BioPsych Exam 2

Calcium

What ion is needed for vesicle-fusion with the membrane to occur?

Reuptake, Enzymatic degradation, Diffusion

What are the three methods of removing Neurotransmitters?

Reuptake

Presynaptic terminal sucks it up and repackages for reuse

Enzyme degradation

Special enzymes in the synapse destroy it

Diffusion

NT diffuse out of synaptic cleft (areas of high concentration move to areas of low concentration)

Glumate

Most abundant excitatory neurotransmitter, binds to ligand gated Na Channel, causes EPSP

GABA

Most abundant Inhibitory neurotransmitter, binds to ligand gated Cl channel, causes IPSP

Affinity

Binding likelihood, Molecular strength

ionotropic receptors

ligand-gated ion channels, NT binds to channel, ions flow into the cell, permeable to specific ions

AMPA

Glutamate binds, a lot of Na enters the cell

NMDA

Glutamate binds, Mg is displaced, Na and Ca enters the cell

GABA Receptors

Bound to ionotropic Cl Channels, Causes IPSP on post-synaptic cells, Alcohol and benzodiazepines interact

Gq GPCR

Excitatory, increases levels of IP3, Causes release of Cl from organelle

Gs GPCR

Excitatory, increases levels of adenylyl cyclase, which increases levels of cAMP

Gi GPCR

Inhibitory, decreases levels of AC, which inhibits rise in cAMP levels

autoreceptors

a type of receptor located on the presynaptic membrane and modulates the neurotransmitter release

Agonist

A drug that binds with and activates an endogenous receptor or signaling process

Antagonist

A drug that binds with and blocks the actions of an endogenous receptor or signaling process

Modulators

Change the way a receptor functions, increasing or decreasing the effectiveness of the normal ligand

Tryptamines

psilocybin/psilocin, DMT

5HT2A receptor

Hallucinations and expanded consciousness is theorized to be mediated by psychedelics binding with this receptor

Blocking the 5HT2A receptor with risperidone or other drugs will do what?

Stop hallucinogenic activity

Ayahuasca

DMT is not orally active unless combined with an MAOI

Additive Drug Interactions

Drugs in the same class share targets, Alcohol and Xanax both affect GABA, or Off-target effects may overlap or synergize, Alcohol and opiates both reduce heart & breathing rate

Subtraction Drug Interactions

Drugs may have opposing effects, More commonly used to treat (e.g., Heroin and Naloxone)

Tryptamine Drug Activation

Psilocybin cannot permeate the blood brain barrier and binds with low affinity to the 5HT2A receptor, Psilocybin must be dephosphorylated into psilocin by liver enzyme (Alkaline Phosphate) to affect brain

Withdrawal

Upon stopping use of a drug (after addiction), users may experience the undesirable effects of withdrawal

Dependence

Absence of a drug may lead to a feeling of physical pain, intense cravings (physical dependence), and negative emotions (psychological dependence)

Addiction

A craving for a chemical substance, despite its adverse consequences (physical & psychological)

Dopamine

motors systems, pleasure/reward, mental illness, craving, reuptake is DAT, degraded is MAO

Norepinephrine

sympathetic arousal, stress

Serotonin

sleep, dreaming, mental anxiety/depression

GABA

relaxation, antianxiety

Alcohol and benzodiazepines

What increases the affinity of GABA to GABA receptor?

Opiates

Binds to opioid receptors involved in the perception of pain and in reward, majority are coupled to a Gi GPCR (inhibitory)

Amphetamines

Reverses the orientation of reuptake channels, causes release of NE, DA, and 5HT from intracellular stores and pumps them into the synapse

Cocaine

What drug blocks the reuptake of DA, NE, and 5HT?

MDMA

Reverses the directionality of the 5HT (SERT) reuptake transporter, increasing serotonin concentrations in the synapse and thus serotonergic signaling, Byproduct of 5HT degradation via MAO is hydrogen peroxide - high levels kill cells

THC

binds with cannabinoid receptors, primarily the CB1 receptor, This receptor is a GPCR coupled to the Gi signaling pathway (inhibitory)

Brain Stimulation Reward (BSR)

Direct electrical stimulation of brain regions responsible for reward / reinforcement

James Olds and Peter Milner

These two men Implanted electrodes into many brain regions and stimulated rat in a particular location, then observed that some rats stayed in spot associated with stimulation

Intra Cranial Self Stimulation (ICSS)

rats self-administer stimulation to a lot of brain regions, allowed them to determine where reward was encoded in the brain

medial forebrain bundle

one of the most active brain pathways involved that influences rewarding behavior and perceptions of pleasure, Ventral tegmental area - Nucleus Accumbens

PFC

involved in decision making and reward seeking

NAc

plays role in evaluation of reward-seeking behaviors (motivation; filters & processes)

D1

postsynaptic excitatory, metabotropic

D2

presynaptic inhibitory, metabotropic

Blocking dopamine

What impairs motivation?

Channelrhodopsin 2 (ChR2)

excitatory, specific wavelength of light (blue) opens Na+ channel

Halorhodopsin (NpHR)

inhibitory, specific wavelength of light (yellow) opens Cl- channel