NURS 165 Study Guide - Final Guide: Prefrontal Cortex, Kidney Failure, Monoamine Oxidase
Neurotransmitters – Depression & Anxiety
• Basic Neuronal Physiology
o Conduction of action potential → release of neurotransmitter →
postsynaptic binding → postsynaptic effects
o Neuro meds can alter
▪ Synaptic transmission
• More common
• Can be selective
▪ Axonal conduction
• Less common
• Less selective
▪ These meds influence receptor activity on target cells!
o AP opens voltage-gated calcium channels → depolarization → influx
of calcium → fusion of synaptic vesicles with cell membrane →
release of neurotransmitter into synaptic cleft via exocytosis → NT
diffuses across cleft → binds to receptors on postsynaptic cell
membrane
• Synaptic Transmission Steps
o Synthesis of transmitter from precursor molecules
o Storage of transmitter in vesicles
o Release of transmitter
▪ This is response to action potential
o Action at receptor
▪ Binds reversibly to receptor on postsynaptic cell (neuron,
muscle, etc. → causes response)
o Termination of transmission – happens by:
▪ Reuptake into nerve terminal transporter protein
• Secondary active transport
• Uses movement of sodium down concentration
gradient to transport neurotransmitter against its
concentration gradient back into presynaptic terminal
• There it is usually stored. Sometimes broken down.
▪ Enzymatic degradation
• AChase
▪ Diffusion
• Classes of Neurotransmitter receptors
o Ionotropic
▪ Neurotransmitter binding directly opens ion channel
▪ Very rapid
o Metabotropic
▪ Neurotransmitter binding activates G protein → second
messenger production and/or ion channel opening
▪ This takes more time – slower signaling
find more resources at oneclass.com
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• Ionotropic: ligand-gated ion channels
o Have ligand-binding site for NT
o Central pore with specific ion selectivity
▪ Can open/close
o Rapid activation!
o Can rapidly change membrane potential to either:
▪ Depolarize (create excitatory postsynaptic potential)
▪ Hyperpolarize (create inhibitory postsynaptic potential)
o Excitatory synapse
▪ Excitatory: receptor permeable to sodium → inside becomes
LESS NEGATIVE → easier to reach threshold for AP
▪ Inhibitory: receptor permeable to chloride → inside becomes
MORE NEGATIVE → harder to reach threshold for AP
▪ NT binds to ionotropic receptor → pore on receptor permeable
to sodium opens → sodium movement into cell →
depolarization
▪ Multiple excitatory inputs → action potential!
• Summation
• IONOTROPIC CAN ALSO BE INHIBITORY!!
o Rapid transmission doesnt always mean its excitatory!
o Inhibitory ionotropic – opening of ligand gated channel to chloride
▪ Inside of cell becomes MORE negative → HARDER to get action
potential
• Metabotropic
o Characteristics of these receptors
▪ G-Protein coupled receptors with binding site for NT
▪ Work through enzymes that generate second messengers
• Take home message: metabotropic uses 2nd
messengers and that’s why it’s slower
o Slower changes b/c produce changes in gene expression
o Types of neurotransmitters
▪ GABA is inhibitory
▪ Glutamate is excitatory
Thick arrows
indicate most
common pathway.
So, fast
transmission
usually goes
through ligand
channels, and vice
versa.
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Less negative easier to reach threshold for ap. Inhibitory: receptor permeable to chloride inside becomes. More negative harder to reach threshold for ap: nt binds to ionotropic receptor pore on receptor permeable to sodium opens sodium movement into cell depolarization, multiple excitatory inputs action potential! Ionotropic can also be inhibitory: summation, rapid transmission doesn(cid:495)t always mean it(cid:495)s excitatory, inhibitory ionotropic opening of ligand gated channel to chloride. So, fast transmission usually goes through ligand channels, and vice versa: glutamate consciousness , gaba. Why: almost like a hot potato did your job, now get out. In parkinson"s disease, a deficiency of dopamine upsets the normal balance between dopamine and acetylcholine. In behavioral medicine: there is an important role for da in motivated, norepinephrine nuclei behaviors. Says stop when too much is present: all have excess transmitter metabolized by mono-amine oxidase (mao, dopamine and ne can also be metabolized by comt, when mao is inhibited, increased dopamine and ne treatment for depression.
