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Midterm 2- Neuro Flashcards

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1
Q

Name 5 motivational states and behavior

A
  1. Hunger- Feed
  2. Thirst- Drink
  3. Cold- Shiver
  4. Rage- Attack
  5. Pain- Avoidance
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2
Q

What type of infection/disease can cause rage?

A

Infected with rabies can produce rage.

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3
Q

What can override the Neocortex and limbic cortex in terms of rage?

A

If there was a reward associated with slap on the face, than it can override the rage from limbic and neocortex

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4
Q

What structure is associated with avoidance in limbic cortex?

A

Cingulate cortex is associated with the emotion of the pain. Somatosensory is associated with location, timings and intensity of the pain. If there is lesion in cingulate cortex, than you will not be bothered by the pain.

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5
Q

Draw the diagram for the interation of hypothamus

A

Limbic -> hypothalamus -> medulla -> Spinal Cortex
Retina -> Hypothamaus
Hypo -> Thalamus OR Posterior pituitory (for Oxytonin) OR releasing inhibitory hormone via Hypophysical portal vein to Anterior pituitory for LH, FSH, etc

Circulating blood acts on hypothalamic osmo, temp gluc, temp, Na, fat/leptin hormone-> Hypo

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6
Q

What is leptin; where is it produced and its relation to obese?

A

Leptin is produced by the fat cells and conveys the size of the fat cells. Obese people probably resistant to leptin

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7
Q

What are the 5 major functions of hypothalamus?

A
  1. receives wide range of sensory input
  2. comapres the info to set point
  3. coordiantes wide range of responses : Auto, Endo and Behavioural
  4. Regulates the internal environment
  5. Coordinates certain motivated behavioural
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8
Q

What is the 7 major function of hypothamus?

A
  1. regulate body temperature
  2. control blood pressure and electrolyte
  3. Regulation of reproduction
  4. Control of energy metabolism
  5. Emergency response to stress
  6. Threatening situation
  7. Control cardia rhythm
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9
Q

What are the Autocrine, endocrine and behavioural response for regulation of body temperature - hypothalamus?

A

Autonomic - metabolic rate, Vasoconstriction
Endocrine- Thyroxin
Behavioural- Shivering, Wear clothes

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10
Q

What are the Autocrine, endocrine and behavioural response for regulation of blood pressure and electolyte - hypothalamus?

A

Autonomic - vasomotor tone
Endocrine- ADH
Behavioural- Drinking

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11
Q

What are the Autocrine, endocrine and behavioural response for regulation of reproduction - hypothalamus?

A

Autonomic - genital response, ejaculation
Endocrine- lactation, mentral cycle
Behavioural- parental behaviour

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12
Q

What are the Autocrine, endocrine and behavioural response for controling energy metabolism - hypothalamus?

A

Autonomic - metabolism (sym) and digestion (para)
Endocrine- none
Behavioural- feeding

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13
Q

What are the Autocrine, endocrine and behavioural response for emergency response to stress - hypothalamus?

A

Autonomic - epi
Endocrine- cortisol
Behavioural- none

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14
Q

What are the Autocrine, endocrine and behavioural response to threatening situation - hypothalamus?

A

Autonomic - pupil dilate, increase BP, HR
Endocrine- adrenaline
Behavioural- Rage/Fear behaviour

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15
Q

What are the Autocrine, endocrine and behavioural response to control cardiac rhythm - hypothalamus?

A

Autonomic - increase BP, HR
Endocrine- ADH
Behavioural- Sleep

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16
Q

Cardiac rhythm for most homeostatic function is controlled by _______

A

Hypothalamus

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17
Q

If you remove basal ganglia, thalamus and cerebral cortex but keep the hypothalamus and brainstem intact, what happens to the function of hypothalamus?

A

the function of hypothalamus would be intact

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18
Q

What is the neural center of Hypothalamus?

A

particular parameter are not contorleld by one neural center. Neuons in limbic, hypothalamus, spinal cord and medulla can control blood pressure

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19
Q

What are the problems with stimualtion/lesion in hypothalamus?

A

Hypothalamus is very small and packed with cells. There are numberous pathways from brianstem and cerebral cortex that pass through hypothalamus. Thus, the result of lesion or stimulation are result of the pathways

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20
Q

Set Point of hypothalamus and what happens when there is damage to set point?

A

compares sensory info with biological set point. Fever would reset the thermo state to higher than normal t emp, thus increase temp and it will incrase even more due to fever. Treatment with advil, tylenol or asprin (not for children)

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21
Q

Describe the feedforward mechanism of Hypothalamus. What are the advantages?

A

Hypothalamus produces mechanism before regulated variable in body has changed. Advantages: 1. Improvement in speed of homeostatic responses. 2. Minimizes the flucutation in regulated variables. If feedforward worked perfectly, there would be no change in regualted variable.

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22
Q

What is controlled by feedforward in hypothalamus? And where do the signals originate from?

A

Body temp, Blood pressure and feeding. These signals originate in limbic cortex

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23
Q

In which three parts do responses to motivational states occur?

A

ANS, Endocrine and Actions

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24
Q

What is ANS?

A

portion of the Nervous system that is responsible for visceral functions of the body

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25
What are the three divisions of ANS
Sympathetic, Parasympathetic, and Gut (Entric)
26
What is the overall function of ANS
control of organ function and maintain homeostasis. It operates in the background (housekeeping gene)
27
ANS exerts its function by controlling what three organs?
Cardiac muscles, skeletal muscles and Glands
28
What are some of the specific functions of the ANS?
Control HR, BP, body temp, GI, bladder, sexual function, etc
29
Compare the Somatic NS with ANS (Name 5 differences)
1. controls the internal enverionment rather than external 2. largly involuntary rathe than voluntary 3. some organs intrinsically active which is regulated by ANS 4. Dual innervations (symp or parasymp) 5. Denervation (loss) of organ - No atropy (Wasting)
30
Draw a diagram of the autonomic reflex arch
Sensor organs (Oxygen, nocioreceptor, Pressure) -> via para/symp afferent pathway) to CNS -> Preganglionic Myelianted B on cell body of post gang -> post gang unmyelinated C -> effector organ (cardiac, skeletal and glands)
31
Describe the 6 characteristics of the autonomic reflex arch
1. Impulses are generated in the visceral sensory receptors : pressure, nocioreceptor and oxygen receptors 2. They are relayed via afferent sym/parasym nerves to CNS 3. The sensory info is processed at various levels within the CNS (spinal cord, brainstem, hypothalamus, cerebral cortex) 4. Info is transmitted via efferent pathway to viscereal effectors (smooth, cardiac or glands) 5. Efferent pathway is made of pre-gang and post gang 5. Pregang all have their cell bodies within CNS; axons mostly myelinated synapse on cell bodies of post gang located outside the CNS; the axons of post gang are mostly unmyelianted C fibers end on visceral effectors
32
Draw the diagram of Whole nerve, Pre gang and psot gng
Check Neuro 15
33
Indicate the differences between Sym and ParaSym based on pre-gang and post-gang size
Sym: short pre and long post ParaSymp: long pre- and short post
34
Name 6 functional features of ANS?
1. Adrenal Medulla: symp innervation is unique. Pre gang axons end directly on cellss of medulla which secrete 80% epi adn 20% nor. Adrenal medulla is a collection of post gang neurons that has evoled as an endocrine gland 2. Distribution to limbs: Most symp post gang re-enter spinal cord via gray ramus and are than redistributed to effector organs: sweat glands, blood vessels and pilorector 3. Antagonist effect: most organs are innervated by syn and para divisions whos actions are antagonist 4. Only symp innervation- most arterial blood vessel, adrenal medulla, sweat galnds, and pilorector muscles 5. Enteric system- controls GI, brain blood flow, and GI, can function independelty from ANS but AND usually moduates enteric system 6. There are more neurons in enteric nervous system than spinal cord. Function- secretion, vaso constriction dilation which controsl fluid movement or gut movement
35
Draw the efferent pathway of Somatic, Symp and Para
Somatic: -> Ach/nicotine - skeletal muscles Sym -> Ach/nicotine-> Ne/abAdrenergic - smooth, cardiac or glands -> Ach/Nicotine (adrenal medulla) -> E(80%) and NE (20% Para -> Ach/nicotine-> Ach/Muscuranic - smooth, cardiac or glands
36
List the 4 characteristics of efferent pathway of pre gang and psot gang axons.
1. All pre-gang are cholinergic 2. Post gang PNS release ANS - thus PNS is totlly cholinergic 3. Most post gang SNS release NE 4. Some post gang Sns release Ach instead of NE a. Post gang fibers to sweat glands secrete ANS b. Post gang vasodilator nerves to blood vessels of skeletal muscles secrete ANS c. Post gang symp to piloerector muscles secrete Ach
37
Name the agonist, Antagnoist, Action and Mehanism for Nicotine Skeletal muscle
Ach/Nicotine; d-Tubocuranic and alpha-Bungarotoxin; ligand gatd; opens K and Na channels and Fast EPSP
38
Name the agonist, Antagnoist, Action and Mehanism for Nicotine ANS Ganglion
Ach/Nicotine; hemamethoniumu; ligand gatd; opens K and Na channels and Fast EPSP
39
Name the agonist, Antagnoist, Action and Mechanism for Muscarinic ANS Ganlia
Ach/Muscurane; Atrophine; GPCR; Modify K and Ca channels and slow EPSP, IPSP
40
Name the agonist, Antagnoist, Action and Mechanism for Adrenergic alpha
NorE; Pentolamine; GPCR, Slow EPSP, IPSP
41
Name the agonist, Antagnoist, Action and Mechanism for Adrenergic beta
EPi; Propanolol; GPCR, slow EPSP, IPSP
42
Namae the 6 features of ANS Trnasmitters
1. The nicotine receptors at ANS ganglion are different than the ones at skeletal 2. Nicotine ganglion recepto is inotropic (fast EPSP) like skeletal 3. Muscuranic receptors also occur at ANS ganglion. Ach act on Nicotine ANS and muscuranic ANS ganglion. 4. Muscaranic and adrenergic receptors are metabotropic (GPCR) 5. There are many types of muscranic, adrenergic receptors. 6. In the ANS, each and NorE are released together with diff peptides to produce wide variety of short-term and long term effects.
43
For Ach at ANS ganglia, provide the rate of transmission and whatis caused.
Nicotine: fast EPSP -> Inititate AP Muscuranic: slow EPSp -> increased excibility Peptidergic: very slow
44
What are the effects of diff subtypes of adrenergic receptor- B1 and B2
B1- increasaed Hr and contractile strength | B2- relaxes smooth muscles in airway
45
If you need a drug that dialtes aiways awithout increasing HR, what type of receptor would you choose?
B2 agonist- Epi
46
Adrena medula stimualtion characteristics
1. releases 80% Epi 2. lasts longer (2mins) 3. has a greater effect on heart becasue Heart has Bi receptors with are strongly affected by epi
47
What is Epi Pen used for and what is the treatment?
During anaphylactic shock (allergic reaction) there is 1. Decrease blood pressure 2. bronchial constriction (Cannot breathe) Treatment: B1 Cardioaccele (increasae HR) B2 Branchodilation Choose to give Epi pen- with caution as too much Epi can cause cardiac arrest
48
What is the mechanism of symp tone in arteries
- arteries have only symp innervation normally: symp and parasymp are continouslly active with 1Ap/Sec (full activation is 20 AP/sec less than somatic NS with is 300 AP/sec) Tone - suppress arteries by 1/2- allows for a single system to increase or decrease activity of stimulated organ increase symp discharge- constriction 20AP/sec decrease symp discharge- dilatin 1Ap/10sec
49
What is the effect of parasymp on different organ?
- organized mainly for discrete localized discharge - rmotes visceral functions concerned with vegetative aspects (housekeeping chores) of day to day living - helps to conserve and restore energy rather than expand energy (slow HR, decrease Bp, promotes digestion - empties bladder and rectum - stimulates male and female sexual organ
50
What is the effect of symp on diff organs?
- Regulates parameters (Bp, temp) in a continous fashion - can discharge as a unit in emergency situations (Attack/defense) This can help body: 1. perform vigorus muscle activity 2. Respond appropriately in states of stress 3. Participate in fight/flight
51
Sym and Para on blood vessels, gut motility, Bladder, Sweat, Sexual function, HR
Blood Vessel- constrict most blood vessel and dialte in skeletal muscles SYM Gut Motility- decrease SYM and increase PARA Bladder- relax SYM and Contract PARA Swear- Increase SYM Sexual function- Ejaculation SYM and Erection PARA HR- Increase SYM and decrease PARA
52
What is shy-Grader syndrome? What is the treatment? and characteristics
- rare progressive disorder where multiple atropy and damage occurs to ANS - there is no cure - Treatement is directed at signs and symptoms Characteristics: 1. Orthostatic hypotension decrease in BP when standing up 2. Reduced sweating (Heat control) 3. Loss of bladder control and bowel control 4. Impotence
53
What are the three parts of the brain that ineract with motor cortex in production of movement?
Basal ganglia (supplemenraty motor cortex), Premotor corex, Parietal Cortex
54
Name the 5 nuclei of the basal ganglia and the neutransmitter that they release
1. Caudate/Putamen (Neostatrium)- release Ach and GABA 2. Internal globullis- GABA 4. Subthalamic Nucleus- GLutamate 5. Substantia Nigra Pars COmp- Dopamine1 + and D2-
55
What are the six features of the Basal Ganglia loop
1. Atleast 4 separate loops from cerebral cortex through thalamus back to cerebral cortex 2. Direct inhibition and indirect via external globullis from putamen to Internal globulus 3. Two inpts to Neostratium from cerebral cortexand substantia Nigra pas imperfecta 4. There are four neutransmitters in cautate/putamen- Dopamine, Acetylcholine, glutamate and GABA 5. Inhibitory GABA reelased from itnernal globullis to thalamus 6. GABA is inhibitory transmitter
56
Name the 4 places on brain that Caudate/Putamen gets singal from, their function and disorder associated with it
1. Motor- Movement- Parkinsons and hungtinsons 2. Occulomoter- Eve movement- fewer saccades- slower 3. Limbic- Emotion- Depression, anxiety 4. Cognitive- Attention, memory, planning - Absentminded, dementia, obsessive compulsive disorder
57
What is the function of basal ganglia for motor loops
- provide continous inhibition whichc prevents unwanted movements - when a movement is to be made, the basal gang selects neutral programs by releasing them from inhibition
58
Whaat is the patholog of parkinsons disease
- loss of dopaminergic neurson in substantia nigra pars compacta - changes balance of activity in direct and indirectp athway
59
What are the other disorders associated with parkinsons disease?
Shuffling gait, masked like face, flexed posture
60
What are the features of parkinsons disease
- resting tremor (not intentional tremor) stops during movement - akinesia (loss of movement) - bradykinesia (slowed movement) - dementia (involvement of frontal cortex) - rigidity- not spaticity, ie. flexonrs and extensors; not velocity depended, lead pipe
61
What are the treatmenet options for parkinson disease
- lesion in internal globulus- improv in specific motor depends on lesion position - Deep brain stimulation to sbthalamicc nucleus or internal globulus abolishs low freq synchronized ossilations in motor cortex by replacing the mwith high - normalizes motor cortex oscillations and improves suymptoms - Use L-Dopa to increase dopamine and decrease acetylcholine (anti-cholinergic)- not a cure but relieves symptoms decreasse dopamine- akinesai and increase dopamine- dyskinesia (involunary movement) - inject stem cells (fetal dopamine) into neostritum
62
What is the pathology of Huntingsons disease
- degeneration of neurons in caudate/putamen | - abnormal repeats of huntingson gene- cell death due to abnormal folding
63
What are the features of huntingson disease
- inheritability - Chorea (decrease input form globulus pallidus - other movement disorder (slurred speech) - dementia (limbic, cognitive) - death - no treatment
64
What is the mechanism of Huntingson disease
Subthalamic nucleus -- (+)--> decrease internal globulus -- (-)---> increase thalamus and increase motor cortex - Increase excitatory will decrease inhibitory internal globus, thus increase activity of thalamus
65
What is hemiballismus
- violent movement of limb due to lesion in subthalamicc nucleus
66
What is the pathology of tourettes syndrome
- increased activity of cognitive prefrontal basal ganglia
67
What is the feature of tourettes syndrome
- inappropriate utterances | - tics (brief, repetitive involuntary movement, eye blinks, head tosses
68
What is MPTP and what are the two positive outcomes ? what was the conclusion about parkinson?
- depletes dopamine levels - developed parkinson symptom - rigidity, resting tremor Outocme: 1. MPTP produces animal model of parkinson 2. hypothesis was produced that parkinso nwill resutl from environemtnal toxicity - large twin study -> most parkinson cases due to environmental cause - chronic exposure n rates to rotenone- organic pesticide- produced features of parkinson disease Conclusion: - both genetic and environmental roel in parkinson
69
Whaat is consciousness andd the two components?
Consciousness- awareness of environment and ones self Two comp: 1. content- memory, perception, attention - cerebral cortex 2. level- awake, alert and asleep- brainstem - retrospinal axon send post-synaptic inhibition to alpha motorneuron of proximal muscle during REM sleep
70
What happens when you stimulate the brainstem or put a lesion?
- stimualte brainstem will lead to wake up sleeping animal | - lesion of brainstel will lead to unconscious animal
71
What is the ascendidng arousal system and what are the 5 neurons?
AAS- arises at midbrain - rostral pons and caudal midbrain 1. Noradrenergic neurons - from locus cerulus control cortical attention 2. Serotonergic neuron- raphe nuclei, failure to cause arousal with decrease carbon dioxide 3. Dopaminergic neuron- reward-based learning, addiction 4. Histaminergic neuron- anti-histamines cause drowsiness 5. Cholinergic neuron- Alxheimers disease - widespread projections - function in modualation of conscious states- including sleep/awake states by acting as neuromodulators that alter the memrbane potential of thalamo-cortical and cortical neuron - depolarization when producing awake state
72
What is coma and what are the two causes?
- prolonged consciousness with no response to stimuli causes: - lesion of rostral brainstem (arousal pathway) - lesion of cerebral cortex eg. decrease oxygen (hypoxia), hematoma (blood clot) produces pressures and damage to cerebral cortex
73
What is locked In-syndrome
- lesion below ascending arousal system- midpons - descending limb adn motor pathway destroyed - forebrain awake and conscious but patients can only interact via eye movement (oculomotor cranial nerve intact)
74
What is persistent vegetative state
- damage to fforebrain (hypoxia) decrease oxygen - chronicc - long term - partial arousal- eyelid movement, saccades, swalloing, moaning - sleep-wake cycel occurs but no outward signs of consciousness
75
Draw the diagrma of primary evokedp otential
Neuro 14
76
What are the properties of primary evoked potential by stimulation of siactic nerve (somatosensory)
1. latency of 20ms (80 ms in visual- 60ms to get out of retina) 2. only recorded over somatosensory cortex if electron is placed on surface
77
What is primary evoked potential
- change in voltage - recorded on oscillations - results from summations of extracellular currents ossicated with postsynaptic potential - not due to local currents assocated with APs
78
What is the difference between slwo wave, alphaa and beta?
Slow wave 1-2 Hz - strongest synchronization - Non-REM sleep Alpha 10Hz - synchronization - lots of neurons firing and depolarizing at the same time Beta 12-30Hz - awake and TEM sleep - not synchronized - low amplitude fast frequency
79
What is the origin of electrical currents associated with EEG
- summation of cortical post synp potentia loccuring in neurosn of neocortex, particularly pyramidal cells - not due to local currents assciated AP
80
What are the uses of EEG?
- lcoation of epileptic focus - location of cortical tumors - diagnosis of sleep disorders - brain machine interface
81
Why sleep?
- memory - restoration - energy conservaton
82
What happens when you have lack of sleep?
- fatigue - impaired memory - decreased cognitive ability (decreased judgement)
83
What are the characteristics of Non-REM Slow wave sleep?
- 70-80% of sleep - diff stages seen in EEG - last stage deep sleep slow waves - children: sleepwalk , talk - dreams can occur (shorter, less visual, emotional) - decreased BP, HR, respiratory rate, temp
84
What are the characteristics of REM paradoxial sleep
= 20-25% sleep (4-6 periods/night) - desynchronized EEG - inhibited musle tone due to spinal inhibition from pons -deep sleep -vividdreams (longer, primarily visual) - rapid eye movement, finger twitch = genital response associated with sexual arousal - large flactuation in HR, BP and resporatory rate
85
What is REM disorder?
- muscle atonia not present due to lesion - act out their dream - present in 50% of parkinson patients - too little brainstem descending postynaptic inhibition to alpha motorneurson

Physiolgoy (4 decks)

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