Neuro exam 4

Excitatory Amino Acid Neurotransmitters

glutamate

inhibitory amino acid neurotransmitters

GABA, glycine

GABA location

mainly in brain and brainstem, but also in spinal cord

Glycine location

mainly in spinal cord, also in brain and brainstem

GABA A

ionotropic cl channel

GABA B

metabotropic, k channel, long lasting action

Glycine receptor

ionotropic, cl channel

what happens with a cl influx

hyperpolarization, produces IPSP

IPSP

fast hyperpolarization by ionotropic, slow hyperpolarization by metabotropic

AMPA receptor

ionotropic, fast

NMDA receptor

ionotropic, voltage dependent

NMDA receptor key features

blocked by mg at rest, needs depolarization via AMPA to open, needs glycine as co-agonist

Effect of na influx (and ca influx for NMDA)

depolarization, makes EPSPs

EPSP

depolarization by ionotropic or slow hyperpolarization from metabotropic

ACh synthesis and degradation

synthesized by ChAT enzyme, broken down by AChE

Nicotonic ACh receptor

ionotropic, NMJ and CNS, fast

Muscarinic ACh receptor

metabotropic, CNS and heart, slow

Ionotropic

fast

metabotropic

slow, via gpcrs

Catecholamines

dopamine, epinephrine, norepinephrine, derived from tyrosine

catecholamines function

movement, mood, attention

serotonin

mood, sleep, emotions, derived from tryptophan

How optogenetics works

insert gene into neuron using virus, promoter targets cell of interest, opsin gene and reporter gene, deliver light with fiber optic cable

Channelrhodopsin

blue light, depolarization and activation

halorhodopsin

yellow light, cl hyperpolarization and inhibition

archaerhodopsin

green light, H hyperpolarization and inhibition

what can optogenetics target

cell bodies in a brain region, axons/terminals

reporter gene

visualize neurons that express optogenetic tools

what does light location determine

which circuit is manipulated

what does viral injection determine

which neurons express opsins, inject region does not equal stimulate region

Schizophrenia

working memory deficits, prefrontal cortex dysfunction

Mouse model

impaired working memory, altered PFC structure, impaired synaptic transmission and LTP

findings of mouse model

reduced synaptic strength, PFC deficits