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Pharmacology > CNS Pharmacology > Flashcards

CNS Pharmacology Flashcards

1
Q

Forebrain

A 
Cerebrum 
Thalamus
Hypothalamus
Amygdala 
Hippocampus
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2
Q

Midbrain

A

Midbrain

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3
Q

Hindbrain

A

Pons
Cerebellum
Medulla Oblongata

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4
Q

Chemical synaptic transmission: excitation

A

INCREASES probability that neuron membrane potential reaches threshold and fires action potential.

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5
Q

Chemical synaptic transmission: inhibition

A

DECREASES probability that neuron membrane potential reaches threshold and fires action potential.

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6
Q

Fast neurotransmitters (NT’s)

A

Voltage gated

Ligand gated

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7
Q

Slow Neurotransmitters

A
  1. Receptor–>G-protein–> + Ion channel

2. Receptor–>G-protein–>2nd messenger–> enzyme–> diffusible messenger–> +ion channel

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8
Q

NT class: Amino Acids

A

Excitatory: Glutamate
Inhibitory: GABA and Glycine

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9
Q

Classes of NT’s: biogenic AMINES

A

ACh
Catecholamines: NE and Dopa
Serotonin
Histamine

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10
Q

Classes of NT’s: Purines

A

ATP

Adenosine

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11
Q

Classes of NT’s: Neuropeptides

A

Endorphins

Substance P

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12
Q

Classes of NT’s: NO and Endocannabinoids (anandamide)

A

Not stored in synaptic vesicles

Generated in response to increases in intracellular Ca and freely diffuse out neurons

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13
Q

Antagonist: compensation

A

Upregulation
SENSITIZATION
Ex: chronic antipsychotics (block dopa) induce production of more dopamine receptors=hyperkinetic D.O.
Delayed onset of therapeutic effects

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14
Q

Agonist compensation

A

Down regulation
DESENSITIZATION
Delayed onset of therapeutic effects of antideprssants which block 5-HT uptake

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15
Q

Mechanisms of receptor desensitization:

A

Receptor Phosphorylation
Receptor Internalization
Receptor Down-regulation: decrease expression of that receptor

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16
Q

Glutamate

A

Major UBIQUITOUS excitatory NT

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17
Q

Glutamate’s role in learning and Memory Function

A

Memories stored by enhancing Gluta-synaptic transmission via LTP.
Requires sufficient Ca influx through NMDA receptors.

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18
Q

Glutamate’s role in Epilepsy

A

Imbalance in excitation and inhibition

Some anti-epileptics block glutamate receptors

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19
Q

Glutamate and Excitotoxicity

A

Excessive stimulation–> excessive Ca influx–> neuronal damage–> neurodegeneration
Stroke, ALS, MS

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20
Q

Glutamate and Dissociative anesthesia

A

I.E. catatonia, amnesia, analgesia

Ketamine blocks NMDA receptors

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21
Q

Glutamate and Drug abuse

A

PCP in NMDA receptor antagonist

Reducing NMDA receptor activity can cause HALLUCINATIONS

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22
Q

GABA

A

Major inhibitory NT

2 groups of neurons: interneurons and projecting neurons

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23
Q

Interneurons of GABA

A

Local circuit neurons: neocortex, thalamus, striatum, hippocampus, cerebellum, spinal cord

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24
Q

Projecting neurons of GABA:

Striatum–>globus pallidus–>thalamus/subs nigra

A

Loss of these in HUNTINGTONs chorea

25
Q

Projecting neurons of GABA

A

Septum–> Hippocampus

Substantia nigra–> thalamus/superior colliculus

26
Q

Projecting neurons of GABA that promote sleep

A

Ventrolateral preoptic area–>nuclei of reticular activating system (RAS)

27
Q

2 types of GABA receptors

A

GABA(a)

GABA (b)

28
Q

GABA(a) functions

A

Fast inhibitory transmission:

  1. INcrease in Cl channel hyperpolarization
  2. Decrease membrane resistance
  3. Modulatory sites for: benzo’s and barbiturates
29
Q

GABA(b) functions

A

Slow inhibitory transmission:

Baclofen is a GABA(b) agonist and reduces mm spasms by INCREASING inhibition in spinal cord.

30
Q

Clinical importance of GABA: all drugs stimulating GABA cause an increase in Cl influx

A

Epilepsy (benzo’s and barbiturates)
Anxiety D.O.
Insomnia
Agitation

31
Q

RAS:

A

GABA from VLPO (ventrolateral preoptic nc) INHIBITS RAS.

Orexin neruons EXCITE RAS

32
Q

Cholinergic Neurons in CNS

A

Interneurons: neocortex, striatum, hippocampus
Projecting: brain stem to thalamus, basal forebrain to neocortex, hippo, and amygdala; peripheral neurons (autonomic, motor)

33
Q

Adenosine and forebrain

A

Affects basal forebrain constellation of cholinergic neurons including basal nc of Meynert

34
Q

2 cholinergic receptor types:

A

Nicotinic: fast
Muscarinic: slow

35
Q

Clinical importance of Cholinergic receptors:

A

Modulates: sleep-wake cycle, arousal, attention
Parkinsonism
Memory

36
Q

Parkinsonism and cholinergic neurons

A

Muscarinic receptors oppose dopamine effects in striatum.

Loss of dopa neurons=striatal imbalance, corrected by increasing dopa or reducing muscarinic activity

37
Q

Memory and cholinergic neurons

A

Alzheimers: loss of basal forebrain cholinergic neurons
Antimuscarinic induced delirium
Mutations in nicotinic channels: Autosomal dominant frontal lobe nocturnal epilepsy; congenital myasthenic syndromes

38
Q

Norepinephrine

A

Projecting brainstem neurons in:
Locus coeruleus to neocortex, hippocampus, thalamus, cerebellum, spinal cord–> attention and arousal
Tegmental region of Reticular formation to hypothalamus, basal forebrain, spinal cord–> autonomic and endocrine regulation.

39
Q

Clinical importance of NE

A
  1. Arousal, attention, sleep cycles: LC efferents
  2. ADHD and Narcolepsy treated w/amphetamine-like compounds
  3. Cognition: NE enhances memory formation.
  4. Some TCA’s like amitriptyline block reuptake of NE
  5. Adrenergic stimulation of hypothalamus decreases appetite.
  6. Pain perception (spinal cord): NE excites enkephalin producing interneurons in spinal cord to inhibit pain transmission during stress response.
40
Q

Serotonin: 5HT

A

Released by projecting neurons from 2 different raphe nuclei:

  1. RN to neocortex, thalamus, hypothalamus, amygdala, striatum.
  2. RN to brain stem, cerebellum, spinal cord
41
Q

5HT receptors

A

Different actions: 14 different subtypes

42
Q

Clinical importance of 5HT

A
  1. Depression: SSRI’s
  2. Panic D.O.: SSRI’s
  3. OCD: SSRI’s
  4. Migraine: agonists like sumatriptan, presynaptic meds block release of vasodilators, postsynaptic ones cause DIRECT vasoconstriction***
  5. Chemotherapy induced emesis: 5HT3 receptors in area postrema (medulla): block w/odansetron
  6. Pain perception by spinal cord: serotonin from PT’s stimulate pain sensory nn endings; serotonergic nn stimulate encephalin neruons in spinal cord.
  7. Schizo: atypical antipsychotics block 5ht2
  8. LSD: 5 ht agonist
43
Q

Dopamine’s tuberoinfundibular pathway

A

From hypothalamus to pituitary: regulate prolactin synthesis and release

44
Q

Dopamine nigrostriatal pathway

A

From substantia nigra to striatum: regulate motor planning and execution

45
Q

Dopamine mesolimbic pathway

A

From ventral tegmental area (VTA) to Nucleu Accumbens: regulates goal directed and reward behavior

46
Q

Dopamine mesocortical pathways

A

From the VTA to neocortex

47
Q

Dopamine in Parkinson’s disease:

A

Neurodegeneration of DA neurons in SN: relative loss of dopaminergic activity in nigrostriatal pathways: hypokinetic

48
Q

Dopamine in Huntington’s Chorea:

A

Neurodegeneration of striatal GABAergic neurons: relative excess of dopaminergic activity in nigrostriatal pathway: HYPERkinetic

49
Q

Dopamine in Schizophrenia

A

Relative excess of activity in mesolimbic and mesocortical pathways.
Extrapyramidal side effects from Antipsychotics.

50
Q

Dopamine in Drug Addiction

A

Increase of dopamine in mesolimbic pathway

51
Q

Dopamine in hyperprolactinemia

A

Dopamine inhibits prolactin

52
Q

Histamine

A

Posterior hypothalamus–> CNS
Regulation of arousal
Many drugs block it=sedation

53
Q

Opioid peptides

A

Regulate pain pathways at spinal and supraspinal levels

Clinically: Agonists (morphine) analgesic, important addiction drugs

54
Q

Role of tissue damage

A

releases many compounds which enhance nociceptive transmission to dorsal horn of spinal cord.

55
Q

What do enkephalins do?

A

inhibit pain transmission in dorsal horn by inhibiting release of glutamate and substance P from C fibers and stimulation of K+ channels on projection neurons.

56
Q

Enkephalin 2:

A

Enkephalin or morphine

inhibits presynaptic release of glutamate and substance P and postsynaptic increase K+

57
Q

Adenosine receptors

A

ATP, co-transmitter
Metabolized to adenosine upon release
Clinically: Xanthines block adenosine receptors producing arousal.

58
Q

Endocannabinoids

A

Cannabinoid (CB) Receptors: G-protein coupled receptors
Derived from arachidonic acid
Reuptake pump and intracellular degradation
Often located on axon terminals: stimulation inhibits neurotransmitter release.

59
Q

Endocannabinoids:

A 
Modulation of: 
Pain
control of movement
regulation of body temperature
Emesis
Appetite
learning and memory
cognition and neuroendocrine control

Pharmacology (14 decks)

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