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lesion/ablation
destroy part of the brain for experimental purposes
Different ways to cause lesions
Radio frequency, excitotoxic lesions, sham lesions
electrolytic lesion/radio frequency
lesion caused by electrode dropped on the brain. burns everything that electrode touches.
excitotoxic lesions
use chemicals to cause lesion, can be more specific on what part/ which neurons is destroyed
ex:kainic acid>binds to glutamate and causes neuron to overexcite and die.
Sham lesion
control group. animal has everything else done to them except for the actual lesion.
stereotaxic surgery
how they put a tip of an electrode to a precise location.
stereotaxic apparatus
what is used to steady head and position electrode of stereotaxic surgery. halo is an example for this.
bregma
when the coronal and sagittal fontanelle fuses... this becomes 0 on the stereotaxic atlas. where they base all of the movements from
fixation
process of preserving brain tissue
formalin
most commonly used fixative, halts autolysis (rotting)
cryostat
meat slicer within a fridge.
microtome
meat slicer
nissil stain
stains cell bodies.
antigen
forgein object that antibodies bind to
antibody variable region
top of y... also called antigen binding site
light chain
top half of Y antibody
heavy chain
bottom half of Y antibody
amplification of signal
secondary antibody attaches to heavy chain of first to tag another anti-antibody
immunofluorescence
antibodies with fluorescence properties (tags) co label things
Computer axial tomography(CAT or CT)
x-rays. have to do several to get several angles and low resolution
MRI (Magnetic Resonance imaging)
uses extremely strong magnetic field to disrupt protons. measures radio waves and has better resolution than CAT
Diffusion tensor Imaging (DTI)
monitors hydrogen atoms (water) movement because those detects white matter tracts. can tract axons coming from particular part of brain
microelectrodes
used to record neural activity of individual neurons.
macroelectrodes
records neural activity of bigger area of neurons. used in EEGs
EEGs
record of electrical activity on paper from macroelectrodes
positron emission tomography (PET)
injection of radioactive deoxyglucose, emit positrons, areas that use most glucose emit most signal. expensive
functional MRI (fMRI)
detects oxygen levels in blood. more blood flow in a region of brain=more activity. can assess neural activity during event... works by light sensitive neuron channels
optogenetics
taking gene from light sensitive algae... put it into neuron... now you can activate neuron with a certain light.
transgenic
add gene from another species to animal; ex: amyloid beta is something mice don't have aka no alzheimers
knock out animals
delete a gene and see effects
conditional knock out
delete gene at specific: organ, age, or cell type
psychopharmacology
study of the effects of drugs on nervous system and behavior
drug
chemical or compound that is taken in to the body and has potential to produce some effect
site of action
pt where molecules of drugs interact with molecules located on or in cell
pharmacokinetics
process in which drugs are absorbed, distributed within the body, metabolized, and excreted
ligand
the drug/neurotransmitter
cognate receptor
what ligand binds to
endogenous
ligand that the body makes like neurotransmitters
exogenous
ligand that is synthetically made ex:alcohol
dose response curve
best way to determine effectiveness of drug. increasingly stronger dose of drug produce larger effects until max effect reached. after that the risk of adverse effects increases
therapeutic index
used to measure margin of safe doses for drugs. most desirable drug has high affinity for sites of action that produces therapeutic effects and low affinity for sites of action that produces toxic effects
tolerance
reduced effect of drug after repeated admin.
physiological tolerance
body becomes more efficient in metabolizing drug
behavioral tolerance
learning how to run drunk
placebo effect
control group; no physiological effect; sugar pills
antagonist
block or inhibit postsynaptic effect
agonist
facilitate postsynaptic effect
direct agonist
drug attaches to postsynaptic receptor directly and mimics same potential
direct antagonist
drug attaches to postsynaptic receptor directly and does not open ion channel
indirect antagonist
drug attaches to a site on receptor and does not open ion channel
indirect agonist
drug attaches to a site on receptor and ion channel opens
Otto Loewi
experiment where one pig heart stimulated and the fluid made the other heart stimulate.
vagusstoff
acetylcholine in solution that caused second heart to beat.
neurotransmitter criteria
1. presynaptic(synthesis and storage)
2. action potential
3. postsynaptic receptors
4. change in postsynaptic cell
Dales law
every neuron uses one neuron receptor... NOT TRUE
glutamate
amino acid neurotransmitter
precursor: glutamine
learning and memory
EXCITATORY
NMDA
inotropic GLU receptor... blocks Mg to depolarize dendrite. eventually causes influx of Ca
AMPA
Na channel... GLU receptor
GABA
Inhibitory NT
precursor:glutamate
Acetylcholine (ACh)
Amine NT
synthesis: acetate and choline
muscles: NMJ
memory: alzheimer's disease
ACh distribution
projection neurons-basal forebrain
interneurons
Serotonin
mood, eating, sleeping, arousal, pain regulation. emotional behavior
precursor: tryptophan
serotonin distribution
Raphe nucleus
Dopamine
movement, emotional responses, and reward/pleasure.
precursor:tyrosine>L-DOPA
Dopamine distribution
ventral tegmental area
substantia nigra
ventral tegmental area
area of brain that is associated with addiction
Norepinephrine
ADHD
stimulate
precursor: dopamine
converts to epinephrine/adrenaline...
Norepinephrine distribution pathway
locus coeruleus
Monoamine oxidase (MAO)
degrades dopamine, norepinephrine, serotonin
inactivation of neurotransmitters
1. diffusion
2. degradation by enzyme,
3. reuptake
4. removed by astrocyte
Cocaine
stimulant
behavioral effects: euphoria, elevated mood, alertness, sense of well-being
Circulatory:BP, heart rate and cardiac arrest
cocaine mechanism
antagonist to dopamine, NE, and serotonin transporters.
amphetamine
behavior: alertness
appetite suppressant (tolerance)
addiction, cardiovascular problems, psychosis
amphetamine mechanism
1. reverses transporters> no reuptake of dopamine
2. inhibits vesicular storage
3. inhibits MAO> dopamine keeps on attaching
amphetamine-induced psychosis
schizophrenia-like
hallucinations
tactile-feeling sensations like bugs on skin
paranoid delusions
stereotyped motor behavior(rocking, hand ringing)
antipsychotic meds help
alcohol
NMDA antagonist
GABA receptor> depressant
alcohol effects
low dose--- stimulant
high dose---- depressant
metabolism of alcohol
converts to acetaldehyde> needs ALDH to convert to acetic acid or
PUKE.
Asians ancestry
more than 50% lack ALDH gene
fetal alcohol syndrome
defects caused by lack of vitamin A... alcohol is a competitor for it.
Neuron communication within
electrical signal from action potential
neuron communication between
chemical signals from neurotransmitters
sodium potassium pump
3 sodium out cell
2 potassium in
resting potential is critical for neuron survival
multiple sclerosis
demyelinating autoimmune disease
Tetrodotoxin (TTX)
blocks Na channels
shuts down action potential
axodendrite
synapse on dendrite
axosomatic
terminal button on somatic membrane
axoaxonic
presynaptic terminal button on top of postsynaptic terminal button. can block neurotransmitter
exocytosis
transport neurotransmitters out of cell with help of voltage gated Calcium channels
inotropic receptor
ligand gated ion channel, when neurotransmitter attaches to it, it opens.
metabotropic receptor
neurotransmitter causes g protein on receptor to activate enzyme to stimulate second messenger. the second messenger goes into cytoplasm and opens ion channels
Excitatory postsynaptic potential (EPSP)
depolarization
sodium channels influx
Inhibitory postsynaptic potential (IPSP)
hyper polarization
Chloride influx
potassium efflux