Brain to Behavior Quiz 2 (Neurophisology Basics, Chemistry of Life, Drugs and Addiction)

neurophysiology

study of chemical and electrical signals within neuronal cells to process

plasma/cell membrane

separates intracellular environment from extracellular envrionment

selectively permable

lipid bilayer

membrane potential (Vm)

interior of neuron usually more negatively charged than exterior space

resting potential (Vrest)

when no inputs are acting upon a neuron

around -70 mV

Na+ and Cl- are highly concentrated ________ of the cell

outside

K+ is highly concentrated _____ of the cell

inside

diffusive force

pushes ions down their concentration gradient

high → low

leak channels

always open

gated channels

open/close in response to environment signal

Cations (Na+,K+) leaving or anions (Cl-) entering the cell =

more negative inferior

Cations entering or anions leaving cell =

more positive inferior

depolarization

inferior = less negative than Vrest

Na+ ions enter the cell

hyper polarization

inferior = more negative than Vrest

K+ ions leave cell

Cl- ions enter cell

Na+/K+ pump

move 2K+ in, 3Na+ out of neuron using 1 molecule of ATP

local

as potential travel away from its source and across the membrane (decays)

graded

larger stimuli → larger response

smaller stimuli → smaller response

initiation

neuron depolarized to threshold

depolarization/rising phase

interior of neuron rapidly becomes more positively charged

depolarization/falling phase

interior of neuron rapidly returns to negatively charged status

after-hyperpolarization / undershoot

neuron bypasses Vrest and is briefly hyperpolarized

voltage-gated K+ channels

Vm returns to Vrest not all the voltage-gated K+ channels have closed yet

return to rest

the neurons return to Vrest

activation gates

open in response to a condition being met

voltage gates

open when Vm reaches certain threshold voltage

voltage-gated Na+ channels

depolarization

open and closes quickly at threshold (around -50mV)

voltage-gated K+ channels

hyperpolarization

opens and closes slowly

fully open when voltage-gated Na+ channels are closed

ligand gates

open when a chemical (ligand) binds to the channel

neurotransmitter receptor

all or none principle

neuron either fires or does not

action potential amplitude always the same

frequency coding

increased stimulus intensity = more action potentials produced

refractory period

period after an action potential where the membrane is unresponsive to firing additional action potentials

propagation

signals moving down the axon due to ion flow

Na+ spreads out as it enters the neuron, triggers action potentials in neighboring sections of the neuron

axon inital segment (AIS)

where actions potential originate

connection between soma and axon

next to axon hillock

the highest concentration of voltage-gated Na+ channels

conduction velocity

speed of action potential propagation

determined by axon diameter and myelination

axon diameter

diameter of myelinated axon

larger diameter axon = faster conduction

myelination

glial cells form a membraneous sheath surrounding axon; insulates the axon

myelination = faster conduction

nodes of ranvier

gaps between sections of myelin where the axon is exposed

action potential only occurs at

Na+ ions flow at high speed along internodes

internodes

sections of axon covered by myelin

saltatory conduction

action potential appears to “jump” from node of ranvier to node of ranvier

saltare = jump/hop (latin)

synaptic vesicles

small, spherical organelles located in presynaptic terminal

filled with neurotransmitters

voltage-gated calcium channels

expressed densely on presynaptic terminal

at active zone\

Ca2+ ions highly concentrated outside the neuron

exocytosis

synaptic vesicles release it’s contents in response to something

neurotransmitters

endogenous chemical specialized for transmitting information between neurons

criteria:

are stored in axon terminals

are synthesized in neurons

are released by receptors on the postsynaptic membrane

evoke change sin postsynaptic cell

endogenous

naturally occurring, originating from organism itself

receptors

protei that receives and transducer signals

typically postsynaptic

binding site

areas dedicated to detecting/binding neurotransmitters

postsynaptic effect

neurotransmitters fit in receptos and activate them

ionotropic receptors

simple receptor = ligand-gated ion channels

open in response to ligand binding

very fast changes in Vm

effects depend on ion selectivity

degradation

rapid breakdown/inactivation of neurotransmitters by an enzyme

ex. ACh and ACh-strase

reuptake

neurotransmitter is reabsorbed by transporters in presynaptic terminal to be reused

diffusion

neurotransmitter molecules diffuse out of the synapse

postsynaptic potentials (PSPs)

brief changes in postsynaptic Vm

small, local, graded potnetial

excitatory = depolarizing

inhibitory = hyperpolarzing

excitatory postsynaptic potentials (EPSPs)

depolarizing postsynaptic potential

Na+ channels

pushes postsynaptic Vm toward the action potential threshold

inhibitory postsynaptic potentials (IPSPs)

hyper polarizing postsynaptic potential

K+ or Cl- channels

pushes postsynaptic Vm away from threshold

signal intergration

how postsynaptic potentials interact on the postsynaptic neuron to influence its firing

happens at axon hillock

spatial summation

adding up of potentials from different locations across the neuron at the axon hillock

temporal summation

adding up potentials that reach the axon hillock based on time of arrival

EPSP-IPSP cancellation

IPSP spatially coincides with an EPSP and partially or totally cancels it out

metabotropic receptors/g-protein-coupled receptors

slow but powerful and diverse effects

signal amplification
effects:

indirectly open ion channels

change ion channel conductivity

add/remove receptors from membrane

alter gene expression

receptor subtypes

can differ in anatomical distribution

work w/ different ions

respond to multiple neurotransmitters

interact w/in / across neuron populations to alter signaling

amino acids

GABA, glutamate, glycine, aspartate, histamine

amines

acetylcholine, dopamine, serotonin, norepinephrine, epinephrine, melatonin

neuropeptides

endorphins (class), dynorphins (class), enkephalins (class), oxytocin, vasopressin, neuropeptide Y, substance P, releasing hormones (class)

gases

nitric oxide, carbon monoxide

breaks neurotransmittger rules → produced outside oxon terminals (in dendrites)

does not require receptors

often retrograde trasmitters

glutamate (glu)

most common excitatory neurtransmitter

key role in memory formation

glu receptors

ionotropic and permable to Na+

ampa

nmda

kainate

metabotropic glu receptors (mGluRs)

gamma-aminobutryic acid (GABA)

most widely distributed inhibitory neurotransmitter

controls excitability

gabaA receptor

ionotropic Cl- channels

gabaB receptors

metabotropic

slow inhibitor via K+ and other channels

amines

typically alter glutamate-GABA signaling balance

neuromodulation

alteration of nerve activity through targeted delivery of a stimulus to a specific neurological site

catecholamines

derived from tyrosine and a six-sided catechol ring in their molecular structure

dopamine

norepinephrine

epinephrine

indolamines

delivered from tryptophan and featuring a five-sided indole ring

serotonin

melatonin

acetylcholine (ACh)

origin = basal forebrain

learning/memory processes

used at neuromuscular junction (NMJ)

released by the parasympathetic nervous system

disruption = impairment of learning/memory processes

loss of ACh neurons in Alzheimer’s disease

nicotine ACh receptor (nAChR)

mostly ionotropic

excitatory

muscarinic ACh receptor (mAChR)

metabotropic

excitatory or inhibitory

dopamine (DA) in mesostriatal pathway

origin in substantina nigra

motor control

loss associated w/ Parkinson’s disease

dopamine (DA) in mesolimbocortical pathway

origin ventral tegmental area (VTA)

reward, reinforcement, and associative learning

abnormalities associated w/ schizophrenia

dysfunction = addiction, attentional disorders, psychosis

D1-like receptors

metabotropic

D1 and D5

excitatory

D2-like receptors

metabotropic

D2 - D4

inhibitory

norepinephrine (NE) / noradrenaline (NA)

locus coeruleus (LC)

alertness, emotion, stress/anxiety, attention

norepinephrine (NE) / noradrenaline (NA)

lateral tegmental area (LTA)

sympathetic nervous system

beta blockers

norepinephrine (NE) / noradrenaline (NA)

drugs given to help treat abnormal heart rhythms, protect against heart attacks, and lower anxiety/stress response

adrenergic response (adenoceptors)

shared receptors for norepinephrine (NE) / noradrenaline (NA) and epinephrine/adrenaline

alpha receptors

norepinephrine (NE) / noradrenaline (NA)

metabotropic

alpha 1, alpha 2

beta receptors

norepinephrine (NE) / noradrenaline (NA)

metabotropic

beta 1, beta 2, beta 3

serotonin (5-HT)

5-hydroxytryptamine

origin in apid nuclei

mood, anxiety, sexual behavior

neuropeptides

chains of typically 10 amino acids or more

large molecules → expensive to synthesis

typically synthesized on demand where/when needed

opioid peptides

neuropeptides

mimicked by opiate drugs

reward/pleasure

control of pain

endorphins, enkephalins

pituitary hormones

neuropeptides

reproductive bheavior

socialization

oxytocin, vasopressin

peptides in gut, spinal cord, or brain

neuropeptides

feeding

neuropeptide Y

retrograde transmitters

travel from postsynaptic back to presynaptic neuron

passes through the cell membrane and directly activates intracellular processes

increases chances of voltage-gated Ca2+ channels opening

increases neurotransmitters synthesis

pharamcology

study of how drug affects the body as a whole

neuropharamcology

study of drug effects specifically on the brain

ligand

a substance that binds to a receptor

agonist

initiates normal effects of the transmitters on that receptor

antagnoist

binds to a receptor and does not activate it

prevents the binding of other ligands

inverse agonist

initiates the reverse of the normal effects

competitive

drug directly competes w/ endogenous ligand at binding site

noncompetitive

drug does not directly compete

binds to modulatory site instead

modulatory site

when a molecule bound with a ligand alters the primary receptor

binding affinity

degree of chemical attraction between ligand and receptor