Biancardi Study guide Flashcards
Autoreceptors
Negative feedback
Says to stop producing Calcium ions
Inotropic receptors
Ion channels
rapid post-syn events
Metabotropic Receptor
G proteins activate channels
Slower onset events
Mechanisms by which GABA and Glycine hyperpolarize the membrane and where they
are mainly found
Opening of ligand-gated chloride ion ( Cl-) channels
Gaba= brain
Gly= spinal cord
Monoamines – Norepinephrine, Dopamine, and Serotonin - review their
reuptake/degradation, and their implication in pharmacological uses (i.e: Selective
serotonin transporter proteins reuptake inhibitors, and monoamine oxidase
inhibitors).
Know that monamines are
Norepinephrine, Dopamine, and Serotonin
Norepinaphrine
Arousal, vigilance, anxiety
Reuptake/ degradation: monoamine oxidase ( MAO)
Pharmacological uses: MAO inhibitor–> antidepressant
Dopamine
Control movement, reward center, emotion, motivation, inhibit prolactin release
Reuptake/ degradation:monoamine oxidase ( MAO)
Pharmacological uses: MAO inhibitor–> antidepressant
Serotonin
Mood, memory, sleep-wake cycle, cognition
Reuptake/degradation: plasma membrane through serotonin transporter proteins (SERT)
Pharmacological Uses: SERT inhibitor
Amino Acids – Glutamate and GABA – Correlate imbalance of both
neurotransmitters with increase or decrease of neuronal activity (implication in
seizures). Review their actions depolarizing or hyperpolarizing the target neuron and
their reuptake and degradation.
these are amino acids
Glutamate
Learning, memory, nociception pathways
Increase in neuronal activity–> excitable (depolarize)
Prolonged stimulus= neuronal death/ injury and seizure
Degradation= reuptake through excitatory amino acid transporters (EAAT)
- recycled by glia cells
Gaba
Inhibitory
Role in sleep, induction, relaxation, suppression in seizures and anxiety
Degradation: GABA transporters and glia cells
Review division of Lower Motor Neurons
Review clinical implications of NMJ dysfunction – review mechanisms of organophosphates toxicity, myasthenia gravis, botulism, and tick paralysis.
Review function of Acetylcholinesterase
Cleaves Ach ( breaks up) for uptake and to be re-synthesized
