DRUGS AND BEHAVIOR

Corpus Callosum

Fiber that connect two hemispheres, people who have severe seizure disorder can have them severed and this can help researchers to understand where information is process

Thalamus

Nicknamed sensory relay station, all sensory information passes through the thalamus before it gets sent elsewhere, such as visual information, auditory, and tactile

Basal ganglia

Important for motor movement

Amygdala

Emotional information, if you have a traumatic experience amygdala activates

• epinephrine activates amygdala

• can lead to ptsd

• ptsd is over consolidation of fear, amygdala can help cotribute

• gets activated in other arousing situations

Hippocampus

• memory consolidation

• time limited but crucial area of the brain for laying down new memories

• long term potentiation

  • lots of drugs prohibit this (roofies), can give amnesia

• spatial imagination (ability to visualize places)

• lays down spatial maps - damage can impact ability to navigate through space

olfactory blub

smell

Brain stem

most protected area of the brain, consciousness and breathing (if you drink too much brain stem will go quiet/in respiratory failure), alc poisoning

Cerebellum

little brain, motor coodination, balance

can have stroke in this area

Blood brain barrier

Brain has lots of blood vessels

protected mechanism that makes sure that certain toxins don’t get in the brain

• barrier favors only allowing smaller, fat soluble molecules in, like nutrients

• endothelial cells that make up blood brain barrier are fused together

• for targeted chemo they make drugs that get to brain and can break past barrier

Nucleus accumbens (na)

pleasure center of the brain

found by placing electrodes in brain, dopamine is neurotransmitter

most drugs that people report liking all have in common that they increase dopamine in na

dopamine

some drugs cause explosion of dopamine

• ventral tegmental area in midbrain, sends dopamine to amygdala which deals with emotions

• nucleus accumbens (controls motor functions)

• prefrontal cortex (attention and planning)

• hippocampus (memory)

mesolimbic pathway

big part of reward circut in brain

addiction can have physiological components as well

• evidence for biological basis of drug dependence can come from animal models

• essentially the negative consequences don’t have the same impact, like your drug of choice paired with a substance that makes one sick does not cause the same aversion in the way that a non addictive substance would

Biology of the nervous system

basic building block - neuron

100 billio neurons

communication system

Terminal buttons

• bulb like structures that release neurotransmitter substance to other neurons

• contains vesicles full of transmitter substance

• cleft is space between descending and receiving neurons

neuron

• within neuron communication is electrical

• electrochemical communication

• neurons are affected by changes in electrical charges around them (inside negative, outside positive), diff is resting membrane potential

• moving depolarization is action potential

communication between neurons

• chemical

• when action potential reaches terminal buttons

• vesicles fuse to membrane and break open, will release NTS (CHECK)

Synapse

• to clasp

• junction where the terminal button of one neuron meets the membrane (usually dendrites) of another neuron

presynaptic neuron

sending neuron

post synaptic neuron

recieving neuron

exocytiosis

• finite period of activity after which 3 things could happen

• NTS binds to the post synaptic neurons receptors

if receptor is exitatory

excitatory post synaptic potential (epsp) will occur in the receivng neuron, causing it to fire

if receptor is inhibitory

inhibatory post synaptic potential (IPSP) occurs and the receiving neuron is less likely to fire

what happens afte exocytiosis

after binding for (or if no binding occured) neurotrnasmission is terminated by one of three mechinisms

• catabolism: process of enzymatic breakdown of nts into other molecules

• reuptake: nts returned to pre synpatic neurn by protein channel (transporter) and recycled

• diffusion: transmitter dreifts away from cleft

Glutamate

• amino acid nts

• most abundant “excitatory” nts

• present in all synapses

• glutamate receptors present on virtually all neurons receptors

• causes ion channels to allow positively charged ions into cell, depolariszing it

• important for the formation of memories

• involved in most all aspects of normal brain function including learning and memory (long term potentiation)

• some dissociative anesthetics such as ketamine or pcp can inhibit glutamate

how does alc effect glutamate

decreasing it

what can glutamate bind to?

ampa, kainate, nmda

• nmda is dense in hippocampus, will have amnesia if blocked

glutamate exciotoxicity (check)

• when a person has a stroke blood gets cut off from brain

• one of reasons that strokes are so devastating is bc transporters die first, greatly increasing scope of dameg

• even minor stroke scope of damage can be impactful bc of scope of damage, with stroke 4 hours before damage is permanent

GABA - Gamma amino butyric acid

• most abundant inhibitory nts

• if you didn’t have enough gaba you’d have seizures

• binds to gaba a and gaba b

• opens channels allowing CI to enter, causing ipsp

• alc, benzos increase gaba a lot which can quiet brain too much, alc is potent gaba agonist

• detox from alc can be dangerous bc brain can become hyper excitable and have seizures

action potential*

happens when membrane potential of a specific cell rapidly rises and falls (depolarization)

resting potenital

electrical potential difference across the plasma membrane of a cell in a non excited state

Monoamines

two subgroups

catecholamines

• dopamine, norepinephrine, epinephrine

and Indolamines

• serotonoin and melatonin

dopamine

• dopamine is important for movement (why not having enough can indicate parkinsons)

• emotions and mood regulation

• reward

• catabolized (broken down) by monoamine oxidase (mao) and catechol-o-methyltransferase (comt)

  • or eliminated by reuptake

• you cant have a drug that just produces dopamine, it’s difficult to target transmitters specifically

• more dopamine - get more norepinephrine and epinerphrine

• 
  

l dopa

prescription medication used to manage movement symptoms of parkinsons disease by turning into dopamine

what if you have underactive dopamine

this can translate to adhd, people who are sensation seeking can get addicted easier bc their baseline for the receptor is lower, their brains need extra stimulation to feel the same reward

• adhd is at higher risk to be addicted and the brain will actually look different on a scan

receptor subtypes for dopamine (many but these are main)

d1 and d2

• they are most likely to become addicted to psycho stimulants if you don’t have enough d2

• if you’re low in d2 and try ectasy or cocaine it will light up your brain more than a normal brain

• people low in d2 receptors are more likely to compulsively use stimulants

dopamine and psychosis

• schizophrenia associated with excessive dopamine activity

  • stimulants (like cocaine) increase monoamine activity and high doses can cause paranoid delusions, loss of contact with reality

  • DA antagonists are effective antipsychotics

norepinephrine

• causes physical changes associated with activation of sympathetic nervous system

• orginates from locus coeruleus and projects to many areas involved in stress response and emotion regulation

• dysregulation associated with severe clinical depression (think lack of behavioral motivation, fatigue, loss of interest in things one usually enjoys)

sympathetic nervous system

• pupils dialate, heartbeat goes up, lung bronchi expand, dry mouth

• muscles and blood flow, feelings of anxiety can come with it too

• doesn’t feel great when paired with smth threatening

• regulates mood, energy, alertness, and motivation

what adrenoceptors does norepinephrine bind to?

a1 a2 (alpha)

b1 b2 (beta)

exitiatory or inhibitory effects depending on subtype

b beta blockers slow heart rate

serotonin

(5hydroxytryta mine, 5ht abbreviation)

• binds to 5ht receptors 1-7, each have multiple subtypes

• raphenuclei (in brain stem) dense with cell bodies of serotonergic neurons that terminaste widely throughout brain

• mood states, emotional disorders, sleep regulation, satiation (feeling satisfied or full)

• trytophan is a precursor

  • catabolized by MAO or undergoes reuptake via serotonin transporters

risks of improper amount of serotonin

• risk of suicide when deficient

• excessive activity can lead to schizophrenia

• not enough can lead to migranes

• too much can cause body temp to go too high and internal organs can shut down

Acetycholine (ACH

• binds to cholingeric receptors 2 types

  • nicotinc

  • muscarinic

• parasympathetic nervous system activation

• released at neuromuscular junction (where nerve and muscle fibers meet one another), binding to nicotinic receptors at neuromuscular junctions, causing muscle cotractions

• in heart muscle, binds to muscarinic 2 (m2) receptors, slowing muscle contractions

• botox blocks ach release

• alzheimers disease (deteritiation of ach releasing neurons required for learning

  • hippocampus rich in ach

  • aricept (ach agonist via enzyme inhibition)

black widow spider venom

• causes synapses to flood with ACH, excessive muscle contraction

• muscle cramps, spasm, convusion, tremor, and possible death in rare cases

ach biological weapon

• sarin nerve gas inhibits acetycholinenesterase (causing buildup of ach) causing spasm of diaphragm, suffocation, and death

Neuropeptides

endorphin

• endogenous morphine or morphine within

• opiate/opioid drugs

  • morphine, heroin, opium are endorphin agonists

  • runners high is endorphins

  • natural painkiller produced by body

  • slows heart rate, respiration, metabolism