MT2 Flashcards

(33 cards)

1
Q

What structures make up the hindbrain (parts and location)?

A

the myelencephalon (enterance of the spinal cord), and metencephalon (the cerebellum and pons)

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2
Q

What is the formal name for the midbrain?

A

Mesencephalon

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3
Q

What are the 2 important functions of the hindbrain?

A

the autonomic nervous system and the reticular formation (alertness and consciousness)

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4
Q

What are the 2 important structures in the midbrain and their function?

A

Substantia nigra (motor and reward) and ventral tegmental area (reinforcement and reward)

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5
Q

What are the important structures in the forebrain? (3 structures)

A

the diencephalic (thalamus and hypothalamus) and the telencephalic (basial ganglia)

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6
Q

What makes up the basial ganglia?

A

dorsal striatum (caudate and putamen) and globus pallidus

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7
Q

difference between dorsal and ventral striatum?

A

Dorsal: found in the basial ganglia of the forebrain. Is made up of caudate and putamen)
ventral: found in the limbic system and includes the nucleus accumbens

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8
Q

What 5 parts of the limbic system do we need to know?

A

The septal nucleus, the nucleus accumbens, the cingulate gyrus, the hippocampus, and the amygdala

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9
Q

What are the two catagories of monoamines? How do they differ?

A

Catacholamines (DA and NE) and serotonin. Catacolamine are derived from tyrosine, and serotonin is derived from tryptophan

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10
Q

What is the rate limiting enzyme in monoamine creation

A

first step from tyrosine base (tyrosine hydroxylase)

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11
Q

What is the mechanism of D1 and D2 class receptors in the cell?

A

D1: up regulates cAMP and depolarization the cell (Gs)
D2: down regulates cAMP by increasing K+ conductance (Gi)

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12
Q

What are the four pathways in the brain relevant for DA? where do they come from, where do they go (where do ya come from cotton eyed joe?) ?

A

Nigrostriatal: from substaintia nigra to dorsal striatum (caudate and putamen)
mesolimbic: ventral tegmental area to nucleus accumbens, amygdala, and hippocampus (limbic system)
Mesocortical: ventral tegmental area to limbic/prefrontal cortex
Tuberoinfudibular: hypothalamus to pituitary (i.e. hormonal control pathway)

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13
Q

What is the core component of amphetamines?

A

Phenylethylamine and some methyl groups

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14
Q

What are the progressive effects of psychomotor stimulants (hint: what is our model psychomotor stimulant? I put down 5 effects)

A

Meth is our model psychomotor stimulant. Its effects are euphoria, antianxiety, alertness, toxic paranoid psychosis, and sensory hallucinations

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15
Q

what two pathways in the brain are activated by psychomotor stimulants?

A

Nigrostriatal and mesolimbic

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16
Q

What are the three causes of AMPH neurotoxicity?

A

Oxidative stress: due to increased DA in the environment
Mitochondrial inhibition: due to increased Ca++
Cytoskeletal damage: due to increase Ca++ dependent proteases

17
Q

What does AMPH do to the BBB?

A

Degrades it by degrading tight junctions, increasing inflamation, and activation matrix metalloproteinases (MMPs) (leads to further degredation)

18
Q

What transporters reuptake glutamate? where are they located?

A

EAAT3: located on the presynaptic cell

EAAT1/2: located on neighboring glial cells

19
Q

Which ionotropic receptors can glutamate activate?

A

AMPA, Kainate, NMDA

20
Q

What cellular mechanism do the glutamate ionotropic receptors use to depolarize cells? what does NMDA do differently?

A

All of them increase the amount of sodium in the cell. NMDA can also increase the amount of calcium inside the cell, leading to the activation of additional cellular mechanisms.

21
Q

What is long term potentiation?

A

When a pre-synaptic and post-synaptic cell are allowed to fire together repeatedly, it will cause a greater change in voltage during the AP.

22
Q

What are three possible mechanisms of LTP?

A
  • change in voltage leads to unblocking/activation of more postsynaptic channels
  • increased presynaptic release
  • increase in number of receptors
23
Q

What glutamate receptors govern necrosis versus apoptosis?

A

Necrosis: AMPA and Kanaite
Apoptosis: NMDA mediated

24
Q

What channels does GABA get reuptook thru? where are they located?

A

GAT1: on presynaptic cell and glial cells

GAT1 thru 3: on glial cells

25
What are four effects of cocaine on the cardiovascular system?
- increased myocardial oxygen demand - increased oxidative stress - decreased myocardial oxygen supply - vasoconstriction
26
What are the sympathomimetic functions of cocaine?
increased HR, BP, and vasoconstriction. dilation of pupils and airways, and increased fat breakdown
27
How can you block and unblock a NDMA channel?
NMDA channels can be blocked by Mg+. Cell depolarization can cause the outflux of Na+ and the Mg+ will release and unblock
28
What are the different effects of psychostimulants on the two relevant pathways?
- Nigrostriatal: Increases locomotor acitivity | - Mesocorticolimbic: increases stereotyped activity
29
What can the addition of calcium from an NMDA receptor do inside the cell?
- It can activate Calmodulin, which can insert additional AMPA receptors or phosphorylate present AMPA receptors - It can send out retrograde messengers
30
What does GABA interchange into?
Glutamate
31
what is GABA's rate limiting step?
glutamic acid decarboxylase
32
What is the half life of cocaine, benzoylecgonine, and cocaethylene?
- cocaine: 30 - 90 min - benzoylecgonine: 2 days -> 2 weeks - cocaethylene: 150 min
33
Where are TAAR DA and Glu receptors located in the brain?
DA: in the striatum, VTG, and the SN Glu: in the frontal cortex, and amygdala