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Neuroscience > Synaptic Transmission & Neurotransmitters > Flashcards

Synaptic Transmission & Neurotransmitters Flashcards

1
Q

Types of synapses

A

Axodendritic
Axosomatic
Axoaxonic

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2
Q

Axodendritic

A

b/w axon of presynaptic neuron and dendrite of postsynaptic cell

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3
Q

Axosomatic

A

b/w axon of presynaptic neuron and cell body of postsynaptic cell

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4
Q

Axoaxonic

A

b/w axon of presynaptic neuron and axon of postsynaptic cell

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5
Q

Electrical potentials @ synapses

A
  • Axosomatic & Axodendritic generate local post-synaptic potential
  • Axoaxonic modulates membrane potential of the postsynaptic cell (Presynaptic facilitation and inhibition)
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6
Q

Presynaptic Inhibition and Facilitation

A

Axoaxonic synapses regulate presynaptic neurons to release NT by changing Ca++ influx to presynaptic neurons

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7
Q

Presynaptic Inhibition

A

1) Interneuron releases NT
2) NT bind to presynaptic neuron, reduce Ca++ influx
3) Presynaptic neuron releases less NT when an action potential arrives at its terminal

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8
Q

Presynaptic Facilitation

A

1) Interneuron releases NT
2) NT bind to presynaptic neuron, increase Ca++ influx
3) Presynaptic neuron releases more NTwhen an action potential arrives

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9
Q

What is a Neurotransmitter?

A
  • synthesized in the neuron
  • transported to pre-synaptic terminal
  • released in amounts sufficient to exert an action on the post-synaptic neuron or effector organ
  • removed from synaptic cleft by a specific mechanism (Synaptic vesicle cycling)
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10
Q

Function of Neurotransmitters

A
  • excite or inhibit post-synaptic membrane
  • depends on the molecule released and the receptors present
  • act directly = fast acting and short-lived (Ligand gated theory)
  • act indirectly = slow acting
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11
Q

Direct activation: Ligand-gated ion channels

A
  • NT bind to receptors part of the ligand-gated ion channels and directly open the ion channels.
  • Na influx
  • Fast acting
  • “lock and key”
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12
Q

Indirect activation: G-proteins

A
  • NT bind to receptors and triggers action of G-protein
  • G-protein then initiate process to open ion channels
  • changes in the metabolism of the cell
  • slow acting
  • can also cause persistent opening of membrane channels
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13
Q

Signal transmission at G-protein

A

A. In the non-stimulated state, the αβγ–chain is associated with a membrane receptor.

B. NT binds to membrane receptor and activates G-protein. The α-chain detaches from the membrane receptor.

C. The (GTP) binds to membrane-spanning G-protein channel. Channel opens and Na flows in

D. The α-chain is inactivate and release from protein channel. Channel closes and the α-chain returns to its host membrane receptor to bind with the βγ-chain.

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14
Q

What is a Neuromodulator?

A
  • Act at a distance away from the synapse
  • Modulate activity of many neurons @ same time
  • Released into extracellular fluid
  • Last minutes to days
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15
Q

Co-transmission of a neurotransmitter and a neuromodulator

A

Depolarization of pre-synaptic terminal membrane triggers events that result in the simultaneous release of neuromodulator (substance P) into extracellular space and NT (Glutamate) into synaptic cleft.

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16
Q

Medications/Drugs (Exogenous vs. Endogenous)

A

When administered “exogenously”, medications mimic action of endogenously released NT or neuromodulators exactly.

17
Q

Common NT’s and Neuromodulators

A

1) Amino acid: GABA and Glutamate
2) Cholinergic: ACh
3) Amine: DA
4) Peptides: Substance P

18
Q

GABA and Glutamate

A

most prevalent fast-acting neurotransmitters

Ligand-gated channels

19
Q

Amino acid: Glutamate (Glu)

A
  • MAJOR Fast-acting excitatory NT
  • Involved in learning and memory
  • Glutamate is present in a wide variety of foods, e.g. MSG
  • may cause seizures

-Excitotoxicity: Excessive glutamate may produce neuronal damage
Ex) TBI or CVA (Glu is 1000 X higher than normal)

20
Q

Amino acid: GABA

A
  • MAJOR Fast-acting inhibitory NT
  • Prevents excessive neural activity.
  • Barbiturates mimics the action of GABA and are used for sedation or anticonvulsants.
  • Baclofen, a muscle relaxant to control muscle spasticity, increases pre-synaptic release of GABA.
21
Q

Cholinergic: Acetylcholine (ACh)

A

MAJOR NT in PNS, ANS, CNS

Fast-acting effect
-@ neuromuscular junction: (Nicotinic receptors)

Slow-acting effect
-regulate HR, ANS: (Muscarinic receptors)

-Controls…
Locomotion
Arousal
Facilitate attention, memory, learning

22
Q

Nicotinic vs Muscarinic

A

Nicotinic = bind nicotine, link ion channels, fast and brief, @ neuromusclular junction, mediate excitation

Nuscarinic = bind muscarine, linked to 2nd messenger through G-protein, slow and prolonged, @ myocardial muscle, mediate inhibition

23
Q

Amines: Dopamine (DA)

A
  • Produced in substantia nigra pars compacta of BG
  • inhibitory effect in the CNS
  • 2nd messenger systems to suppress the activity of Ca++
  • Affects motor activity, motivation/reward behavior, and cognition
24
Q

Dopamine Projecting System

A 
BG = movement
Limbic = reward/wanting addiction
Prefrontal = working memory and attention
25
Q

Neurologic Conditions: Dopamine

A

Parkinson’s disease

↓DA in basal

26
Q

Schizophrenia

A
  • delusions, hallucinations, disorganized, tangential speech; flat affect
  • catatonia = decrease in spontaneous activity
  • working memory is affected.
  • Abnormalities in limbic system, frontal lobes, and BG
  • S/S improve with antidopaminergic agents
  • NT involved = glutamate, GABA, serotonin, and norepinephrine.
27
Q

Peptides: Substance P

A

-Neuromodulator and NT

Neuromodulator in chronic pain syndrome
-increases pain perception

NT in the nociceptive pathway

-stimulates free nerve endings @ site of injury and transmit pain signals from PNS to CNS

28
Q

Peptides: Endogenous opioids (endorphin, enkephalin, dynorphin)

A

Body’s natural pain killers
Inhibit CNS neurons involved in perception
Exercise increases them!

Neuroscience (11 decks)

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