Neuronal Synaptic Transmission Flashcards

(55 cards)

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
Latency period of slow EPSP in sympathetic ganglia
5sec | Duration is 30mins
26
Slow EPSP is noticed in?
corticalneurones,autonomic ganglia,cardiac, and smooth muscles
27
Physiology significance of IPSP
Used to reduce excess signals and abolish unwanted signals
28
NT in IPSP is?
Glycine
29
When does IPSP peak?
1.5msec and crashes exponentially in constant time
30
Reason for slow IPSP
K’s influx | Increase in conductance of K
31
Presynaptic inhibition can be found only in?
CNS
32
Inhibitory NT in presynaptic inhibition is ?
GABAa or GABAb | Gamma amino butyric acid
33
How long can N1 in presynaptic inhibition transmission release gaba for
100msec
34
Gaba agonists can be used to treat?
Multiple sclerosis and spastic spinal cord injury
35
Examples of gaba blockers
picrotoxin,strychnine,bicchulin
36
NT in presynaptic facilitation is?
Serotonin
37
What causes schizophrenia
No one fucking knows
38
Symptoms of schizophrenia
Disordered thinking, reduction in gray matter
39
Schizophrenia effect on dopamine receptors
They increase drastically
40
Treatment for schizophrenia
Dopamine receptors blockers
41
Multiple sclerosis is caused by?
due to formation of plaque by the demyelination of the nerves in the cns without affecting the axons
42
Treatment of multiple sclerosis
treatment is by treating the symptoms | Rational treatment
43
Symptoms of multiple sclerosis includes?
Paraesthias, optic neuritis, motor and sensory disability etc
44
Define paraesthias and optic neuritis
abnormal sensation caused by damage or pressure to peripheral nerves, inflammation of optic nerve
45
Cause of epilepsy
abnormal focus of excitation in cns
46
Treatment of epilepsy
Anticonvulsant
47
Epilepsy involves one or both hemispheres | T/F
T
48
Characteristics of epilepsy
loss of consciousness, systemic jerking of the limb, convulsions,sustained contraction of limbs, momentary loss of motor response
49
Cause of Parkinson’s disease
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
Symptoms of Parkinson’s disease
muscle rigidity, gait disturbance,bradikinesia, impaired autosomal postural
51
Treatment of Parkinson’s disease
injection of L-dopa because dopamine can’t cross the blood brain barrier
52
Brain stem divisions are 3. | List them from top to bottom
Mid brain Pons Medulla
53
Anti-choline esterases slow down the progression of Senile Dementia significantly T/F
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
Alzheimer’s is caused by too much or too little ach??
Too little
55
Citrulline is a by-product of the synthesis of Nitric Oxide from Serine T/F
F