DBM - Chapter 5

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30 Terms

1
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adrenal medulla (kidney)

secretes EPI and NE into the bloodstream

act as hormones

2
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vesicular monoamine transporter (VMAT)

packages monoamines into vesicles

VMAT1 - adrenal medulla; VMAT2 - brain

DA, NE, 5-HT

3
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independent release

some drugs of abuse cause DA and NE release independent of cell firing (Ca2+ - independent release)

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somatodendritic autoreceptors

on cell bodies or dendrites

slows rate of neuron firing

reduces rate of NT release

“impulse modulating”

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terminal autoreceptors

on presynaptic nerve terminal

inhibit further NT release

“release or synthesis modulating”

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somatodendritic DA autoreceptors

midbrain in VTA and SN

enhances opening of K+ channels

slows firing rate

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terminal DA autoreceptors

enhances opening of voltage-gated K+ channels

inhibits Ca2+ entry to VGCCs

enhancing DA uptake via DAT

inhibiting TH

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somatodendritic NE autoreceptors

enhance opening of K+ channels

9
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terminal NE autoreceptors

inhibit VGCCs

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clonidine

treats high blood pressure and opioid withdrawal

NE autoreceptor agonist

reduces NT release

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yohimbine

antagonizes NE autoreceptors

increases NE release

exacerbates opioid withdrawal

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membrane transporters

DAT and NET

non-selective, each can take up the other NT

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SNRI

inhibits reuptake of both NE and 5-HT

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cocaine

inhibits reuptake of all monoamine NTs: DA, NE, 5-HT

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catchecol-O-methyltransferase (COMT) and monoamine oxidase (MAO)

metabolize catecholamines

DA → HVA

NE → MHPG in the brain

NE → VMA in the PNS

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ascending DA pathways

innervate forbrain regions and release DA

  • nigrostriatal

  • mesolimbic

  • mesocortial

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nigrostriatal dopamine tract

substantia nigra → caudate-putamen (striatum)

facilitates voluntary movement

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Parkinson’s Disease

massive loss of DA neurons in SN

denervation of the striatum

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mesolimbic dopamine pathway

ventral tegmental area → nucleus accumbens

motivated behaviors

positive symptoms in schizophrenia

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mesocortical dopamine pathway

ventral tegmental area → prefrontal cortex

working memory

negative and cognitive symptoms in schizophrenia

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dopamine receptor subtypes (metabotropic)

D1 and D5 (D1-like)

  • stimulates AC via Gs

D2, D3, D4 (D2-like)

  • inhibits AC via Gi

  • enhances K+ channel opening

  • inhibits VGCCs

D2 are autoreceptors and postsynaptic receptors

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dopamine hypothesis of schizophrenia (1967)

excess DA function results in symptoms of schizophrenia

high doses of amphetamine can produce psychotic reaction in health individuals » can be reversed by DA antagonists

psychotic behavior driven by excess post-synaptic D2 receptor activation

“typical” antipsychotic drugs: D2 receptor antagonists

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D2 receptor antagonists: acute administration

increased firing rate after antipsychotic administration

increased DA turnover (synthesis, release, metabolism)

enhanced release accompanied by post-synaptic blockade

no worsening of symptoms

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D2 receptor antagonist: chronic administration

decreased DA turnover

two theories:

  1. initial increase in synaptic DA followed by gradual decrease

    • chronic blockade leads to up regulation of autoreceptors

    • regulation of DA turnover

  2. after initial increase in DA turnover, DA neurons temporarily inactivate (depolarization block)

    • resulting decrease in turnover

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D2 receptor antagonist: side effects

extrapyramidal symptoms (EPS)

  • dystonia (continuous spasms + muscle contractions)

  • akathisia (motor restlessness)

  • Parkinsonism (rigidity, bradykinesia, and tremor)

tardive dyskinesia » permanent

  • irregular, jerky movements

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dopamine system stabilizers

partial DA agonists: compete with DA for receptors, reduces DA effect » reduces positive symptoms

stimulates DA receptors in brain regions with too little DA » reduces negative symptoms

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noradrenergic system

CNS: brainstem » locus ceruleus (LC)

  • ascending fibers project to many forebrain structures

PNS: post-ganglionic NT in sympathetic division of ANS

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noradrenergic receptors (metabotropic)

α1: operates via Gq, increase in Ca2+ ions in post-synaptic cell, PKC activation

α2: inhibits AC via Gi, increase K+ channel opening, inhibit VGCCs (like D2)

ß1 and ß2: stimulates AC via Gs (like D1)

postsynaptic receptors throughout cortex, thalamus, hypothalamus, cerebellum, limbic system

α2 receptors function as autoreceptors in LC and nerve terminals

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α1 and α2 receptors in PFC

NE has higher affinity for α2 than α1 in PFC

activation of post-synaptic α2 in PFC enhances working memory

stress stimulates NE release in the PFC

  • activation of α1 receptors » negative effect on cognitive functions of the PFC

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ß-antagonists (beta blockers)

hypertension, cardiac arrythmias

generalized anxiety disorder (GAD): propranolol

  • reduce physical component associated with excess NE activity

  • psychological component still present