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Synaptic Transmission Flashcards

1
Q

Membrane potential at rest?

A
  • polarized -70mV
  • positive on outside
  • negative on inside
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2
Q

Depolarization?

A
  • Na flows inside and charges become reversed

- positive charge on inside

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3
Q

What do local anesthetics do?

A
  • block entrance of Na into cell, causing it be inactive
  • sensory: pain transmission blocked
  • motor: muscle paralyzed
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4
Q

Repolarization?

A
  • K flows out of the cell and charges return
  • positive outside
  • negative inside
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5
Q

Absolute refractory period?

A
  • membrane is completely inactive

- another stimulus has no effect

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6
Q

Relative refractory period?

A
  • membrane is excitable

- needs stimulus above threshold

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7
Q

Na-K pumps?

A
  • actively pump Na out of the cell, K into the cell

- against concentration gradients

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8
Q

Single cell gradation?

A
  • no gradation

- all or none response

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9
Q

Nerve conduction gradation?

A
  • each individual axon has different threshold
  • full nerve has graded response
  • AP height can increase as stimulus strength increases
  • limit reached when threshold of all axons making nerve have been reached
  • potential for increased nerve conductance
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10
Q

Types of ion channels?

A
  1. Non gated: passive, always open
  2. Gated: active, always open
    - independent from each other
    - open channels are activated= increased conductance
    - closed channels are inactive= decreased conductance
  3. Voltage gated:
    - voltage sensitive
    - operation related to membrane potential inside cell
    - shifts open
    - Na, K, Ca
    - Ca and beta blockers can slow HR
  4. Chemical gated:
    - ligand gated or receptor gated
    - operation dependent upon interaction of biological chemical (NTs) with receptors
    - ligands: ACh or GABA
    - Chloride
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11
Q

Channelopathies?

A
  • diseases caused by genetic defects in ion channels

- some types of arrhythmias and convulsive disorders (epilepsy)

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12
Q

Duration of action potential?

A
  • 15 msec

- all or none

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13
Q

Saltatory conduction?

A
  • signal jumps from small unmyelinated regions called Nodes of Ranvier to another node
  • pathway is myelinated
  • AP propagates
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14
Q

Non propagated action potential?

A
  • nonmyelinated
  • no nodes of ranvier
  • signal is slow and weakly transferred as it moves away from origin
  • occur at junction of nerve terminal and dendrite
  • Multiple Sclerosis (clinical demyelination)
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15
Q

Autoreceptors?

A
  • function as part of negative feedback loop
  • when activated, decreases amount of NT released into synapse
  • prevents over stimulation of post synaptic membrane
  • homeostasis mechanism
  • excessive stimulation of post synaptic membrane causes down regulation and physical dependence
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16
Q

What type of effect is a chloride channel?

A

-inhibitory

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17
Q

Spacial summation?

A
  • multiple presynaptic terminals located at different release NT on one postsynaptic membrane
  • release at exact same time
  • each change of 1mV can be summated to 15 mV, cumulative effect
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18
Q

Temporal summation?

A

-rapid repetitive stimulation from one presynaptic terminal can release sufficient NT to trigger post synaptic potential

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19
Q

Monosynaptic vs polysynaptic transmission?

A
  1. Mono
    - signal across just one synapse
    - very rapid (throw football from point A to B)
    - reflex responses
  2. Poly
    - transmit signals across multiple synapses
    - takes much longer (students passing football along)
    - can be impaired
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20
Q

What you need in order to classify a chemical as a neurotransmitter?

A
  1. must be in nerve terminal
  2. has capacity to synthesize substances and accumulate substance
  3. capacity to store substance
  4. released upon nerve stimulation
  5. causes change at postsynaptic membrane
  6. process to inactive substance
    - catabolic enzymes
    - reuptake mechanism
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21
Q

How many directions can a synapse travel?

A
  • one direction

- presynaptic to postsynaptic

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22
Q

Duration of postsynaptic potentials vs time NT can act on postsynaptic membrane?

A
  • PSP: 15 msec

- NT: hundreds of msec, secs, mins, hours

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23
Q

Amount of voltage needed to change cell activity on postsynaptic membrane?

24
Q

Steps of synaptic transmission?

A
  1. Synthesis of NT
  2. Storage of NT
  3. Release of NT
  4. Binding to postsynaptic receptors
  5. Effect of binding to postsynaptic receptors
    - increased ionic permeability (Na, Cl, K, Ca)
    - interaction with G proteins
    - effect can be stimulatory or inhibitory
  6. Termination of NT activity
    - diffusion
    - enzymatic inactivation
    - reuptake
25
Cholinergic NT synthesis?
- occurs in cytoplasm - anabolic enzyme (choline acetyl transferase) facilitates combination of choline and acetyl CoA - Acetylcholine is formed
26
Where is Choline acetyltransferase synthesized?
- synthesized in perikaryon - transported down axon to presynaptic terminal - large quantity in cytoplasm of cholinergic terminal
27
Where is acetyl CoA synthesized?
synthesized by mitochondria in presynaptic terminal
28
Where does choline come from for NT synthesis?
-enters presynaptic terminal from extracellular fluid via active transport
29
Adrenergic NT synthesis in presynaptic terminal?
1. Tyrosine is converted to DOPA via Tyrosine Hydroxylase (rate limiting, has fixed rate) 2. DOPA is converted to Dopamine by decarboxylase 3. Dopamine is converted to NE by dopamine beta hydroxylase
30
Why is L-DOPA given to parkinson's patients?
-it can cross the BBB whereas DOPA cannot
31
Adrenergic NT synthesis in Adrenal Medulla?
1. NE is converted to Epinephrine by N-methyltransferase - stress hormone - increases cardiac function, relaxes bronchioles, increases blood flow - Glucocorticoids are also released in stress and increase the synthesis and release of Epi
32
Effect of Glucocorticoids?
Increase action of: - Tyrosine Hydroxylase - Dopamine beta-hydroxylase - N-methyltransferase - increase synthesis of Epi
33
Storage of Cholinergic NT?
-ACh stored presynaptic vesicles
34
Storage of Adrenergic NT?
-catecholamines stored in presynaptic vesicles
35
Resting state release of NT?
1. continual release of small quantity of NT to maintain physiologic responsiveness of post synaptic cell 2.
36
Active state release of NT?
1. Arrival of action potential at presynaptic membrane 2. Activation of Na channel (voltage gated) 3. Influx of Na 4. Depolarization of presynaptic membrane 5. Activation of voltage gated calcium channel 6. Influx of Ca (vesicles fuse) 7. Vesicles next to membrane fuse, NT discharged into synapse, called Exocytosis 8. Amount released sufficient to change activity of target cell - contraction of skeletal muscle - reduced beat of heart cell
37
Inhibitory release of NT?
1. Receptors located on presynaptic membrane are auto receptors 2. Autoreceptors decrease release of NT form presynaptic membrane 3. Due to decreased Calcium influx
38
Agonist vs Antagonist binding to postsynaptic receptors?
1. Agonist - mimic NT at its receptor 2. Antagonist - bind to receptor and block it, do not activate it
39
NT binds to postsynaptic membrane and causes opening of voltage gated Na channels?
1. Increase in Na permeability 2. Na channel opens 3. Na influx 4. Depolarization 5. Excitatory Postsynaptic Potential (EPSP) 6. activation of target cell
40
NT binds to postsynaptic membrane and causes opening of voltage gated K channels?
1. Increase in K permeability 2. K channels open 3. Efflux of K (loss of positive) 4. Hyperpolarization (increased negativity on inside of cell) 5. Inhibitory Postsynaptic Potential (IPSP) 6. Inhibition of target cell (same of Cl coming in)
41
NT binds to postsynaptic membrane and causes opening of voltage gated Ca channels?
1. Increase Ca permeability 2. Ca channels open 3. Influx of Ca 4. Exocytosis - EPSP in skeletal muscle contraction - IPSP if calcium dependent K channels open (relaxation of smooth muscle in GI)
42
NT binds to postsynaptic membrane and causes opening of chemical gated GABA channels?
1. Increases Cl permeability 2. Cl channels open 3. Influx of Cl 4. Increased negativity inside cell (hyper polarization) 5. IPSP produced 6. inhibition of target cell
43
Na channels opened?
Excitatory
44
Cl or K channels opened?
Inhibitory
45
Diffusion to terminate NT activity?
- minor process | - small portion diffuses out of synapse
46
Cholinergic enzymatic inactivation of NT activity?
1. Acetylcholinesterase - principal catabolic enzyme - hydrolyzes ACh to Choline and Acetate - very rapid enzyme to break down ACh 2. Butylcholinesterase - found only in small amounts in neurons - more located in liver, other organs and plasma - used to treat Alzheimers
47
Adrenergic enzymatic inactivation of NT activity?
1. Monoamine Oxidase - located on outer surface of mitochondria - catabolizes (by deamination) adrenergic NTs which circulate in blood and those in nerve terminal - MAO-A: prefers 5-HT and NE - MAO-B: prefers Dopamine 2. Catechol-Oxymethyltransferase (COMT) - primarily extracellular - catabolizes (by methylation) NE and Epi released by nerve terminals and Adrenal Medulla
48
Reuptake of NT to inhibit activity?
1. Adrenergic: major process for inactivation of NT | 2. Cholinergic: does not exist
49
Factors affecting activity of CNS?
1. Reduction of synaptic transmission 2. Hypoxia 3. Changes in blood pH 4. Drugs
50
How synaptic transmission is reduced?
1. Exhaustion of NT supply - released faster than it can be replenished - synaptic transmission fatigue 2. Development of IPSP - rapid firing leads to Ca buildup - K channels open - K efflux, hyper polarization 3. Inactivation of Postsynaptic receptors
51
Hypoxia to reduce synaptic transmission?
- CNS need continual supply of O2 | - disruption in circulation for 3-5 seconds will produce unconsciousness
52
Changes in blood pH to reduce synaptic transmission?
- normal pH = 7.4 1. Acidic pH < 7.0 - coma produced 2. Alkaline pH > 7.8 - CNS activated, convulsions - breathe rapidly, CO2 will decrease and pH increases - dangerous for person with epilepsy
53
Drugs to increase or decrease synaptic transmission?
1. stimulate NT action by binding to and activating receptor - amphetamine similar to Epi 2. block receptor and inactivate it
54
GABA-A effect?
- decreases CNS activity - Benzos - non benzos
55
Melatonin effect?
- decreases CNS activity | - Ramelteon (Rozerem)
56
Histamine H1 effect?
- increases CNS activity | - antagonist: Doxepin (Sinequan)
57
Orexin effect?
- increases CNS activity - Narcolepsy: orexin deficient - neuroprotective effect in alzheimers - decreased Orexin receptors in alzheimers patients

SPOM (17 decks)

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