Neuro NT exam 1 Flashcards
-learning
-memory
excitatory
Glutamate
-muscle contraction
-cognitive processing
-project into cerebellum + pons (respiratory + breathing)
-hippocampus, amygdala, + cortex –> Alzheimer’s
ACh
-activated by nicotine
-iontropic
-found in brain + striated muscles
Nicotinic
-activated by muscarine
-found in brain, cardiac heart muscles, + smooth muscles
muscarine
-motor function
-optogenetic approach to understanding DA function
-reward + addiction
- increase cognitive processing
Dopamine (DA, Monoamine)
-fight-or-flight
-arousal
norepinephrine
-mood
-sleep
-increase cognitive processing
serotonin
-inhibition
-active until process needed
GABA
-ionotropic
-opens cl channels
-prevents seizures
GABA a
-leads to K+ channels opening
-leads to greater degree of hyper polarization than GABA a
GABA b
-ionotropic
-opens cl channels + stay open longer than gaba A
-important in retina functioning
GABA c
-increase efficiency learning drug out of body
metabolic tolerance
-change w/in neurons that decrease effectiveness
functional tolerance
study of neural bases of behavioral & mental processes
behavioral neuroscience
-apply magnetic field pulses through coil
*changes in magnetic field cause weak electrical currents on surface of brain
*stimulate neuron activity & stop neurons from communicating
*measuring behavioral/cognitive perception
Pros:
-ask causal questions about activity
-temp lesion
Cons: surface structures only
Transcranial Magnetic Stimulation (TMS)
-measures electrical potential of brain through electrodes
*measures timing of activity in brain well not good for spatial location
-used on kids kids + infants
-for research –> present stimuli + record event related potential (ERPs)
-can be measured when a person is at rest
EEG
how long after stimulus did ERP occur
latency
how large is neural response
amplitude
have latency and amplitude + measures across different electrode sites
-relates to cognitive function
ERPs
-measures localized activity in the brain/bloodgoing to region
-BLOOD OXYGENTATION LEVEL DEPENDENT (BOLD) signal
-have participant perform tasks in scanner
*great spatial not temporal resolution –> blood flow sluggish
fMRI
-removes brain structure or sever connections
-study effect on animal’s behavior
ablation
-cool down regis of interest to slow/stop neural activity
-pharmacologically disrupts neurons from firing
temporary lesions
use micro electrodes to measure electrical activity of cells
electrophysiology
-place micro electrode in extracellular space near a cell
-1-100s neurons detected
-electrodes used to activate neurons/brain areas
extracellular recording
measures brain chemistry + how many neurotransmitters there are
micro dialysis
use of genetic tools to induce neurons or other cells to become sensitive to light –> can execute/inhibit cell by shining light
-introduce genetic material into ells that allow them to express a channel sensitive to light
-shine light into Brain –> only cells with channels will be excited
-studies specific set of neurons that release NT
optogenetics
records electrical events within neurons and not just signaling
-measures sub threshold activity within neuron
intracellular signaling
uses probes to find neurons within specific mRNA sequence
in situ hybridization
synthetic radioactive probes bind to protein of interest
autoradiography
-antibodies detect expression of specific proteins
-can tell what cells express a certain protein & where protein is expressed
immunohistochemistry
structure + organization of nervous system
neuroanatomy
anatomical features of nervous system that are apparent to naked eye
gross neuroanatomy
take info from outside to inside
sensory neuron
communicate from central to peripheral nervous system
motor neuron
see both hemispheres + more oval
horizontal plane
slice vertically *only see 1 side of hemisphere
sagital plane
back of brain to front
-looks boxy
coronal plane
towards back
posterior
towards front
anterior
towards top + superior
dorsal
inferior; towards bottom
ventral
towards outside of Brain
lateral
white matter tract connecting both hemisphere
corpus collosum
sensory, emotions, problem solving, decision making
cerebral cortex
cell bodies * not myelinated
gray matter
sensory (touch) + perception
parietal lobe
pre-motor planning + basic function
frontal lobe
large, gray matter + lots of connections with other regions
*deep in brain
subcortical structures
motor control
basal ganglia
learning + emotion
limbic system
sensory relay station
thalamus
feeding, fleeing, fighting, + f’ing
hypothalamus
motor-coordination + learning *affected by alcohol
cerebellum
branching
arborization
-neurons –> 100-150 billion
-develop up to 20 weeks in womb
cells in brain
-structural support
-storing energy
-insulation
-cleaning up dead cells + waste
-influence communication btw neurons
glial cells
- brain composed of separating neurons + other cells independent, structurally, metabolically, + functioning
- info transmitted cell to cell across gas (synapses)
neuron doctrine
integration of messages form neurons & determine if message will be sent
*integration zone
axon hillock
receive into “ears”
*input zone
dendrites
moves action potential quickly
myelin sheath
sends NT into synapse
*output zone
axon terminals/synaptic button
conduction zone
axon
w/o myelin sheath; A.P to regenerate
nodes of ranvier
sends messages/ A.P
presynaptic neruon
receives messages
postsynaptic neuron
oligodendrocytes
CNS
Schwann cells
PNS
-directly controls ion channel (ligand binds to open channel)
-fast synapse
ionotropic
-indirectly opens/controls ion channels
-NT binds to G-protein
-slow synapse
-prolonged + magnified effect
metabotrobic
binds to identical site as NT
competitive binding affinity
binds to different part of receptor
noncompetitive affinity
propensity of ligand to activate receptor to which it is bound
(whether conformational change will occur)
efficacy
opposite effect than the NT would normally bind to receptor
*high efficacy
inverse agonist
lack of effect - drug doesn’t activate receptor & may block receptor site so NT can’t act
*low efficacy
antagonist
-same effect as NT
*high efficacy
agonist
down regulate by taking away receptors
counteract agonist
up regulate by putting more receptor sites
counteract antagonists
