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Insulation of axons
- CNS= oligodendrocytes
- PNS= Schwaan cells
What does tetrodotoxin do?
Inhibits sodium voltage gated channels (inhibits saltatory conduction)-> Death
What do Ouabain and digitalis do?
Inhibit sodium/K Atpase
Similarities between NMDA and GABA receptors
- a) ligand bindingn site (NT)
- B) channel binding side (regulators, poisons)
- c) modifiers/co-activator site
Differences: NMDA lets in calcium, GABA lets in chlorine
What enzyme turns Glutamate into GABA
actions of Methylxanthines
- Inhibits PDE-> Increases cAMP
- increase intracellular calcium (cardiac contractility)
- blocks adenosine receptors
- inhibits prostaglandins
- stimulates gastric acid secretion
metabolism of methylxanthines
metabolized by liver cyps
OH-hydroxylations and demethylation
actions of nicotine
- Stimlates sympathetic ganglia/adrenal medulla
- increaased BP, heart rate, vasoconstriction
major metabolite= cotinine, N'-oxide
Actions of Cocaine
- Stimulation of cortex and brain stem
- blocks presynaptic reuptake of NE, serotonin and DA by blocking DAT
Sympathetic potentiator (vasoconstriction, tachycardia etc. )
Local anesthetic by inhibition of voltage-dependent Na channels
What do imipramine and amitriptyline do?
Synthetic drugs that inhibit DAT
- NT elevated through increased release from intracellular stores
- inhibition of monamine oxidase
structurally most similar to NE and 5-ht (some convergence with DA), thus mostly noradrenergic effects
Hallucinations largely auditory and tactile in nature with a strong paranoia component
What's special about methamphetamine
higher ratio of CNS:PNS effects
moa of LSD
- Serotonin agonist (note that serotonin is derived from tryptophan, and LSD looks like tryptophan/5-ht) @ midbrain-presynaptic membrane
- activation of sympathetic neurons
- visual hallucinations
- high potency
What can you use haloperidol for?
Blocks LSD effects
MOA of phencyclidine
Blockade of NMDA by PCP induces/exacerbates psychotic symptom
Partial agonist at Dopamine D2 receptors
Usually have a magnesium block, glutamate binds MG2+ allowing calcium to enter, increasing depolarization
PCP binds an adjacent site on NMDA, blocking the receptor from activation, thus downstream neurons have greater Dopamine activity
MOA of benzodiazepines
- Binds GABAa receptor subtype at a co-activator site, crowding the normal conformation of the receptors, causing excessive opening of chloride channels when GABA binds
- reduces anxiety by selectively inhibiting limbic circuits
- no anti-psychotic effects
- sedative properties, hypnotic at higher levels
- muscle relaxant-> presynaptic inhibition on spinal cord
highest density of binding sites in cerebral cortex, amygdala, hippocampus, hypothalamus
What is flumazenil used for?
Anaonist for diazepam
MOA: blocks reuptake of neurotransmitters DA, NE, 5-HT; take time to exhibit effects possibly due to cellular changes. Also inhibit a-adrenergic, histamine, muscarinic receptors
- don't exhibit their anti-depressive effects in normal individuals.
- mood elevation slow in onset, but effects are persistent.
- tolerance to anti-cholinergic adverse events and autonomic effects develops.
- strong component of psychological and physical dependence.
TCAs and their effects on various other drugs
- TCA+ethanol: toxic sedation
- TCA+ indirect sympathetics: blocks effects by preventing indirect mimmetic from getting to their intracellular site of action
- TCA+ direct sympathetics: potentiates the effects
- TCA+MAO-I: potentiation, can cause hypertensive crisis.
- Delta 9 Tetrahydrocannabinol most potent cannabinoid
- THC binds to GPCR (CB1=CNS, CB2=PNS)
- CB1 activation=pleasure perception and reward
Oxidized to inactive THC-COOH in the liver, reation p450 mediated
- subtype of stroke, characterized by decrease in cerebral blood flow to brian tissue (87% of all strokes)
- Focal ischemia: CBF reduced at specific region of the brain
- Global ischemia: CBF reduced at most parts of the brain
ATP decrease due to lack of CBF leads to excessive influx of Ca2+, and activation of apoptosis. Involves: elevated calcium activated lipases, kinases, endonucleases, and ROS
t-PA is an effective current treatment
- decreases severity and frequency of manic episodes in bipolar disorders.
- Lithium carbonate mostly prescribed
- Lithium modulates activity of NT(primarily glutamate) to protect neurons from excitotoxicity. Lithium inhibits GSK3 and IP3
- Lithium decreases brain inflammation
- Lithium is absorbed in GI tract, well distributed, and excreted in urine.
Lithium has a number of adverse effects, thus concentrations should be regularly monitored
Amyloid B hypothesis: Abnormal elevation or insufficent clearance of AB oligomers may underlie AD pathology. AB oligomers thought to be more injurious than AB-plaques
AB Oligomers diffuse into synaptic cleft and disrupt signal transmission. Oligomers will eventually aggregate forming plaques
Tau hypothesis: aggregates of hyperphosphorylated tau protein form NFT. Amyloid B is thought to promote phosphorylation of Tau.
Mitochondrial hypothesis: APP induces mitochondrial dysfunction in neuronal cells
- Donepezil= cholinesterase inhibitor to increase Ach levels
- Memantine= prevent glutamate reuptake by nerve cells
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