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BB Test 3 > CNS Neurotransmitters > Flashcards

CNS Neurotransmitters Flashcards

(61 cards)

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1
Q

What are the monoamine neurotransmitters?

A
  • Norepinepherine (NE)
  • Serotonin (5-HT)
  • Acetylcholine (ACh)
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2
Q

What are the amino acid neurotransmitters?

A
  • Glutamate (Excitatory)
  • GABA (Inhibitory)
  • Glycine (Inhibitory)
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3
Q

What are the neuropeptide neurotransmitters?

A
  • Endorphin
  • Angiotensin
  • Substance P
  • Many others
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4
Q

What type of staining showed the nervous system was a collection of individual neurons?

A

Golgi staining

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5
Q

Describe the two types of transmission speeds and the charactestics of each.

A
  • Fast
    • Rapid, point-to-point, transient (doesn’t last long)
    • Involve transmitter-gated ion channels (ionotropic)
    • Typicall triggered by a single depolarizatoin
  • Slow
    • Slow, diffuse, lasting
    • Involve G-protein coupled receptors (metabotropic)
    • Typically triggered by prolonged or repetative depolarization
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6
Q

What functional groups do monoamine neurotransmitters consist of? What is the exception to this?

A
  • Amine group connected to an aromatic ring by a two carbon chain
    • ACh is not a monoamine but is clumped together with this group
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7
Q

What enzyme converts glutamate (excitatory) to GABA (inhibitory)?

A

Glutamic acid decarboxylase (GAD)

  • Wherever there is glutamate, there is also GAD
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8
Q

What determines if a neuron is inhibitory or excitatory? What is the exception?

A
  • It’s receptor
    • Gluatamate - Always excitatory
    • GABA - Always inhibitory
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9
Q

What neurotransmitters work together to tightly regulate different neural functions?

A

Glutamate & GABA

  1. Glutamate released into cleft
  2. Binds post-synpatic neurons
  3. Neurons can take up Glutamate and convert to GABA
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10
Q

What receptor is believed to be the source of learning?

A

Glutamate-NMDA receptor

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11
Q

Describe the Glutamate-NMDA recptor firing.

A

NMDA is a slective agonist to glutamata

  1. NMDA, Glutamate, and depolarization from -80mV to -40mV are required to fire
  2. Depolarization frees a Mg<strong>2</strong>+ that blocked channel
  3. Ca2+ influx results (Voltage gated)
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12
Q

What is synaptic plasticity?

A

Regulation of strength of connection between two synapses

  • Seen in Glutamate-NMDA receptor
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13
Q

What is glutamate toxicity?

A

Too much glutamate from:

  • Excessive gluatamate release
  • Poor glutamate reuptake

Excessive Ca2+ intake triggers neuronal injury/death

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14
Q

What can cause glutamate toxicity?

A

Stroke: Anoxia can release toxic amounts of glutamate

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15
Q

What is the mechanism of the GABAA receptor and what drugs act on it?

A

Hyperpolarization via Cl- influx into neuron

Drugs:

  • Benzodiazepines
  • Barbituates
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16
Q

What is the mechanism of the GABAB receptor and what drugs act on it?

A

Hyperpolarization via K+ outflux from neuron

Drugs:

  • GHB
  • Baclofen
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17
Q

What is the disease model for Huntington’s?

A

Destruction of GABAergic neurons in basal ganglia

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18
Q

What is the disease model for Tetanus and Strychnine?

A

Inhibition of presynaptic GABA release (results in shortage of GABA in synaptic cleft)

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19
Q

What is the disease model in Stiff-Person Syndrome?

A

Antibodies destroy GAD and prevent GABA production, causing autoimmune or paraneoplastic syndrome

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20
Q

What drugs can treat excessive glutamate? (Increased glutamate can cause seizures)

A
  • Benzodiazepines (increase GABA efficiency)
  • Valproate (Inhibit enzymes that deactivate GABA)
  • Topiramate (Inhibit GABA re-uptake)
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21
Q

What are the side effects of treating excessive glutamate with GABA?

A
  • Sedation
  • Cognitive slowing
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22
Q

What are the non-therapeutic uses of drugs that increase GABA?

A
  • Anxiolysis, hypnosis, amnesia (occasionally)
  • High addictive potential
  • “Date-rape” drugs
    • GHB (Gamma-hydroxybutrate)
    • Benzodiazepines
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23
Q

What nuclei produce Dopamine?

A
  • Pars compacta (substantia nigra) - largest
  • Ventral tegmental area
  • Hypothalamus
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24
Q

Describe the Nigrostriatal tract.

A
  • Substania nigra → Striatum (D2 receptors)
  • Regulates fluid and smooth muscle action
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25
Describe the Mesolimbic tract.
* **Ventral tegmental area** → **N. accumbens (D1** receptors; part of limbic system) * Associated with fear & reward responses
26
Describe the mesocortical tract.
* **Ventral tegmental area** → **Frontal lobe** * Associated with motivation and response
27
Describe the Tubero-infundibular tract.
* **Hypothalamus → Pituitary** * Regulates secretion of hormones, notably **prolactin**
28
What are the 4 clinically imporant tracts associated with dopamine?
* Nigrostriatal tract * Mesolimbic tract * Mesocortical tract * Tubero-infundibular tract
29
Parkinson's disease is associated with death of what structures?
**Pars compacta** (within **substantia nigra**) - Decreased dopamine
30
What are the primary and secondary symptoms related to Parkinson's disease?
* **Primary: Movement-related** disorders * Shaking, rigidity, slowness, difficulty with gait * **Lack of DA** to reach receptors to gait/initiate movements * **Secondary: Cognitive** disorders * Dementia, sensory, sleep, emotional lability
31
What illicit drugs block the re-uptake of Dopamine? What is the effect?
* **Cocaine** and **methamphetamine** * **Excessive dopamine** can cause paranoia, hallucinations, delusions, disorganized thoughts * Results in **reward dysfuntion**
32
What can be used to treat Parkinsons (decreased dopamine)?
**L-DOPA** (bypasses rate limiting step of converting **tyrosine to DOPA** by **tyrosine hydroxylase**)
33
What are the neurotransmitters changes associated with **depression** and what can be used to treat it?
* **Decreased dopamine** and **serotonin** * Buproprion/Methylphenidate (prevent DA re-uptake)
34
What are the neurotransmitter changes associated with **ADHD** and what drugs can be used to treat it?
* **Decreased dopamine** and **norepinepherine** * Bupropion/Methylphenidate (prevent re-upatke of DA)
35
What are the neurotransmitter changes associated with **Schizophrenia** and what drugs can be used to treat it?
* **Increased dopamine** * **Antipsychotics** (operate via **D2 receptor antagonism**)
36
What nucleis produce **serotonin (5-HT)**?
**Raphe** nucleus (pons/midbrain)
37
What tracts are associated with **serotonin (5-HT)**?
Many; extensive projections throughout brain including: * Cortex * Cerebellum * Hypothalamus * Spinal column * PNS
38
What disorders are associated with **decreased serotonin**?
* **Major depressive** disorder * **Anxiety** disorders * Nausea (increased, not decreased)
39
What are the drugs used to treat major depressive disorder?
* **SSRIs** * TCA * MAO inhibitors
40
What are the drugs used to treat anxiety disorders?
* **Benzodiazepines** (DOC) * **SSRIs** * TCA * MAO inhibitors
41
What are the drugs used to treat nausea?
Ondansntron (5-HT3 receptor antagonist)
42
What is the rate limiting step in serotonin production?
Tryptophan → 5-HTP **TPH** (Tryptophan hydroxylase)
43
What is serotonin syndrome and what are the symptoms?
* Excessive serotonin * Cognitive symptoms: Headache delerium * Autonomic symptoms: Hyperthermia, hypertension * Somatic symptoms: Tremor, hyperreflexia, clonus
44
What drugs of abuse can causes serotonin disorders?
* LSD * MDMA
45
What food and beverages can cause serotonin disorders?
* Cheese (tyramine) * EtOH
46
What nuclei produce **norepinepherine**? What is it responsible for?
* **Locus ceruleus** (pons) * Fight or flight response * Smooth muscle contraction or relaxation, heart muscle contraction, glycogenolysis
47
What tracts are associated with norepinepherine?
Broad projectsion throughout cortex (frontal), limbic, spinal
48
What neurotransmitter changes are associated with **Parkinsons**?
* **Decreased NE** (locus ceruleus destruction) secondarily due to **decreased DA** (substania nigra destruction) - Must have dopamine to make NE * Increased 5-HT * Increased ACh
49
Panic attacks are associated with increased levels of what neurotransmitter?
**Increased norepinepherine** (due to re-uptake deficiency)
50
What drugs can be used to treat norepinepherine disorders?
* **Antidepressants** (increase NE availability) * Selective NE/DA re-uptake inhibitor (**Bupropion**) * SSNRIs (**Vanlafaxine, duloxetine**)
51
What nucleus produces ACh?
* **Nucleus Basalis of Mynert** (inferior to anterior commissure) * **Pedunculopontine nucleus** (brainstem, caudal to substantia nigra)
52
What tracts are associated with ACh?
Pedunculopontine - Projects to: 1. Thalamus, basal ganglia 2. Brainstem, deep cerebellar nuclei Nucleus Basalis of Mynert - Projects to: 1. Cortex, associated with memory, learning, defecits with Alzheimer's Parasympathetic nervous system 1. Heavily involved with limbic system and homeostasis
53
Alzheimer's disease is associated with what neurotransmitter changes?
* Decreased ACh (degeneration of NBM) * Loss of nACh receptors in hippocampus
54
The hippocampus in normal, healthy adults is rich in what?
Nicotnic ACh receptors Linked to cognition
55
Schizophrenia shows reduction of what type of receptors?
Nicotinic ACh receptors in hippocampus and frontal cortex Cigarette smoking is commonly believed to be form of self-medicatoin
56
What is required for nictonic ACh receptors to fire?
* ACh * Nicotine
57
What is required for muscarinic ACh receptors to fire?
* ACh * Muscarine
58
What can cause ACh toxicity and what is used to treat it?
Organophosphates/Sarin gas Atropine (anti-muscarinic)
59
What are the symptoms of ACh toxicity at nicotinic receptors?
**SLUDGE** * **S**alivation * **L**acrimation * **U**rination * **D**efacation * **G**I upset * **E**mesis
60
What are the symptoms of too little ACh (anticholinergic toxicity) at muscarinic receptors?
* Increased body temperature and sweating (**hot as a hare**) * Loss of accomidation (**blind as a bat**) * Decreased secretions (**dry as a bone**) * Disorientation from CNS manifestations (**mad as a hatter**)
61
What drugs can cause anticholinergic toxicity (too little ACh)?
* Anti-nausea medications * Antidepressants * Antipsychotics * Anti-histaminics

BB Test 3 (26 decks)

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