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PHG 203 > Neuronal Synaptic Transmission > Flashcards

Neuronal Synaptic Transmission Flashcards

1
Q

Difference between orthodromic and antidromic conduction

A

Ortho moves in the right direction and always gets to its destination no matter the hurdles it has to cross

Anti goes the wrong way and dies out fast

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2
Q

Rough ER can be found in which parts of a neurone

A

Soma and dendrites but not axon

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3
Q

Structure of synapse in the cerebral and cerebellar cortex

A

Axodendritic

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4
Q

Structure of synapse in the cerebellum and autonomic ganglia

A

Axosomatic or axodendritic

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5
Q

Chemical synapse increase or decrease based on use or experience
T/F

A

T

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6
Q

How many synapses are in the CNS

A

2 x 10^14

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7
Q

Division of the synapses in cerebral cortex

A

98% on dendrites (received 8k nerve endings)

2% on soma ( receives 2k nerve endings)

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8
Q

Examples of dense vesicles

A

NE, EPI, dopamine

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9
Q

Location of active zones on the presynaptic nerve terminal

A

On the subsynaptic membrane

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10
Q

Location of Ca channels on the presynaptic nerve terminal

A

Active zones of the subsynaptic membrane

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11
Q

Size of synaptic cleft in EPSP

A

20-40nm

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12
Q

Contents of the synaptic cleft of EPSP

A

Enzymes that breakdown NTs
By-products of NTs
CSF

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13
Q

Location of receptors on the post synaptic cell

A

Subsynaptic membrane of post synaptic cell

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14
Q
    • -+ -= post synaptic density
A

Receptors , enzymes, proteins

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15
Q

Function of neurexins

A

bind pre terminal to post cell;protein to receptor

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16
Q

What guides and binds the vesicle to the cell membrane

A

V-snare protein synaptobrevin

T-snare protein syntaxin

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17
Q

What’s the kiss-and-run discharge in neuronal transmission

A

contents leave through a small hole in the active zones and this hole closes up immediately after NT passes through

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18
Q

Relate one EPSP to threshold and rmp

A

It’s above rmp but below threshold

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19
Q

Time between:
Stimulation and response
To reach peak
To crash

A

0.5
1.5
3 msec

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20
Q

EPSP obeys all or none law

T/F

A

F. It doesn’t

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21
Q

Spatial summation of EPSP

Temporal summation of EPSP

A

S: more than one adjacent knobs needs to be stimulated at the same time
T: just one adjacent knobs need to be stimulated repititively

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22
Q

Lesser the duration of EPSP the less the opportunity for summation
T/F

A

T

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23
Q

What causes slow EPSP

A

Closure of K gates

Reducing conduction of K

24
Q

Latency period of slow EPSP generally

A

100-500msec

Duration is a few seconds

25
Q

Latency period of slow EPSP in sympathetic ganglia

A

5sec

Duration is 30mins

26
Q

Slow EPSP is noticed in?

A

corticalneurones,autonomic ganglia,cardiac, and smooth muscles

27
Q

Physiology significance of IPSP

A

Used to reduce excess signals and abolish unwanted signals

28
Q

NT in IPSP is?

A

Glycine

29
Q

When does IPSP peak?

A

1.5msec and crashes exponentially in constant time

30
Q

Reason for slow IPSP

A

K’s influx

Increase in conductance of K

31
Q

Presynaptic inhibition can be found only in?

A

CNS

32
Q

Inhibitory NT in presynaptic inhibition is ?

A

GABAa or GABAb

Gamma amino butyric acid

33
Q

How long can N1 in presynaptic inhibition transmission release gaba for

A

100msec

34
Q

Gaba agonists can be used to treat?

A

Multiple sclerosis and spastic spinal cord injury

35
Q

Examples of gaba blockers

A

picrotoxin,strychnine,bicchulin

36
Q

NT in presynaptic facilitation is?

A

Serotonin

37
Q

What causes schizophrenia

A

No one fucking knows

38
Q

Symptoms of schizophrenia

A

Disordered thinking, reduction in gray matter

39
Q

Schizophrenia effect on dopamine receptors

A

They increase drastically

40
Q

Treatment for schizophrenia

A

Dopamine receptors blockers

41
Q

Multiple sclerosis is caused by?

A

due to formation of plaque by the demyelination of the nerves in the cns without affecting the axons

42
Q

Treatment of multiple sclerosis

A

treatment is by treating the symptoms

Rational treatment

43
Q

Symptoms of multiple sclerosis includes?

A

Paraesthias, optic neuritis, motor and sensory disability etc

44
Q

Define paraesthias and optic neuritis

A

abnormal sensation caused by damage or pressure to peripheral nerves, inflammation of optic nerve

45
Q

Cause of epilepsy

A

abnormal focus of excitation in cns

46
Q

Treatment of epilepsy

A

Anticonvulsant

47
Q

Epilepsy involves one or both hemispheres

T/F

A

T

48
Q

Characteristics of epilepsy

A

loss of consciousness, systemic jerking of the limb, convulsions,sustained contraction of limbs, momentary loss of motor response

49
Q

Cause of Parkinson’s disease

A

caused by lesion on the nerve terminal of the nigro -striatum pathway of the substantial nigra
-making the substantial nigra to not produce enough dopamine to inhibit the striatum of basal ganglia leading to
Low inhibitory dopaminergic function and
Excess excitatory cholinergic function

50
Q

Symptoms of Parkinson’s disease

A

muscle rigidity, gait disturbance,bradikinesia, impaired autosomal postural

51
Q

Treatment of Parkinson’s disease

A

injection of L-dopa because dopamine can’t cross the blood brain barrier

52
Q

Brain stem divisions are 3.

List them from top to bottom

A

Mid brain
Pons
Medulla

53
Q

Anti-choline esterases slow down the progression of Senile Dementia significantly

T/F

A

F. F

Senile Dementia is Alzheimers. Even though the condition is related to a reduced concentration of Acetylcholine within the CNS and anticholine esterases would otherwise increase the concentration of Ach by preventing its degradation, it has been shown to not have any effect on the progression of Alzheimers.

54
Q

Alzheimer’s is caused by too much or too little ach??

A

Too little

55
Q

Citrulline is a by-product of the synthesis of Nitric Oxide from Serine

T/F

A

F

PHG 203 (22 decks)

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