble molecules in the blood

A

Lipid-soluble molecules need carriers to transport them through the blood, but can pass directly through cell membranes

216
Q

What does the biological half-life of a drug mean?

A

How long it takes the drug to go from maximum to half of that maximum in the body

217
Q

Why do people develop drug tolerance?

A

It is the bodies attempt to maintain homeostasis
- so the body develops mechanisms and adapts to the drug
- either through better elimination/metabolism of the drug
- or by functional tolerance (receptors changing etc.)

218
Q

Why do withdrawal effects happen?

A

Withdrawal effects are basically the body’s tolerance mechanisms still working without the drug actually being active in the system

219
Q

What are withdrawal effects often like ?

A

The opposite effects of the drug itself

220
Q

What is intro-cranial self-stimulation?

A

Studied in rats:
Implanted electrodes in the brain of the rats and if the rat will press the lever for stimulation in that certain brain area then that suggests that brain area is most likely rewarding

221
Q

Which 2 brain areas were found to be rewarding from the rat studies of intracranial self-stimulation?

A

A lot but we are specifically focusing on:
Nucleus accumbens
Ventral tegmental area

222
Q

What is the Mesotelencephalic Dopamine System?

A

Release of dopamine from the ventral tegmental area (VTA) into the nucleus accumbens is crucial in the reward system
- that is this pathway

223
Q

How is dopamine involved in reward?

A

If you take away dopamine’s action the reward part goes away which shows dopamine must have a crucial role in the connection between stimulation and reward
- study with the rat using a dopamine antagonist and because of this the rats didn’t learn to press the lever

224
Q

What evidence is there that suggests dopamine may not be involved in reward but seeking instead?

A
  • Overtrained rats do not release dopamine upon reward ( already used to pressing the lever for food etc. )
  • Dopamine increases in rats when they are put into a new environment

Psychology Stage 2 (6 decks)

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