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Neuro anatomy Exam 1 > Phys Neurotransmitters > Flashcards

Phys Neurotransmitters Flashcards

1
Q

What are the two types of neurotransmitter receptors?

A

Ionotropic (ligand-gated channels)

Metabotropic (G-coupled receptors)

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2
Q

What is an Ionotropic/ligand-gated raceptor?

A

Receptor activated by a ligand, any substance that can bind to a target protein

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3
Q

Describe Ionotropic/ligand-gated receptor mechanism

A

NT binds to the binding site of the post synaptic neuron -> channels open -> ions permitted to flow into the neuron -> change membrane potential -> send AP down neuron

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4
Q

Describe Metabotropic/G-coupled receptor mechanism
Is this mechanism slower/faster?
Specific/widespread?

A

NT binds to binding site -> activate G-protein -> can open ion channels or activate intercellular signaling molecules (secondary messengers) -> initiate signaling cascade within cell
Slower
More widespread

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5
Q

Which NT is the most abundant NT in brain/CNS and is involved in most every major excitatory brain function?

A

Glutamate

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6
Q

What are the two functions of Glutamate?

A
  1. Learning/memory

2. Synaptic Plasticity

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7
Q

What are the 2 main receptors glutamate binds to? Be specific

What is 3rd receptor it can bind to?

A
  1. Ionotropic: NMDA, AMPA, Kainate
  2. Metabotropic

Kainate receptors

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8
Q

When glutamate binds to ionotropic receptors, is it slow or fast transmission?
What are three functions?

A 
-Fast transmission
3 functions:
1. Neuronal plasticity
2. Synaptic pruning
3. Apoptosis (controlled cellular death)
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9
Q

When glutamate binds to metabotropic receptors…
…what is it’s function?
…does it affect presynaptic or postsynaptic excitability?

A

Function - modulate glutamate release

Affect - postsynaptic excitability

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10
Q

Describe Kainate receptors affect on pre/post synaptic actions (which is Gaba and which is glutamate binding)

A

Presynaptic - GABA

Postsynaptic - Glutamate

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11
Q

Function of glutamate binding to Kainate:

A
  1. Less well known
  2. Minor role in synaptic plasticity (decrease affect of likelihood postsynaptic cell will fire in response to future stimulation)
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12
Q

What does a NT/drug that acts as an agonist do?

A

Binds to same receptors and have same effect as the NT

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13
Q

What does a NT/drug that acts as an antagonist do?

A

Block the effects of the NT

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14
Q

What does a NT/drug that acts as an inverse agonist do?

A

Bing to the sit the NT binds to and have the exact opposite effect

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15
Q

What does a NT/drug that acts as an neuromodulators do?

A

Binds to a site on the receptor that is separate from the site where the NT binds, and affect the likelihood that NT will bind

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16
Q

Phencyclidine (PCP) (Antagonist) will inhibit the reuptake of…
will inhibit the action of…

A
  • Inhibit reuptake of dopamine, ne, and serotonin

- Inhibit the action of glutamate by blocking NMDA receptors

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17
Q

Initial impact of PCP -
Eventual impact -
Continued Usage -

A

Initially - less glutamate binding to receptors -> less APs (Relaxation, numbness, sensory distortions)
Eventually - excess glutamate overcrowding the synaptic cleft (confusion, agitation, analgesia, fever, schizo type behavior)
Cont’d usage - seizures, resp failure, coma, fever, stroke, death

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18
Q

What two ways does Riluzole decrease excess levels of glutamate in cases of ALS?

A
  1. Block release of glutamate from nerve cell
  2. Reduce glutamate vesicle fusion with the presynaptic cell membrane -> decrease amount of glutamate released into the synaptic cleft
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19
Q

Describe the clinical pathology of glutamate excitotoxicity

A

Increased glutamate -> continuous binding of AMPA and NMDA receptors and channels remain open for too long -> too much Ca++ ends up in cell -> apoptosis (cascade of cell death)

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20
Q

Describe positive/negative symptoms of Schizophrenia.
What are the two NT focuses on in this pathology?
Describe the possible pathology of SZ.

A
  • Positive symptoms: delusions and hallucinations
  • Negative: deficits, such as social withdrawal and lack of motivation
  • Focus on dopamine and glutamate
  • Possible pathology: NMDARs are hypofunctional
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21
Q

Describe the clinical pathology of epilepsy.

Describe what type of medication is used as anticonvulsants

A
  • Excessive glutamate leads to overactive NMDA receptors -> thought to cause epileptic seizures
  • Glutamate antagonists selective for NMDA or non-NMDA receptors are potent anticonvulsants
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22
Q

Describe the clinical pathology of Alzheimer’s Disease

What are the 2 primary symptoms?

A
  • Excessive NMDAr activity -> excitotoxicity and promotes cell death
  • Primary symptoms: memory deficits and inability to form new memories
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23
Q

What is GABA?
Is it excitatory/inhibitory?
Describe functions

A
  • Gaba: major inhibitory NT in CNS
  • Function:
    1. Treats anxiety and used in rehab for drug abuse
    2. Inhibits motor, sensory, and cognitive neurons -> sedation, muscular/cardiorespiratory, relaxation, pain inhibition
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24
Q

Describe the Ionotropic Gaba receptor:
GABAa or GABAb?
What ion does it control?
Describe mechanism of action

A
  • GABAa found in nearly every neuron
  • Controls Cl- entry into cell
  • When Cl- enters cell, it will hyperpolarize making it harder for the AP to propagate
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25
Q

Describe the Metabotropic Gaba receptor:
GABAa or GABAb?
What ion does it control?
Describe mechanism of action

A
  • GABAb will reduce muscle contraction
  • Controls K+ out of cell
  • When activated, cause opening of K+ channels -> K+ ions travel out -> hyperpolarize cell -> inhibits presynaptic release of NTs (ACh)
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26
Q

Describe the agonist action of Alcohol on GABA receptors (2 mechanisms):

A

Alcohol will increase GABA activity:

  1. Act on presynaptic neuron ->causing increase in GABA release (increase K+ out of presynaptic)
  2. Act on postsynaptic neuron -> facilitating activity of GABAa receptor (CL- into postsynaptic cell)
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27
Q

Describe the agonist action of Benzodiazepines on GABA receptors:
Used to treat what?
Affect pre/post synaptic?

A
  • Psychoactive drug used to treat anxiety and insomnia

- Increase post synaptic receptors sensitivity to GABA binding

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28
Q

Describe the agonist action of Barbiturates on GABA receptors:
Used to treat what?
Affect pre/post synaptic?

A
  • Sedation, decrease anxiety, and anticonvulsants for seizures
  • Prolong opening of individual GABA operated Cl- channels
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29
Q

Describe the agonist action of Baclofen on GABA receptors:
Used to treat what?
Affect pre/post synaptic?

A
  • Antispasticity

- Increase presynaptic release of GABA in spinal cord -> increase activity of GABAb receptors -> relaxation of muscles

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30
Q

Epilepsy treatment:
GABA agonists -
GABA antagonists -

A

Agonists - suppress seizures

Antagonists - produce seizures

31
Q

Huntington’s Disease:

A
  • Fatal genetic disorder that causes the progressive breakdown of nerve cells in the brain
  • Symptoms: personality changes, forgetfulness/impaired judgment, unsteady gait, involuntary movements (chorea - hallmark symptom), slurred speech, difficulty swallowing, and significant weight loss
    1. Loss of NT (GABA, ACh, Glutamate) -> loss of neurons
    2. Decrease GABA a receptors available in the brain
32
Q

What is Glycine?
Where is it found?
Inhibitory/excitatory and pre/post synaptic response?
Describe mechanism (what type of receptor?)

A
  • Glycine functions alongside GABA and is found in the brainstem and spinal cord
  • Inhibitory post-synaptic response
    Mechanism: when glycine receptors are activated -> Cl- enters the neuron via ionotropic receptors -> blocks AP
33
Q

Describe Glycine antagonist Strychnine:

A
  • Poisonous natural substance
  • Used as pesticide
  • Causes muscular convulsions and death by asphyxia
34
Q

Describe clinical pathology of Spasticity

A
  • Loss of inhibitory interneuron activity -> poorly coordinated muscle response -> spasticity
35
Q

Describe clinical pathology of Spinal Shock:

A

Spinal shock - acute phenomenon seen after spinal cord injury

  • Pt presents with LMN symptoms, despite UMN injury (low tone, absent reflexes,) that last hours to about 1 week
  • Elevated levels of glycine found in SCI
36
Q

Is Acetylcholine excitatory/inhibitory in pre/post synaptic neuron?

A
  • Excitatory post-synaptic response
37
Q

What are the functions of AcH

A

Functions:

  1. Triggers muscle contraction
  2. ANS involvement - slows HR, constricts pupils, increases digestive secretions and smooth muscle contraction
  3. Stimulates secretions of certain hormones
  4. CNS - wakefulness, attentiveness, anger, sexuality
38
Q

What are the ionotropic and metabtropic receptors ACh binds to?
Excitatory or Inhibitory

A

Ionotropic - nicotinic (excitatory)
Metabotropic - muscarinic (excitatory or inhibitory)
- Regulation of cardiac muscle, smooth muscle, and glandular activity

39
Q

What is the antagonist affect of Botulin Toxin?

A
  • Inhibit ACh release into cleft
40
Q

What are the 4 locations Botulin Toxins act on in the body?

A
  1. NMJ
  2. Autonomic ganglia
  3. Postganglionic parasympathetic nerve endings
  4. Postganglionic sympathetic nerve endings that release ACh
41
Q

How is Botulin Toxins used as treatment? (2)

A
  1. Overactive smooth muscle

2. Abnormal activity of glands

42
Q

Describe the use of Antagonist Atropine?

A

Blocks inhibitory effects of ACh on HR leading to Tachycardia (antagonist to muscarinic receptors)

43
Q

Describe the use of Agonist Nicotine of the CNS?

A
  • Increase ACh release -> enhanced cognition and attention
  • Binds to nicotinic receptors and mimics ACh -> causes depolarization of post synaptic neuron
  • Can cause increase dopamine levels in brain (addictive qualities)
44
Q

Describe the use of Agonist Nicotine of the PNS?

A
  • Increases sympathetic ns activity (increased HR and BP)

- Increase release of catecholamines like epi from adrenal glands -> increase SNS activity

45
Q

Describe Alzheimer’s Disease and Dementia in regards to nicotinic receptors

A
  • Loss of nicotinic-expressing neurons in the brain
46
Q

Myasthenia Gravis:
What is it?
What symptoms?
Describe affect on nicotinic receptors

A
  • Autoimmune disease, repetitive muscle use (eye and eyelids often) that leads to weakness
  • Ptosis (dropping of eyelid) and strbismus (cross eyed apearance)
  • Antibodies attack and destroy nicotinic receptors on muscle cells, so normal ACh but few receptors
47
Q

Tabacco Addiction:

A
  • Nicotine activates nAChR’s -> cause receptors to become desensitized -> brain upregulates (adds more) -> plays role in withdrawal and craving
48
Q

Serotonin (5-HT):
Where is it found?
Excitatory/Inhibitory and pre/post synaptic?

A
  • Found in the brain and brainstem (cluster of neurons called Raphe Nuclei)
  • Excitatory and Inhibitory post-synaptic response
49
Q

What are the functions of Serotonin?

A
  1. Emotions
  2. Sleep-Wake cycle
  3. GI Tract Regulation/ Appetite
  4. Cardiovascular growth factor (clotting)
  5. Increased -> can decrease sexual function
50
Q

What are the ionotropic and metabotropic serotonin receptors?

A

Ionotropic - 5-HT3 excitatory

Metabotropic - 5-HT1-7 excitatory or inhibitory receptors

51
Q

Describe role of agonist SSRIs

What are some examples?

A

Ex: Prozac, Zoloft, Celexa

- Increase levels of serotonin by inhibiting the reuptake

52
Q

Describe serotonin’s role in depression

A
  • Low levels of serotonin are linked to clinical depression
53
Q

Describe serotonin’s role in Autism

A

45% of tested ASD subjects contained high levels of 5-HT in their blood

54
Q

Describe serotonin’s role in serotonin syndrome

Signs and symptoms?

A
  • High levels of serotonin as an adverse effect of serotonergic therapy
  • Agitation, restlessness, confusion, tachycardia, HTN, loss of muscle coordination, muscle rigidity, heavy sweating
55
Q

What is Dopamine?

Where is it found in the CNS and ANS?

A
  • Amine function as neuromodulators
  • Found in:
    1. CNS: substantia nigra, midbrain, hypothalamus
    2. ANS: sympathetic neurons
56
Q

Is dopamine inhibitory/excitatory on pre/post synaptic?

Name some functions

A 
- Excitatory and inhibitory on post-synaptic neuron
Functions:
1. Drive
2. Attention, memory
3. Motor functions (extrapyramidal)
4. Addictive for narcotics
57
Q

What are the ionotropic and metabotropic serotonin receptors?

A

Ionotropic - none

Metabotropic - excitatory and inhibitory

58
Q

Describe Agonist Amphetamine on dopamine

A
  • Bind to dopamergic receptors on presynaptic cell and enters -> increased release of dopamine into synaptic cleft
59
Q

Describe Agonist L-dopa on dopamine

A
  • Primary drug for parkinson’s

- L-Dopa (can cross BBB) is precursor to synthesis of dopamine (can’t cross BBB)

60
Q

Describe Dopamine’s role in Parkinson’s
Where does PD develop in brain?
What are PD symptoms?

A
  • Dopamine dysregulation in substantia nigra where cells begin to die
  • Symptoms: resting tremor, rigidity, bradykinesia and loss of postural reflexes
61
Q

Describe Dopamine’s role in Schizophrenia

What part of brain is affected for positive/negative symptoms?

A
  • Recent studies suggest hypodopaminergic state in prefrontal cortex = negative symptoms -> leads to hyperdopaminergia in mesolimbic system and striatum = positive symptoms
62
Q

Describe Dopamine’s role in ADHD

A
  • Higher [ ] of dopamine transporters in brain -> remove dopamine from brain cells -> less time to exert its effects
63
Q

Describe Dopamine’s role in Substance Dependency:
Acute
Chronic
Discontinuation of cocaine

A

Acute - increase synaptic dopamine because cocaine blocks presynaptic reuptake
chronic - down regulate dopamine receptors in response to overstimulation
Discontinuation - dopamine depletion and intense depression/agitation

64
Q

Norepinephrine (noradrenaline):
Found in cortex and ANS -
Inhibitory/Excitatory on pre/post synaptic?

A

Found in:

  1. Cortex - locus ceruleus (pons), medulla
  2. ANS: sympathetic neurons (fight or flight)
    - Excitatory post-synaptic response
65
Q

What are the ionotropic and metabotropic norepinephrine receptors?

A

Ionotropic - none
Metabotropic - A1,A2 and B receptors (activation of B increase HR and force of contraction)
- Called adrenergic receptors

66
Q

Describe beta blockers role on norepinephrine

A
  • Bing b receptors -> prevent activation -> prevent increased NE (sweating, rapid HR)
  • Can help with anxiety, HTN
67
Q

Describe Amphetamines role on norepinephrine

A
  • Increase blood and brain levels of NE:
    1. Block reuptake
    2. Increase its release from cells
68
Q

Describe Cocaine’s role on norepinephrine

A

Block reuptake of NE

69
Q

Describe Tricyclic antidepressants (TCAs) role on norepinephrine

A

Increase levels of NE and serotonin and block action of ACh

70
Q

Describe NE on ADHD

A
  • Increase brain levels of NE (but difficult to determine)
71
Q

Describe NE on Hypotension

A
  • Agonist activity on A1 and A2 causing vasoconstriction
72
Q

Describe NE on PTSD

A
  • Excessive NE in Veterans who experience PTSD
73
Q

Describe NE on Parkinson’s

A

NE markedly decreased in various regions of PD brain

Neuro anatomy Exam 1 (13 decks)

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