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Neuro Part 1 > Lecture 9+10 +DLA 14 > Flashcards

Lecture 9+10 +DLA 14 Flashcards

1
Q

traditional criteria for neurotransmitters

A
  1. synthesized by presynaptic neurons
  2. stored in preparation for release
  3. released by presynaptic neurons in a Ca dependent way
  4. have a special receptor
  5. mechanism for removal from synapse
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2
Q

Dopamine transport and removal (catecholamine)

A
  1. dopamine is synthesized from tyrosine
  2. Reuptake-1 actively transports DA into presynaptic neuron
    some is loaded into vesicles and some is metabolized by MAO
  3. Reuptake-2 actively transports DA into the postsynaptic neuron for metabolism by COMT

Remaining synaptic DA diffuses and is absorbed by blood for peripheral metabolism

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3
Q

norepinephrine transport and removal (catecholamine)

A
  1. DA enters the vesicle and is converted to NE by dopamine beta hydroxylase
  2. Reuptake-1 actively transports NE into presynaptic neuron
    Some NE reloaded into vesicles
    Remainder metabolized by MOA
  3. Reuptake-2 actively transports NE into postsynaptic cell for metabolism by COMT

Remaining synaptic NE diffuses and is absorbed by blood for peripheral metabolism

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4
Q

epinephrine transport and removal (catecholamine)

A
  1. NE leaks into the cytoplasm where is is converted to epinephrine by PNMT
  2. Reuptake-1 actively transports epinephrine into presynaptic neuron
    Some E reloaded into vesicles
    Remainder metabolized by MOA
  3. Reuptake-2 actively transports epinephrine into postsynaptic cell for metabolism by COMT

Remaining synaptic epinephrine diffuses and is absorbed by blood for peripheral metabolism

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5
Q

serotonin (indolamines)

A

synthesized from tryptophan

Serotonin actively transported into vesicles for storage and then release

Synaptic serotonin can undergo reuptake or metabolism by monoamine oxidase to 5- hydroxy-indoleacetyldehyde

Aldehyde dehydrogenase then converts 5-
hydroxy-indoleacetyldehyde to 5-hydroxyindoleacetic acid for urinary excretion

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6
Q

synthesis and removal of glutamine (AA neurotransmitter)

A

synthetic pathway 1:
Krebs cycle (alpha oxoglutarate transaminase yields glutamine)
starts with glucose

synthetic pathway 2:
glutamate recycling
glutamine is converted to glutamate by the astrocytes and neurons working together; can go through vesicular reloading

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7
Q

synthesis and removal of GABA (AA transmitter)

A

Glutamine can be converted to GABA
(glutamine to glutamate to GABA)

after release GABA receptors can reuptake and glia can take up GABA to form glutamine

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8
Q

synthesis and removal of glycine (AA transmitter)

A

Glycolysis of glucose yields 3- phosphoglycerate and subsequently serine

Serine transhydroxymethylase folatedependently converts serine to glycine

Membrane-spanning transporters take up synaptic glycine

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9
Q

synthesis and removal of ACh

A

Choline retrieved from the synapse interacts with acetyl coenzyme-A in presence of ACh transferase to yield ACh

ACh enters vesicles

ACh esterase hydrolyzes ACh (choline can be taken up for reuse)

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10
Q

low molecular weight synthesis of transmitters

A

synthesized in the cytosol

load into vesicles (small and clear)
vesicles are tethered awaiting release

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11
Q

high molecular weight synthesis of transmitters

A

propeptides synthesized in the somata

loaded into large dense-core vesicles with cleaving enzymes

peptide-containing vesicles are stored farther from release sites compared to the small clear vesicles

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12
Q

synthesis, removal, and function is histamine

A

histamine is derived from histidine by histidine decarboxylase

removed by histamine methyltransferase and diamine oxidase; forms acids and excreted in urine

function:
can be inhibitory or excitatory

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13
Q

The hypothalamic tuberomammillary nucleus

A

the major aggregation of histamine producing neurons

innervate cortex, hypothalamus, posterior pituitary, cerebellum, medulla, and spinal cord (histaminergic)

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14
Q

H1 receptors

A

increase excitability by suppressing activity of potassium channels

excitatory

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15
Q

H2 receptors

A

receptor activation stimulates protein kinase activation which inhibits calcium activated potassium channels

excitatory

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16
Q

H3 receptors

A

receptors are negatively coupled to adenylate cyclase. Subunits of the G-protein also suppress voltage-gated calcium channels to decrease transmitter release

inhibitory

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17
Q

beta endorphin

A

synthesis:
arises from anterior and intermediate pituitary and the arcuate hypothalamic nucleus (RER)

degraded by peptidases

inhibitory at most synapses in the medulla and spinal cord
(opioid peptides are important in pain regulation)

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18
Q

Enkephalins

A

originate from spinal and caudal bulbar neurons

degraded by peptidases

inhibitory at most synapses in the medulla and spinal cord

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19
Q

substance P

A

Synthesized in peripheral unmyelinated nociceptive
fibers

Released into spinal dorsal horn and spinal nucleus of the trigeminal nerve

inhibited by serotonin and norepi

degraded by peptidases

inhibitory and excitatory

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20
Q

electrical synapses

A

synchronize electrical signal activity among cells

mediated by cap junctions
voltage sensitive
intracellular communication

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21
Q

chemical synapses

A

most common

neurotransmitters are released into the synapse to lead to a reaction.

synapses can change to mediate learning

22
Q

what are the different kinds of chemical synapses?

A

axodendritic = influence likelihood of AP at target cells

axosomatic = often reduce probability of AP at target cell

axoaxonic = diminish magnitudes of AP’s and thus reduce transmitter release

23
Q

ACh receptors: ionotropic and metabotropic

A

ionotropic = nicotinic
change in ion flux (Na, K)
rapid effects

metabotropic = muscarinic 
metabolic changes (phosphorylation) 
slow effects
24
Q

metabotropic receptors

A

receptor couple to G-proteins

ligand binds and dissociates alpha subunit

alpha subunit can be both excitatory and inhibitory

effects on ions channels, metabolism, gene expression

25
Q

neurotransmitter release

A
  1. activation of Ca channels
  2. fusion of the vesicle and release of the transmitter into cleft
  3. diffuse to postsynaptic neuron
  4. transmitter binds
  5. ionic flux or induction of enzyme activity
26
Q

botulism toxin

A

breaks down synaptobrevin, thus no vesicle docking and no ACh release. irreversible.

protease produced by Clostridium botulinum

leads to: 
diplopia (double vision) 
dysphagia 
xerostomia (dry mouth)  
dysarthria (trouble speaking) 
muscle weakness

used for the treatment of dystonia
can be used as botox

27
Q

tetanus toxin

A

from Clostridium Tetani

degrades synaptobrevin
inhibits glycine release
sustained hypertonia
irreversible

28
Q

Beta-bungarotoxin

A

snake venom

binds to actin and cytoskeleton
inhibits the phosphorylation of synapsin 1
no vesicle release

29
Q

aminoglycoside antibiotics

A

neomycin and streptomycin (for example)

Block presynaptic calcium channels (reversible if extracellular calcium increased)
High concentrations can block nAChR

30
Q

lambert eaton syndrome

A

risk factors:
cancer

causes muscle weakness

due to 4-aminopyridine therapy

31
Q

temporal vs spatial summation

A

temporal:
Repeated high-frequency firing by a unitary presynaptic input

spatial:
Activity from different pre-synaptic neurons converge
onto one neuron

32
Q

central cholinergic neurons are for??

A

arousal and memory

33
Q

Alzheimer’s disease treatment

A

nucleus basalis of meynert degenerates

AChE inhibitor (non disease modifying)

34
Q

role of peripheral cholinergic neurons

A

smooth muscle, cardiac, muscle, and gland innervation

Cholinesterase quickly degrades ACh to prevent tetany and desensitization

35
Q

myasthenia gravis treatment and pathology

A

Disrupted cholinergic transmission at neuromuscular junction

Treatment
AchE (esterase) inhibitors

36
Q

overactivation of cholinergic neurons in the periphery

A

salivation
lacrimation
urination
defecation

treatment: atropine (muscinaric antagonist)

37
Q

ionotropic glutamate receptors

A

AMPA and Kainate receptors induce Na/K influx after glutamate binding

EPSP summation unblocks the NMDA channel pore, thus Ca flux

38
Q

seizures and glutamine

A

Heightened release of glutamate through hypersynchronization of neuronal populations

NMDA antagonists can be used to suppress seizures
Reduced influx of calcium

also could use GABA agonists

39
Q

weakness and glutamine

A

Reduced release of glutamate into bulbar and spinal
motor nuclei

(As seen in Upper Motor Neuron Syndrome)

40
Q

anxiety and glutamine

A

Mediated through altered excitability of limbic cells

Treatment:
Benzodiazepines

41
Q

strychnine

A

The alkaloid blocks glycine receptor on lower motor neurons, reducing chloride influx

tetany

reversible

42
Q

effect of tetrodotoxin and saxitoxin

A

inhibit Na channels

43
Q

effect of w-conotoxin

A

block Ca channels

44
Q

role of Neostigmine, Physostigmine, Sarin & Tabun

A

inhibit acetylcholinesterase’s

45
Q

role of Tubocurarine and Alpha- Bungarotoxin

A

inhibit nicotinic receptors

46
Q

what does 4-Aminopyridine inhibit

A

K channels

47
Q

GABAa vs GABAb

A

A:
prolonged opening of the Cl- channels
less chance for AP
anxiolytic drugs

B:
metabotropic
2nd messenger to increase K
slow inhibition

48
Q

D1/ D5 dopaminergic receptors

A

metabotropic

increase cAMP

49
Q

D2-D4 dopaminergic receptors

A

metabotropic

decreases cAMP

50
Q

alpha1/beta1 norepi receptor

A

metabotropic

excitatory

51
Q

alpha2/beta2 norepi receptor

A

metabotropic

inhibitory

52
Q

serotonin receptors

A

5-HT1 and 5-HT5 are inhibitory

5-HT2 = excitatory

5-HT3 = excitatory (ionotropic)

5-HT (4,6,7) = excitatory

all but HT3 are metabotropic

Neuro Part 1 (18 decks)

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