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Neuroanatomy Block 5 > Synaptic Transmission And Neurotransmitters > Flashcards

Synaptic Transmission And Neurotransmitters Flashcards

1
Q

Electrical synapses

  1. Conductance is thru __ junctions
  2. Uni or bidirectional?
  3. Is there a synaptic delay?
A
  1. Gap
  2. Bi
  3. No
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2
Q

Chemical synapse:

  1. Transduce __ impulses into __ signals
  2. Neurotransmitters are __ and __ by neurons
  3. Neurotransmitter release by presynaptic terminal is dependent on __. why?
A
  1. Electrical into chemical
  2. Synthesized and stored
  3. Ca; needed for depolarization
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3
Q

What needs to happen to open the voltage gated Ca channels?

A

AP needs to reach terminal

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4
Q
  1. Ionotropic and metabotropic are types of __synaptic receptors
  2. Ionotropic vs metabotropic?
A
  1. Post

2. Ion= opens an ion channel; metabo=G coupled receptor

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5
Q

How are neurotransmitters removed from the synaptic cleft? (4)

A

Terminal reuptake, glial reuptake, diffuse away or enzymatically transformed to inactive substances

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6
Q

Ionotropic post synaptic receptors:

  1. __ gated ion channels
  2. Open rapidly or slowly?
  3. Stay open for long or short?
  4. Name an excitatory NT
  5. Name 2 inhibitory
A
  1. Ligand
  2. Rapidly
  3. Short
  4. Glutamate
  5. GABA and glycine
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7
Q

Metabotropic:

  1. Slow or fast, why?
  2. Stay open for longer or shorter
A
  1. Slow - G protein coupled receptors show a delayed opening

2. Stay open longer

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8
Q
  1. Difference between EPSP and IPSP

2. Both are caused by opening of what kind of channels?

A
  1. EPSP induces depolarization of postsynaptic membrane; IPSP induces hyperpolarization
  2. Ligand gated
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9
Q
  1. Dominant NTs in CNS
  2. PNS?
  3. 2 common other ones
A
  1. GABA and glutamate
  2. ACh and norepinephrine
  3. Serotonin and dopamine
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10
Q
  1. EPSP receptor activation opens what kind of channels?
  2. How does this lead to depolarization
  3. IPSP receptor activation opens what kind of channels?
  4. How does this lead to hyperpolarization
A
  1. Nonselective cation channels (Na, K, Ca)
  2. Cation influx
  3. Cl or K channels
  4. Move according to gradients - Cl will enter neuron to increase negative charge; K leaves the cell so the membrane moves closer to Keq potential
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11
Q

Hyperpolarization leads to __ membrane excitability

A

Decreased (IPSP)

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12
Q
  1. Temporal summation
  2. Spatial summation
  3. Both result in?
  4. Would spatial summation be increased if the axons being stimulated were close or far from each other
  5. Why are these summations important
A
  1. Stimulating the same axon again and again
  2. Stimulating 2 different axons at the same time
  3. Greater depolarization
  4. Closer = increased
  5. With enough input, they can initiate an AP
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13
Q
  1. Can EPSPs and IPSPs cancel each other out?

2. Give an example using patellar reflex

A
  1. Yes
  2. Stimulating stretch receptor of extensor muscle generates an AP that produces a small EPSP in motor neuron of extensor muscle and IPSP in flexor
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14
Q

5 ways that drugs can affect presynaptic strength?

A
  1. Can increase/decrease the degradation of NT in terminal
  2. Can increase/decrease NT release
  3. Can block NT release
  4. Inhibit NT synthesis
  5. Reduce NT reuptake/degradation
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15
Q
  1. From previous slide, what does Botox do?

2. What do SSRI and AChE inhibitors do?

A
  1. Block NT

2. Reduce NT reuptake or degradation

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16
Q
  1. How do agonist drugs affect postsynaptic?
  2. Antagonist?
  3. Other effect drugs can have on postsynaptic?
A
  1. Evoke same response as NT
  2. Block response to NT
  3. Can alter channel function
17
Q

From last slide, which do Benzos do?

A

Alter the channel function

18
Q

Name what category the following NTs are in:

  1. ACh
  2. Glutamate, GABA, and histamine
  3. Dopamine, epinephrine and NE
  4. Serotonin
A
  1. Cholinergics
  2. Amino acid NTs
  3. Catecholamines
  4. Indolamines
19
Q
  1. Glutamate subsection (another AA)
  2. GABA subsection and its location
  3. Location of histamine neurons and function
  4. Location of catecholamines and indolamines neurons
A
  1. Aspartate
  2. Glycine; spinal cord
  3. Hypothalamus; involved in wakefulness
  4. Brainstem neurons
20
Q

Glutamate:

  1. Originates from?
  2. Uses what 2 receptors for fast excitation
  3. Glutamate __ is implicated in some neurodegenerative disorders
  4. When get it be neurotoxic?
  5. Target of some general __
A
  1. Either alpha ketoglutarate or astrocyte-derived glutamine
  2. AMPA and NMDA receptors
  3. Excitotoxicity
  4. Excess release or poor synaptic clearance
  5. Anesthetics
21
Q

Glutamate:

  1. Ionotropic post synaptic receptors are excitatory or inhibitory?
  2. Metabotropic
A
  1. Excitatory

2. Could be either

22
Q

Glutamate: NMDA receptor

  1. How does this receptor amplify depolarization
  2. Why can overactivation of this receptor be neurotoxic?
  3. What inhibits receptor opening?
  4. 2 drugs that are NMDA antagonists
  5. This receptor is key for
  6. What normally blocks Ca inside the channel?
A
  1. It has a role as a Ca channel
  2. Too much intracellular Ca
  3. Zinc
  4. PCP and Ketamine
  5. Synaptic plasticity
  6. Mg
23
Q

Glutamate AMPA receptors:

  1. What does receptor trafficking do and what is it critical for
  2. What promotes insertion of more AMPA receptors
  3. What effect do inhibitory NTs have on these receptors?
A
  1. Regulates neuronal excitability and synaptic plasticity; learning and memory
  2. Ca influx
  3. Can remove them
24
Q

GABA:

  1. 4 main locations
  2. Involved in what brain functions
  3. Main function of glycine
  4. How is synaptic cleft cleared of GABA
A
  1. Brain, interneurons, projection neurons, and spinal cord
  2. Sensation, memory, mood, etc.
  3. Mediates fast inhibitory transmission in the brainstem and spinal cord
  4. Transporters on presynaptic neuron and astrocytes
25
Q
  1. GABAa receptor is what type
  2. What does it do to the cell and why
  3. GABAb receptor is what type
  4. Difference between GABAb pre and post synaptic receptors
A
  1. Ionotropic
  2. Hyperpolarizes because of Cl- influx
  3. Metabotropic
  4. Pre are inhibitory; post are usually inhibitory but could be excitatory
26
Q
  1. GABA deficiencies lead to neuronal __

2. GABA dysfunction could be a key factor in etiology of

A
  1. Excitability

2. Seizures

27
Q
  1. Excitotoxicity of glutamate can result in
  2. Decreased cholinergic input to cerebral cortex can result in
  3. Decreased dopamine can lead to
  4. Dopamine circuits in striatum and frontal lobe reinforce effects of
  5. Central NE and serotonin systems are involved in
A
  1. Cell death in acute chronic neurologic diseases
  2. Memory loss and confusion
  3. Parkinsons
  4. Addictive drugs
  5. Anxiety and depression
28
Q

Neuropeptides: where are they found and function

  1. Substance P
  2. Orexin (hypocretin)
  3. Name the 3 endogenous opiates
A
  1. Pain related; in spinal cord and peripheral nerves
  2. Regulates hunger and sleep; hypothalamus
  3. Enkephalins, dynorphins, and beta endorphins
29
Q

What are retrograde messengers

Give 3 examples

A

Released from post synaptic neuron to regulate NT release from pre synaptic neurons (typically suppression)

NO, CO and endocannabinoids

Neuroanatomy Block 5 (5 decks)

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