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PSY 434 (3)
Lecture

chapter 7 psychopharm

5 Pages
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Department
Psychology
Course Code
PSY 434
Professor
Tara M Burke

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Chapter 7:ACh Synthesis and metabolism of Ach • Synthesis – Precursors • choline – from dietary fat • acetyl coenzymeA (acetyl CoA) – from fats and sugars – Enzyme • choline acetyltransferase • Metabolism – Enzyme • acetylcholinesterase – Metabolites • choline • acetic acid • (carboxyl group) • 5-HTTP: gives more immediate precursor for serotonin • We eat tryptophan to boost our serotonin levels, It gets converted to 5-HT (Serotonin) • To increase brain tryptophan need to ingest in absence of other proteins and high carbs Drugs that affectACh storage and release • ACh is stored in vesicles – Put there by vesicular ACh transporter (VAChT) – Vesamicol • Blocks VACHT ­ Less ACh in vesicles ­ Thus, less available for release • Suppresses REM sleep ­ Cholinergic system interacts with Thalamus to influence  sleep • Increased cholinergic activity = awake and  REM • Decreased cholinergic activity = nREM  sleep Acetylcholinesterase (AChE) • One form is in the presynaptic cell to break down excess intracellular ACh • Another form is present on the postsynaptic membrane. – Breaks down ACh in synapse • Another form is neuromuscular junction – Muscle cells secrete the enzyme to breakdown the ACh released by the  corresponding neuron • Immediately after ACh causes muscle contraction AChE removes  it. Choline Transporter • Choline is reuptaken by choline transporter • Hemicholine­3 (HC­3) – Blocks choline transporter – Reduces ACh production – Impairs attention in rats Block metabolism • Drugs that block AChE (reversible effects) – Physostigmine – Increases levels of ACh • Slurred speech • Hallucinations • convulsions Neostigmine and pyridostigmine • Synthetic analogs of physostigmine – Do not cross blood­brain barrier – Also reversible – Used to treat myasthenia gravis • Autoimmune disorder • Antibodies attach to ACh receptors in muscle • Eventually the receptors are broken down • Lack of receptors leads to insensitivity to ACH – Severe weakness – Fatigue – Blocking AChE prolongs ACh activity which stimulates the remaining  receptors. Irreversible AChE inhibitors • Insecticides – Weak versions • Nerve Gas – Sarin and Soman  • Strong irreversible AChE inhibitors – over­activates cholinergic synapses • Sweating • Salivating • Vomiting • Convulsions • Death by asphyxiation due to paralysis of diaphram muscles Antidote for Nerve Gas • Pyridostigmine bromide (PB) – Reversible AChE inhibitor protects against nerve gas – Apparently the reversible inhibition protects from the irreversible  inhibition. – Must be administered ahead of time • During first gulf war soldiers were instructed to take 3 tablets daily when at risk  for nerve gas • Animal studies had shown low risk for crossing blood brain barrier (BBB). • Unfortunately it appears that stress can increase the level at which this drug  crosses the BBB – Forced swim test in rats. – Gulf war syndrome? *Stress increases pyridostigmine entry into the brain Botulinum Toxin • Blocks release of ACh at neuromuscular junction – Stops the vesicles from cleaving to the presynaptic membrane – Very potent poison – Muscle weakness – Paralysis
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