brain and behavior exam 2

pharmacokinetics

what the body does to the drug

pharmacodynamics

how the drug affects the body and behaviors

neurotransmitters

NTs transmit signals between neurons. they are relased at the synapse (ex. GABA, glutamate, and acetylcholine)

neuromodulators

influence the activity of multiple neurons. released into extracellular fluid, can inhibit or enhance the release of NTs. (ex. dopamine, norepi, histamine)

agonist

activates a receptor, mimicking the natural ligand. increases activity of receptor, leading to a biological response (ex. epi increases HR)

antagonist

blocks the activation of a receptor. inhibits a biological response (ex. propranolol inhibits the release of epi and decreases HR)

how does a drug cross the blood-brain barrier

it slips past your brains natural defense system and enters the brain through your blood (ex. benadryl and polysorbate 80, found in vaccines)

competitive (direct) antagonist

binds to the same site as the agonist, preventing its action. can be overcome by dose increase (ex. naloxone)

noncompetive (indirect) antagonist

antagonist binds to allosteric site, prevents the agonist from acting. cannot be overcome by dose increase. (ex. ketamine)

mimetic agonist

mimicks the function of a natural antagonist to target and inhibit NT

how do drugs act as agonists

by activating a receptor to produce a response

how do drugs act as anatagonists

by blocking a receptor without activating it

short acting (reversible) drugs

rapidly distributed to the brain because of high lipophilicity. have a ____ duration because they are quickly distributed from brain to other tissues, designed to be distriubuted to the bs fast. last for 2-4 hours (ex. stimulants)

long acting (irreversible) drugs 

slower, more sustained release into the ns, providing a longer lasting effect due to slow absorption/distribution. last 10-12 hours (adderall xr extended release). has fewer peaks and valleys in the bs leads to a smoother experience, longer presence in the bs can lead to reliance.

functions of neurotransmitters

NTs are the brains chemical messengers that carry signals between neurons that affect mood, movement, learning, and overall behavior

acetylcholine

precursor: choline. AcH: ache = muscles. essential for muscle movement.

nicoticic receptors

ionotropic (fast, excitatory). found in muscles, autonomic ns (PNS). increase firing; involved in movement and attention (nicotine, agonist)

muscarinic receptors

metabotropic (slow, modulatory). found in brain and PNS. affect HR, digestion, memory. Ex. atropine (antagonist)

dopamine

precursor: tyrosine. D1,D5- excitatory, D2,3,4- inhibitory. what sets them apart is nature of channels.  found in VTA. functions: reward, motivtion, movement, emotion. ex. antipsychs: block D2

serotonin

functions; appetite/mood regulation,

5-HT1: inhibitory; regulates anxiety and mood

5-HT2: excitatory; linked to perception and hallucinations (LSD target)

5-HT3: ionotropic; involved nausea and gutbrain signaling (appetite)

ex. SSRIs (enhance serotonin) and SNRIs (enhance serotonin and norepi)

norepi

functions: stress response (fight or flight)

alpha receptots

a1: excitatory; increases alertness and BP

a2: inhibitory; regulates NT release

beta

b1 and b2: excitatory; increase HR and arousal 

ex. beta blockers block b receptors to reduce anxiety and HR 

GABA

functions: relaxation

gaba_a: ionotropic; opens chloride channels, ca+ permeable ex. alcohol and benzos 

gaba_b: metabotropic; activates potassiam channels. inhibitory (slow) ex. baclofen (muscle relaxant, gaba angonist)

glutamate

functions: learning/memory

NMDA: involved in learning and memory; calcium permeable

AMPA: fast excitatory signaling

Kainate: excitatory, less studied

mGlu: metabotropic gluatmate receptors, modulate neural activity

ex. ketamine, blocks NDMA receptor

endorphins 

mu: pain relief, euphoria (target of morphine and heroin)- endorphins 

delta: mood regulation- enkorphins 

kappa: stress and dysphoria- dynorphins 

ex. naloxone blocks mu receptors to reverse an overdose 

presynaptic inhibition

where the activity of one neuron reduces the amount of NT released by another neurons axon terminal. it happens before the signal reaches the postsynaptic cell. the effect is to dampen or control how much NT is let into the synapse, which weakens the signal to the next neuron

depression eitiology 

explained by monomine hypothesis (low levels of s, norepi, and d contribute to low mood and reduced motivation. low serotonin. 

SIGECAPS- must have 5/9sx for +2w (DSM5 crit).

ssris boost monomine levels and aleviate symptoms

treatment: combo of CBT and SSRIs

bipolar eitiology

bipolar is associated with alternating manic and depressive episodes tied to ion regulation and NT imbalance. irregular sodium and calcium activity can cause unstable mood states- excess glutamate and dopamine occur during mania 

lithium modulates ion channels n intracellular signaling. lamotrigine reduces neuronal firing (mania), and atypical antipsychs block dopamine (d2) and serotonin (5-HT2A) receptors to control manic symptoms

treatment: psychotherapy and antipsychs 

scizophrenia eitiology

dopamine hypothesis (excess d activity,  particualy at d2, produce pos sx like hallucinations and delusions). glutamate hypothesis (underactivity of NMDA receptors contribute to cognitve and neg sx)

5As 2x sx +6m (DSM5 crit)

typical anipsychs (haloperidol) block D2 receptors reducing pos sx. atypical antipsychs (clozapine) block D2 and 5-HT2A receptors, improving broader sx

serotonin and appetite

reduces caloric intake through 5-HT(2c). serotonin alone cannot mediate weight loss for obese pts. ex. lorcaserin (5-HT(2C) agonist)

dopamine and appetite 

released in VTA when we consume pleasurable food, such as sugary, salty, or fatty items. da regulates the body’s hunger hormones (ghrenlin)

endocanabinoids

(1990) lipid discovered, mimicks thc, binds to anadaminde. functions: reward, appetite stimulation, natural anxiolyte. neuromodulatory effect; diffuse, widespread, delayed, but longer lasting

functions: information processing and memory

cb1 + 2 receptors

can have inhibitory effect. take dopamine pathway (VTA) axons → nucleus accumbus

cb1

has receptors in hippocampus 

mechanism of action for canabanoids 

When cannabinoids bind to CB1 or CB2 receptors, they trigger a series of events that modulate the release of neurotransmitters and other signaling molecules. 

• THC:

  Activates CB1 receptors, leading to increased release of dopamine (reward neurotransmitter) and inhibition of neurotransmitter release, resulting in psychoactive effects. 

• CBD:

  Interacts with both CB1 and CB2 receptors, but its mechanism is more complex. It modulates the activity of other receptors and enzymes, reducing inflammation and pain.