Neuro beh sci ch 4-5

Endogenous substance

A substance that occurs naturally within the body.

Exogenous substance

A substance originating outside the body that can affect physiology or behavior.

Ionotropic receptor

A receptor that directly controls an ion channel; usually produces fast transmission.

Metabotropic receptor

A receptor without its own ion channel that indirectly affects channels; usually slower.

Ligand

A chemical that binds to a receptor.

Agonist

A ligand that binds to and activates a receptor, mimicking a transmitter's effect.

Antagonist

A ligand that binds to a receptor without activating it and blocks other ligands.

Inverse agonist

A ligand that binds to a receptor and produces the opposite effect of its usual activity.

Competitive ligand

An agonist, antagonist, or inverse agonist that binds at the endogenous ligand's receptor site.

Noncompetitive ligand / neuromodulator

Binds at a modulatory site rather than the normal transmitter-binding site.

Affinity

The strength of chemical attraction between a ligand and receptor.

Efficacy / intrinsic activity

A bound ligand's ability to activate a receptor and produce a response.

Full agonist

Activates a receptor to produce a full response.

Partial agonist

Binds to a receptor but produces a weaker response than a full agonist.

Four criteria for a neurotransmitter

Presynaptic synthesis/storage; Ca²⁺-dependent release after depolarization; specific postsynaptic receptors; a mechanism to terminate the signal.

Why must neurotransmitter release be Ca²⁺ dependent?

The study guide lists calcium-dependent release following presynaptic depolarization as a defining criterion.

Why is neurotransmitter signal termination important?

A specific mechanism must stop the presynaptic signal.

Three major neurotransmitter classes

Amino acids, amines, and peptides.

Amino acid neurotransmitters

Small organic molecules; examples include glutamate, glycine, and GABA.

Amine neurotransmitters

Small organic molecules; examples include histamine, acetylcholine, norepinephrine, dopamine, and serotonin.

Peptide neurotransmitters

Short amino-acid chains stored and released from secretory granules at axon terminals; examples include dynorphin and enkephalins.

Can one neurotransmitter always predict one behavior?

No. Effects depend on receptor subtype, location, and context.

Can a neurotransmitter be excitatory in one place and inhibitory in another?

Yes; its effect depends in part on the receptor subtype stimulated.

Glutamate

The brain's most prevalent excitatory neurotransmitter; associated with excitotoxicity.

GABA

An inhibitory neurotransmitter in the central nervous system.

Glycine

An inhibitory neurotransmitter that, like GABA, mediates CNS synaptic inhibition.

Glutamate receptor subtypes

AMPA, NMDA, and kainate.

AMPA receptor ions

Primarily Na⁺ and K⁺; most AMPA receptors are not Ca²⁺ permeable.

NMDA receptor ions

Na⁺, K⁺, and Ca²⁺.

Kainate receptor ions

Na⁺ and K⁺.

What type of postsynaptic potential do glutamate receptors generally produce?

An excitatory postsynaptic potential (EPSP).

GABA-A receptor

Ionotropic receptor that produces fast inhibitory effects through a Cl⁻ channel.

GABA-B receptor

Metabotropic receptor that produces slower inhibitory effects; the study guide associates it with K⁺ channels.

GABA-C receptor

Ionotropic receptor with a Cl⁻ channel.

Why can GABA-A receptor modulation be risky?

The receptor has multiple subunits and binding sites; too much inhibition can lead to coma, while too little can lead to seizures.

GABA-A binding sites listed in the study guide

Chloride channel, steroid site, benzodiazepine site, and barbiturate site.

Acetylcholine (ACh) functions

Learning, memory, arousal, attention, and muscle movement.

Cholinergic neurons

Neurons whose cell bodies or projections contain/release acetylcholine.

Neuromuscular junction (NMJ)

A chemical synapse between a motor neuron and a muscle fiber that transmits signals to cause contraction.

Primary neurotransmitter at the NMJ

Acetylcholine (ACh).

What happens at the NMJ after ACh is released?

ACh binds ligand-gated receptors on the motor end plate, causing depolarization; voltage-gated Na⁺ channels then help trigger a muscle action potential and contraction.

Nicotinic ACh receptor

Usually ionotropic and excitatory; skeletal muscles use this receptor type.

Muscarinic ACh receptor

G-protein-coupled, metabotropic, slower, and capable of excitatory or inhibitory effects.

Examples of muscarinic ACh antagonists

Atropine and scopolamine.

Catecholamines

Dopamine, epinephrine, and norepinephrine.

What are epinephrine and norepinephrine also called?

Adrenaline and noradrenaline, respectively.

How can epinephrine and norepinephrine act outside synapses?

The adrenal medulla releases them into the bloodstream as hormones during the stress response.

Dopamine functions listed in the materials

Movement, mood, attention, visceral function, motivation/reward, and addiction-related pathways.

Nigrostriatal dopamine pathway

Originates in the substantia nigra in the midbrain and projects to the striatum.

Mesolimbocortical dopamine pathway

Originates in the ventral tegmental area (VTA) and projects to limbic structures and cortex.

Parkinson's disease and dopamine

A progressive neurodegenerative disorder associated in the slides with degeneration of the nigrostriatal system and loss of dopamine neurons in the substantia nigra.

Norepinephrine (NE) cell-body cluster

The locus coeruleus in the pons of the brainstem.

Noradrenergic projections and functions

Project broadly, including to cortex, basal ganglia, hippocampus, and hypothalamus; modulate mood, arousal, and sexual behavior.

Serotonin (5-HT) functions

Regulates mood, anxiety, appetite, and sleep; also contributes to pain and spinal-reflex modulation.

Serotonin cell-body location

Mainly the raphe nuclei in the brainstem.

Serotonin projections

Project widely, including to cortex, hippocampus, thalamus, basal ganglia, spinal cord, cerebellum, and limbic system.

What does Prozac do according to the materials?

As an SSRI, it increases serotonin activity by blocking serotonin reuptake.

Opioid peptides

Peptides that bind opioid receptors and help relieve pain; examples include enkephalins, endorphins, and dynorphins.

Psychopharmacology

Study of psychoactive drugs and their effects on mood, sensation, thinking, behavior, and brain chemistry.

How can local anesthetics such as Novocaine affect neural conduction?

They block sodium channels.

How can drugs affect presynaptic transmitter production?

They can affect synthesis enzymes, block transport, or inhibit transmitter storage.

Tetrodotoxin (TTX)

Blocks Na⁺ channels and can prevent action potentials.

Amphetamine's transmitter-release effect in the slides

Stimulates release of catecholamines.

Caffeine's mechanism in the slides

Blocks adenosine, an endogenous neuromodulator that normally inhibits catecholamine release; this promotes arousal.

Typical antipsychotics

First-generation antipsychotics described as selective dopamine D2 antagonists; used to treat schizophrenia.

Atypical antipsychotics

Block dopamine and some serotonin receptors; the study guide says they may reduce negative symptoms.

Monoamine oxidase (MAO) inhibitors

Prevent breakdown of monoamine neurotransmitters, allowing them to accumulate and prolong activity.

Tricyclic antidepressants

Block reuptake of norepinephrine and serotonin into presynaptic terminals, increasing them in the synapse.

Selective serotonin reuptake inhibitors (SSRIs)

Block serotonin reuptake so serotonin accumulates in the synapse; examples include Prozac and Zoloft.

Anxiolytics

Drugs used to reduce anxiety; described in the slides as depressants that reduce nervous-system activity.

Benzodiazepine agonists

Act at GABA-A receptors and enhance GABA's inhibitory effects.

Morphine

An analgesic (painkiller) found in opium; the slides describe morphine and heroin as highly addictive.

Endogenous opiates

Body-produced peptides that bind opioid receptors and relieve pain; examples are enkephalins, endorphins, and dynorphins.

THC

The active ingredient in cannabis identified in the slides; effects can include relaxation, mood alteration, stimulation, hallucinations, and paranoia.

CB1 cannabinoid receptors

G-protein-coupled receptors found in the CNS that mediate rewarding properties of cannabinoids.

CB2 cannabinoid receptors

Cannabinoid receptors prominent in the immune system.

Endocannabinoids

Brain-produced cannabinoid-like substances that act as retrograde messengers and can influence presynaptic neurotransmitter release.

Two endocannabinoids named in the slides

Anandamide (AEA) and 2-arachidonoylglycerol (2-AG).

Retrograde messenger

A signal that travels opposite the usual direction, from postsynaptic to presynaptic cell.

Nicotine's receptor action

Acts as an agonist at nicotinic acetylcholine receptors in the body and brain.

Cocaine's main mechanism in the slides

Blocks monoamine transporters, especially dopamine transporters, slowing reuptake and enhancing neurotransmitter effects.

Cocaethylene

An active metabolite formed when cocaine is metabolized in the presence of ethanol.

Biphasic alcohol effects

An initial stimulant phase followed by a depressant phase.

Alcohol and GABA-A

Alcohol activates GABA-A receptors and increases inhibitory effects.

Alcohol and dopamine pathways

Alcohol indirectly stimulates dopamine pathways, contributing to euphoric effects.

Fetal alcohol syndrome

Permanent fetal damage resulting from alcohol abuse during pregnancy, as described in the slides.

Hallucinogens

Substances that alter sensory perception and produce unusual experiences.

Hallucinogens named in the slides

LSD, mescaline, and psilocybin; the slides describe mainly visual effects.

MDMA / Ecstasy effects in the slides

Increases serotonin and changes dopamine and oxytocin levels; chronic use is associated in the slides with depression, memory disturbance, and changes to serotonergic neurons.

Moral model of drug abuse

Attributes drug abuse to poor moral character or lack of self-control.

Disease model of drug abuse

Views addiction as requiring medical treatment rather than moral punishment and emphasizes brain alterations/function.

Physical dependence model

Says drug use may be driven by avoiding withdrawal symptoms.

Positive reward model

Explains drug use as behavior controlled by positive rewards.

Reward circuit

Neural circuit responsible for the acute rewarding and reinforcing effects of abused drugs; also responds to non-drug rewards.

Mesolimbic dopamine pathway

Pathway from the VTA to the nucleus accumbens (NAc), important in addiction-related reward and reinforcement.

Amygdala's role in the reward circuit

Mediates emotional characteristics associated with a drug.

Hippocampus's role in addiction

Stores memories of pleasure and cues such as people, places, and activities associated with use.

Mesocortical pathway

Projects from the VTA to the prefrontal cortex and supports information coordination, planning, and behavioral control.

Dopamine and reinforcement

The materials state that reinforcement generally correlates with dopamine activity and drugs of abuse typically stimulate dopamine pathways.

Factors associated with addiction susceptibility in the slides

Biological factors, family situation, personal characteristics, and environmental/social factors.