CNS neurotransmitters Flashcards

(61 cards)

1
Q

what are the 2 major types of neurotransmitters?

A

small molecules ( classic neurotransmitters) and neuropeptides

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2
Q

name the three main types and examples of other small molecule ( classical neurotransmitters)

A

acetylcholine (ACh), amino acids ( glutamate, GABA, glycine), biogenic amines ( dopamine, norepi, and epi)

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3
Q

what is special about the amino acid neurotransmitters, glutamate, GABAand glycine?

A

they are in every synapse glutamate is excitatory, and GABA and glycine are inhibitory

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4
Q

what are peptide neurotransmitters important for?

A

transmission and blocking of pain.

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5
Q

what does removal of neurotransmitters from the synapse do?

A

terminate synaptic transmission

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6
Q

the concentration of neurotransmitter w/in the synaptic cleft is tightly controlled via regulation of what 4 processes?

A

neurotransmitter synthesis, packaging, release and removal

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7
Q

where are neuropeptide neurotransmitters made?

A

in the ER

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8
Q

where are small molecule neurotransmitters made?

A

in the presynaptic terminal

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9
Q

ligand gated ion channels are?

A

ionotropic

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10
Q

G-prootein coupled channels are?

A

metabotropic

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11
Q

Metabotropic neurotransmitters are ___________ than ionotropic transmitters

A

slower

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12
Q

1 alpha and 1 beta are required to be what type of receptor?

A

GABA

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13
Q

iontoropic receptors have how many subunits that contain how many transmembrane domains?

A

iontoropic receptors are usually 4-5 subunits that contain 3 or 4 transmembrane domains

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14
Q

metabotropic receptors have how many transmembrane domains?

A

7

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15
Q

what are the major biogenic amine neurotransmitters?

A

dopamine, norepinephrine, serotonin

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16
Q

what is the major neurotransmitter in the neuromuscular junction of the peripheral nervous system and where else is it the major neurotransmitter?

A

acetylcholine which is also the major neurotransmitter in the parasympathetics

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17
Q

where is acetylcholine synapse in the peripheral nervous system?

A

in the ganglia of the visceral motor sys

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18
Q

what are the fmcs of Ach in the CNS?

A

attention, arousal, reward plasticity, enhances sensory fnc upon waking

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19
Q

what is damage to the Ach sys ( cholinergic sys) in the CNS associated w/?

A

memory deficits in alzheimer’s

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20
Q

what does acetylcholinesterase do?

A

it cleaves acetylcholine to acetate and choline ( this occurs in the synaptic cleft in the CNS and in the basal lamina in the periphery

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21
Q

where is achetocholine degraded?

A

in the synaptic cleft

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22
Q

sarin gas and other nerve gases and insecticides which inhibit acetylcholinesterase do what?

A

cause Sch to accumulate resulting in continued depolarization of the postsynaptic cell and leads to muscle paralysis at the neuromuscular junction.

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23
Q

are acetylcholine receptors ionotropic or metabotropic?

A

there are both metabotropic (muscarinic)and ionotropic (nicotinic) Ach receptors

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24
Q

where do ionotropic (nicotinic) acetylcholine receptors act?

A

in the periphery in the neuromuscular junction and also in the CNS

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25
where do metabotropic ( muscarininc) receptors act?
they mediate most Ach effects in the brain and they are involved in autonomic effector organs in the heart, smooth muscle etc.
26
name 2 metabotropic Ach receptor antagonists.
atropine ( cause pupil dialation) scopolamine ( motion sickness)
27
what is myasthenia gravis?
an autoimmune disease in which pts have antibodies against the muscle nicotic ( ionotropic) Ach Receptor leading to decreased receptors in the postsynaptic membrane, expanded synaptic cleft, and shallow junctional folds ( see pg 145)
28
what are the symptoms of myasthenia gravis?
weakness, fatiguability in the arms and legs, difficulty speaking and swallowing, chewing , diplopia, and ptosis
29
how do you treat myasthenia gravis?
by giving CHOLINESTERASE INHIBITORS to prevent the sparse number of Ach receptors the pt has from breaking down. or THYMECTOMY surgically remove the thymus or CORTICOSTEROIDS or IMMUNOSURPRESSANTS - to decrease the autoimmune response to AchRs
30
What is the most prominent transmitter for normal brain fnc (CNS)?
glutamate
31
and in crease in extracellular glutamate can lead to ?
excitotoxicity causing neurons to over excite and die
32
excitotoxicity of glutamate is seen in which medical problems or disease?
strokes, hypoglycemia, trauma, and repeated intense seizures
33
can glutamate cross the blood brain barrier?
no but glutamine can
34
what happens to glutamate in glial cells?
they are converted to glutamine ( for transport out of cells) which prevents the excitotoxicity from occurring
35
what are 3 types of glutamate receptors?
NMDA, AMPA and Kainate
36
what are 3 unique properties of NMDA compared to the other glutamate receptors?
- ca2+ can pass through it - ion flow is voltage dependent because of the Mg2+ binding - glycine binding is required to the open channel
37
where is GABA used in the CNS
in 1/3 of brain synapse , used in interneurons and purkinje fibers of the cerebellum
38
where is glycine used in the CNS?
at synapses in the spinal cord.
39
decreased GABA function can cause?
epilepsy
40
excess glycine can cause ?
neonatal disease characterized by lethargy and mental retardation.
41
glycine is made in nerve terminals from?
serine
42
GABA is made in nerve terminals from?
glutamate
43
where is glutamate made and used in the brain?
all over the place ( everywhere)
44
what are GABA receptor agonists used for?
they are tranquilizers and control epilepsy and can be used to treat panic disorders and anxiety.
45
what is an example of aGABA antagonists?
strychnine ( used in rat poison) it causes overactivity in spinal cord and brain stem leading to seizures
46
where are biogenic amines synthesized in the brain compared to GABA?
the amines are synthesized in specific layers but their receptors are more broadly distributed.
47
are biogenic amines released and removed from nerve terminals by the same means or different means?
by the same means ( they are les reliant on glial cells)
48
are biogenic amines greatly used in the brain?
they are used by relatively few neurons in the brain but they are very important in maintenance of mental health
49
a dopamine input to the corpus striatum is seen in what disease?
parkinson's disease
50
cocaine interferes with the reuptake of what receptors?
dopamine receptors, therefore it raises dopamine levels
51
what is the major fnc of dopamine?
involved in ovation, reward and reinforcement ( this takes place in the midbrain dopamine system)
52
what is the minor dopamine fnc?
it is involved in emotional behavior ( localization of this involvement: in the projections to the cortex)
53
dopamine receptors act by?
activating or inhibiting adenlyl cyclase
54
why are ppl on amphetamines hyped up?
because it inhibits dopamine and norepi transporters causing an increase in release of them.
55
although it is hard to clinically distinguish norepi and serotonin how are they different?
norepi is mood activating serotonin is mood altering
56
what is the dopamine hypothesis?
that too much dopamine leads to psychosis
57
what do anti-psychotic drugs block?
drugs block dopamine receptors
58
what do anti- anxiety drugs (MAO inhibitors and _________)?
block the breakdown of biogenic amines and therefore increase biogenic amines and inhibitors of serotonin receptors
59
what are the 3 classes of anti depressants include?
MAO inhibitors ( biogenic amine receptor breakdown) tricyclic anti-depressants ( block reuptake of Norepi) serotonin reuptake inhibiotrs ( like prozac)
60
how are peptide neurotransmitters removed from the synaptic cleft ?
via degradation by peptidases
61
see chart on 165
see chart