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Bloc J - Neuro > Oct3 A1-Neurotransmitters > Flashcards

Oct3 A1-Neurotransmitters Flashcards

1
Q

synapses are from where to where

A
  • terminal axon of one neuron
  • dendrite or cell body of another neuron
  • excitatory or inhibitory post synpaptic potentials occur at each synpase + integration of all of them determines the response*
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2
Q

neurotransmitter systems characteristics

A
  • neurons in the brain send axons to communicate with other neurons either locally or at a distance
  • discrete groups of neurons project to specific locations and use the same neurotransmitter
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3
Q

steps of ntr transmission

A
  • AP
  • depol of terminal axon
  • binding of synpatic vesicles
  • ntr release
  • R binding
  • local effects (Rs are either ionotropic = lead to mvmt of ions across the membrane or metabotropic = GPCRs, cause activation of enzymes producing cell changes)
  • ntr metabolized or taken up by the pre-synaptic neuron and or glial cells
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4
Q

ntr life cycle

A
  • ntr is synthesized from a precursor
  • ntr is incorporated in TAKEN UP in a synaptic vesicle
  • vesicle binds and released ntr in the cleft
  • ntr binds its R on post-syn membrane
  • ntr is metab to inactive form IN the cleft or there is REUPTAKE of the ntr in the pre-syn neuron for reuse or metab
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5
Q

what an ntr agonist does

A

stim the R

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6
Q

myasthenia gravis main symptoms

A

ptosis (drooping of eyelid) + facial weakness

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7
Q

MG cause

A

autoimmune dz where Abs are made against nAchRs at the neuromuscular junction (synapse) = loss of nAchRs, damage to post syn memb, weakness

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8
Q

tx of MG

A

pyridostigmine

  • prevents breakdown of Ach by inhibiting the enzyme AchE in the synaptic cleft
  • Ach floats for longer so more time, more chance of finding a R
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9
Q

conditions related to MG

A
  • botulism (caused by toxin of clostridium botulinum (botox) which blocks docking of vesicles to presyn memb)
  • anaesthesia involves sedation (calm or sleep), analgesia (no pain), amnesia (don’t remember) and neuromuscular blockade: the neuromuscular blockers used also bind nAchRs at the NMJ, like botox.
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10
Q

important charact of diseases related to ntr problem (deficiency)

A

may involve multiple structures and ntrs bc ntrs may have multiple functions or act in multiple systems (have multiple locations and Rs)

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11
Q

anatomy relevant to Alzheimer’s disease (AD)

A
  • the basal forebrain has extensive cholinergic projections to the frontal lobes (cortex)
  • frontal lobes (cortex) are imp for cognitive functions like judgment and planning
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12
Q

pathophgy of AD

A

progressive neurodegenerative dz

  • degeneration of neurons in frontal lobes + other areas of the brain (parietal and temporal cortex = where it starts)
  • lack of Ach in the brain
  • eventually affects other ntr systems and other neurons degen
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13
Q

consequence of AD (symptoms)

A
  • impaired cognitive function
  • language and memory symptoms (caused by initial degen in parietal and temporal cortex, where dz starts)
  • dementia*
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14
Q

how we can tx AD (slow the disease)

A
  • use AchEi that act specifically on the AchE variant that is found in the CNS (brain) (not NMJ)
  • increases levels of Ach in the brain
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15
Q

aside from MG (and ptosis) and AD, where is Ach also imp

A

in the ANS

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16
Q

schizophrenia main symptom

A

psychosis

  • abnormality of form and content of thoughts
  • hear hallucinations
  • delusions in term of thoughts
17
Q

schizophrenia pathophysiology

A

increased norepinephrine, serotonin and dopamine

ARE ALL MONOAMINE NTRS

18
Q

tx for schizophrenia

A
  • old one = chlorpromazine = blocks the Rs for the monoamine ntrs
  • new one = reserpine = blocks a transporter needed for UPTAKE of MONOAMINE NTRS in synaptic vesicles
19
Q

main limitation of anti-psychotic tx reserpine and chlorpromazine

A

cause parkinsonism = symptoms that resemble Parkinson’s dz (PD) (also called extrapyramidal sx)

20
Q

way that they found to reverse the parkinsonism caused by anti-psychotics in schizophrenia

A

give levodopa (a dopamine precursor)

21
Q

PD sx

A
  • bradykinesia (slow mvmts)
  • rigidity (not the same as spasticity from UMN lesion. rigidity occurs in extrapyramidal dz like PD)
  • postural instability
  • tremors
22
Q

pathophgy of PD

A
  • depleted dopamine in the basal ganglia
  • many regions of the brain degenerate, including the substantia nigra (basal ganglia structure located in the midbrain) (is pigmented bc of melatonin) Normally, the SN sends axons with dopamine ntr to the putamen which then outputs on thalamus and then cortex (the basal ganglia, which includes the putamen and the caudate nucleus (bilateral paired structure) + the SN and other structures) has diff pathways communication with thalamus and then cortex
23
Q

tx found for PD

A

levodopa (dopamine precursor) (also called L-dopa)

24
Q

example of meds other than levodopa that act to increase dopamine in PD and help sx

A
  • dopamine R agonists

- inhibition of monoamine oxidase B (which degrades dopamine inside the cell)

25
Q

PD hallucinations (caused by excessive dopamine caused BY THE TREATMENT) vs schizophrenia hallucinations (caused by excessive dopamine caused BY THE DISEASE)

A
  • PD = are aware of their hallucinations and are aware that this is abnormal + hallucinations are well formed (animals, people)
  • schizophrenia = don’t know their hallucinations are not real + not well formed hallucinations (shapes, more auditory hall)
26
Q

one example of important fct of dopamine

A

reward (what makes you feel good about doing something)
-give too much levodopa to PD pts = acts on the reward pathways and they become disinhibited: gambling behavior, hypersexualized, etc.

27
Q

things proving schizophrenia might be caused by too much dopamine

A
  • antipsychotics cause parkinsonian symptoms (bc block uptake of dopamine in vesicles)
  • PD pts tx with levodopa develop hallucinations
  • cocaine and amphetamines block reuptake of dopamine at the cleft and cause psychosis
  • PD pts are more likely to not have smoked in their life (bc cigarette gives you dopamine)
28
Q

ntr Rs subtypes principle

A
  • one ntr can have diff Rs subtypes (dopamine Rs have D1 to D5 subtypes)
  • each subtype of R for a ntr can have diff effects, so same ntr = diff effects
  • can use meds selective for one subtype
29
Q

what are second generation anti-psychotics for schizophrenia

A

D2 selective dopamine R agonists

  • less SE
  • more selective
  • smaller dose
30
Q

what are ‘‘positive’’ symptoms of schizophrenia

A
  • psychosis
  • hallucinations
  • delusions
31
Q

what are ‘‘negative’’ symptoms of schizophrenia

A
  • apathy (lack of motivation)
  • blunt affect
  • etc
32
Q

depression pathophgy

A

disease of ntr linked to decreased serotonin

  • reserpine (blocked uptake of monoamines into synaptic vesicles, used for schizophrenia) caused depression
  • but also other problems in depression, not just serotonin*
33
Q

tx of depression

A

SSRIs (selective serotonin reuptake inhibitors) like fluoxetine (Prozac)

34
Q

principle in serotonin Rs

A
  • 7 main types (5 excitatory and 2 inhibitory)
  • each type has many subtypes, which can also be inhibitory or excitatory
  • *so give SSRI = not sure what you’re doing**
35
Q

what is the trigemino-vascular system

A

trigeminal neurons projecting onto cerebral blood vessels. they signal vessel dilation and inflammation, leading to sensation of pain
dilation = pain = migraine

36
Q

serotonin effect in migraines + consequent medication developed

A
  • it binds to a specific receptor subtype (1B, 1D) to cause vessel constriction
  • triptans = selective agonists of this R. specific migraine tx to lead to vessel constriction = no dilation = no pain
37
Q

common effect of medications treating depression, anxiety and migraines

A

increased serotonin neurotransmission

-bad consequence of that is a possible serotonin syndrome

38
Q

serotonin syndrome def

A
  • tremor, agitation, altered mental status, autonomic instability
  • occurs when multiple seratonergic meds are combined and serotonin Rs are over stim
  • don’t prescribe triptan for migraine if pt already on med for depression*

Bloc J - Neuro (60 decks)

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