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NB1 > Neurotransmitter Pathway > Flashcards

Neurotransmitter Pathway Flashcards

1
Q

What is a nuclei?

A

– Clusters of functionally related central neuronal cell bodies
• Cells forming nuclei may synthesize characteristic neurotransmitters

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2
Q

What are tracts?

A

– Bundled axons allowing communication between nuclei

• Tracts may mediate the release of specific neurotransmitters onto cells forming select target nuclei

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3
Q

Contract ACh receptors

A

Ionotropic: Nicotinic Change in ion flux (Na+, K+) Rapid Effects (milliseconds)

Metabotropic: Muscarinic Metabolic changes, e.g. phosphorylation
Slower effects (seconds to minutes)
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4
Q

What is the pathology of Ahlzeimers to ACh?

A

Alzheimer’s disease
– Nucleus basalis of Meynert degenerates
– AChE inhibitor approved for treatment
• Not disease-modifying

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5
Q

Whaat do peripheral cholinergic neurons have in contact?

A

Somatic and preganglionic efferent fibers are myelinated

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6
Q

What is the function of cholinesterase?

A

Cholinesterase in synaptic cleft quickly degrades ACh, preventing desensitization and tetany

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7
Q

What is Myasthenia Gravis?

A

Myasthenia gravis
– Disrupted cholinergic transmission at neuromuscular junction
– Treatment
• AchE (esterase) inhibitors

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8
Q

What is SLUD?

A

– Salivation, lacrimation,
urination, defecation

• Overactivation of targets of the cholinergic postganglionic fibers
– Treatment

• Muscarinic receptor antagonists
– Atropine

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9
Q

Contrast the types of Glutamate receptors

A

Ionotropic glutamate receptors
• AMPA and Kainate receptors induce
Na/K flux after glutamate binding CAMKII
• EPSP summation unblocks the NMDA channel pore—> Ca2+ flux

Metabotropic glutamate receptors
Group1 mGLUR- (e) 1,5
Group 2 mGLUR- (i) 2,3
Group 3 mGLUR- (i) 4,6-8

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10
Q

What causes seizures?

A

– Heightened release of glutamate through hyper- synchronization of neuronal populations
– NMDA antagonists can be used to suppress seizures
– Reduced influx of calcium

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11
Q

How can glutamate defect oead to weakness?

A

– Reduced release of glutamate into bulbar and spinal motor nuclei
• As seen in Upper Motor Neuron Syndrome

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12
Q

Describe GABA nuclei and projections

A

GABAergic interneurons are ubiquitous

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13
Q

What are the GABAerguc pathways?

A

GABAergic pathways:
• Striatum -> substantia nigra

• Substantia nigra -> superior colliculus
and thalamus

• Medial vestibular
nuclei –> spinal
cord

• Cerebellar cortex ->
deep cerebellar nuclei

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14
Q

How can GABA be used to treat seizures?

A

Seizures
• Heightened release of glutamate through hyper-
synchronization of neuronal populations

  • Treatment
  • GABA agonists can inhibit hyper-excitable cells
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15
Q

How is GABA used to treat anxiety?

A

Mediated through altered excitability of limbic cells
• Treatment
• Benzodiazepines augment GABAergic transmission
• Reducing excitability

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16
Q

What are the nuclei and projections of the glycine?

A

Neurons tend to be small local inhibitiry interneurons
-Common in spinal and bulbar motor nuclei

Only one receptor type
Ionotropic with a Cl- channel
Blocked by strychnine

17
Q

Describe synthesis and removal of glycine

A

Glycolysus of glucose yields. 3-phosphoglycerate, subsequently serine

Serine transhydroxymethylase folate-dependently converts serine to glycine

Membrane spanning transporters take up synaptic glycine

18
Q

What is the mechanism of tetanus?

A
  • Toxic protease suppresses release of glycine from bulbar and spinal interneurons
  • Lower motor neurons are disinhibited

• Deploying muscle-relaxing strategies
directed at central or peripheral targets

19
Q

What is the mechanism of Strychnine poisoning?

A

The alkaloid blocks glycine receptor on lower motor neurons, reducing chloride influx
• Lower motor neurons are disinhibited

20
Q

In what cases can a cell synthesize NE but not E?

A

If a cell is DBH positive but PNMT negative, then it synthesizes NE but not E

21
Q

What are the metabotropic Dopamine receptors?

A

All Metabotropic receptors:
D1-like – increases cAMP (D1/D5) D2-like – Decreases cAMP (D2-D4)

Reward, mood and movement

22
Q

What are the dopamine based ailments?

A

Movement Disorders

Parkinsonism
• Decreased movement
• Treatment
• Dopamine agonists

Psychoses
• Hallucinations and delusions
• Treatment
• Dopamine antagonists(majortranquilizers)

23
Q

What are the central projections of norepinephrine?

A

LC; Locus Coeruleus – diencephalon, limbic system (emotional centre), cerebral cortex (sensory pathways- micturition, cerebellum and spinal cord

24
Q

What are the types of Norepinephrine receptors?

A 
Metabotropic
• Alpha1/Beta1 GS
Alpha 1/Beta 1
   • Excitatory 
• Alpha2/Beta2 
       • Inhibitory
• Postganglionic PKA sympathetic
     neurons excite cardiac muscl
25
Q

How is depression and pain treated?

A
  • Treatment
    • Norepinephrine agonists (re-uptake or MAO inhibitors) • Activates spinal and bulbar opioidergic neurons
      * Suppresses release of substance P onto spinal dorsal horn and spinal trigeminal nucleus
26
Q

How is Parkinsons treated?

A

• Sympathetic insufficiency

  • Parkinson’s disease
  • Orthostatic hypotension
  • Loss of peripheral sympathetic neurons • Treatment
  • Norepinephrine agonists
27
Q

How is serotoninn pathways similar to noradrenergic pathways?

A

Noradrenergic pathways from Locus Coeruleus broadly similar – see previous slide

28
Q

What is the frontal cortex impacted by serotonin?

A

-Social Context
-Appropriate
behaviours

29
Q

How does serotonin impact the limbuc system?

A
  • Emotions/mood

- Anxiety/Fear

30
Q

How does serotoniimpact Ascending affecting system?

A

Arousal/wakeness

31
Q

How does serotonin impact the spinal cord?

A

To spinal Cord, modulates

nociception and sexual reflexes

32
Q

What are the types of serotonin receptors?

A

• Seven families 5-HT1 -5-HT7 and further subtypes, e.g. 5-HT1A

• All metabotropic with exception of 5-HT3
• 5-HT1, 5-HT5: inhibitory
• 5-HT2: excitatory
• 5-HT3: excitatory ionotropic
(cation-permeable)
• 5-HT4, 5-HT6, 5-HT7: excitatory

• Complex interactions of different 5-HT receptor isoforms can co- exist in the same neuron, e.g. spinal neurons governing micturition

33
Q

How can serotonin be hsed to treat depression and pain?

A

Treatment
• Serotonin agonists (re-uptake or MAO inhibitors)

  • Activates spinal and bulbar opioidergic neurons
  • Suppresses release of substance P onto spinal dorsal horn and spinal trigeminal nucleus

NB1 (67 decks)

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