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brain form and function > topic 5 (neurotransmitters in health and disease) > Flashcards

topic 5 (neurotransmitters in health and disease) Flashcards

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1
Q

what receptors are invovled in long term potentiation

A

glutamate receptors

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2
Q

how does glutamate cause excitotoxicity

A
  • follwing injury or death to a glutamatergic neuron glutamate is released
  • this can excite the neighbouring cells and be neurotoxic
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3
Q

what is autoimmune encephalitis

A
  • antibodies are produced by the body against different receptors in the brain
  • this causes a variety of conditions some can be fatal
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4
Q

what are 5 modulatory pathway neurotransmitters

A

dopamine, acetylcholine, serotonin, noradrenaline

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5
Q

what is the function and disease of the nigrostriatal dopamine pathway

A

modulation of movement

parkinsons disease

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6
Q

what is the mesolimbic/mesocortical dopamine pathway involved in

A

behaviour

schizophrenia, addiction

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7
Q

what is the tuberohypophyseal system involved in

A

prolactin

between the hypothalamus and the pituitary gland

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8
Q

why does the substantia nigra lose pigmentation in parkinsons disease

A
  • melanin is a breakdown product of dopamine

- as neurons in the Substantia nigra lose dopamine the area loses pigmentation

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9
Q

what are 5 key parts of the basal ganglia

A 
striatum
thalamus
globus pallidus
subthalamic nucleus (stn)
substantia nigra
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10
Q

outline the direct pathway

A
  • excitatory
  1. motor cortex excities striatum with glutamate
  2. Striatum inhibits the globus pallidus with GABA
  3. because the globus paladus normally inhibits the thalamus with GABA, inhibition on the inhibition causes the thalamus to be excited
  4. The thalamus excites the motor cortex leading to more movement
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11
Q

outline the indirect pathway

A

-inhibitatory

  1. motor cortex excites striatum with glutamate
  2. The striatum inhibits GPe with GABA.
  3. GPe normally inhibits the STN with GABA, so inhibition of this inhibition causes an increased STN activity.
  4. The STN excites the GPi with glutamate
  5. The GPi inhibits the thalamus, so increased activity of the GPi causes less thalamus activity
  6. The thalamus normally excites the motor cortex so inhibition of the thalamus causes less movement
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12
Q

outline the nucleus basalis cholinergic pathway

A
  • projection from the nuclei in the basal forebrain to the cortex
  • function in memory and arousal
  • degeneration in alzheimers disease
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13
Q

outline the serotinergic pathways from the raphe nuclei

A
  • projects across the cns including the cortex, hippocampus and limbic system
  • multiple different receptors
  • involved in mood, sleep, appetite, pain regulation
  • involved in depression, anxiety and chronic pain
  • drugs include SSRI’s and tricyclic antidepressantsq
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14
Q

outline the noradrenergic pathway from the locus correlus

A
  • widespread projection across the CNS
  • involved in arousal, mood and blood pressure control
  • drugs include amphetamines and methyl dopa
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15
Q

what is the uk brain bank criteria for parkinsons diagnosis?

A 
Bradykinasia
AND 1 of
tremor
rigidity
postural instability
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16
Q

what is the pathology of parkinsons disease

A
  • lewy bodies are found in the substantia nigra
  • these contain aggregates of alpha-synuclein
  • these spread up through the brain in Braak stages
17
Q

what are the Braak stages of parkinsons pathology?

A
  1. peripheral and enteric nervous system
  2. medulla oblongata
  3. pontine tegmentum
  4. basal mid and forebrain, hypothalamus and thalamus
  5. mesocortex, allocortex
  6. neocortex
18
Q

what is parkinsons pathology in the basal ganglia circuits

A
  • The STN sends dopamine to the striatum
  • This can either excite or inhibit depending on whether it lands on D1 or D2 receptors
  • In parkinsons disease the STN sends less dopamine to the striatum
  • This favours the indirect pathway leading to inhibition of movement
19
Q

where would Deep brain stimulation in parkinsons disease be

A
  • in the subthalamic nucleus
  • this shuts down its functioning
  • resulting in less excitation of the GPi
  • resulting in less inhibition of the thalamus
  • resulting in more movement
20
Q

name 3 drug treatments for parkinsons disease

A
  • levodopa which is a precursor to dopamine, combined with a peripheral dopa decarboxylase inhibitor to stop it from being broken down in the periphery
  • drugs which stop dopamine breakdown e.g monoamine oxidase inhibitors or COMT inhibitors
  • dopamine agonists
21
Q

what are symptoms of dopamine medication

A

dyskenesia (too much movement)

psychiatric problems

22
Q

what are non motor symtpoms of parkinsons

A

NORADRENERGIC

  • constipation
  • erectile dysfunction
  • urinary urgency

CHOLINERGIC
-cognitive impairement

SEROTONERGIC
- fatigue

OTHER
-Ansomnia
-REM sleep behavioural disorder
-Depression
-Apathy
Pain
23
Q

whats the diagnostic criteria of alzheimers disease

A 
progressive cognitive decline in one or more of the following:
memory
executive function
attention
language
perceptual- motor
social cognition

AND impairement of function

not due to delerium or other mental disorder

24
Q

what age is early onset AZ

A

before age 65

25
Q

in the amyloid cascade hypothesis, what causes amyloid beta plaques in dominant and sporadic forms of the condition

A

DOMINANT
- mutations in APP genes lead to increased AB production throughout life

SPORADIC

  • faliure of AB clearance mechanisms
  • gradually rising AB levels in the brain
26
Q

what is the impact of increased AB according to the amyloid cascade hypothesis

A
  • AB aggregates into plaques
  • this creates microglia and astrocyte inflammatory responses
  • this leads to altered ionic homeostasis
  • this leads to increased protein kinase activity leading to TAU tangles
  • widespread dysfunction leading to dementia
27
Q

how do microglia react to amyloid plaques

A
  • microglia surround amyloid plaques
  • at first this is protective to protect the plaques from damaging the rest of the cell
  • however after a while these microglia change to more destructive forms that can lead to neuronal loss
28
Q

where is neuronal loss due to AD most pronounced

A

in the temporal and parietal lobes especiall the hippocampus

29
Q

what are 2 currently available treatments for AD

A

acetylcholinesterase inhibitors

NMDA receptor antagonists

30
Q

what is the cholinergic hypothesis of AD

A
  • choline acetyltransferase markers are lost in alzheimers disease
  • this is a presynaptic enzyme important in the synthesis of acetlycholine
  • this leads to a reduction in choline uptake and ACh release
  • This leads to neuronal loss in cholinergic nuclei
31
Q

how does memantine work as an alzheimers disease drug

A

its an NMDA receptor antagonist
its thought to inhibit glutamate induced excitotoxicity
its used in moderate to severe alzheimers disease

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