Psychopharmacology Flashcards

Flashcards covering key vocabulary and concepts in psychopharmacology from lecture notes.

Neuron at Rest

Has a negative charge; an action potential is triggered when the charge becomes sufficiently positive.

Myelin Sheath

Fatty substance wrapped around axons; aids electrical conduction of impulses via saltatory conduction at gaps between cells.

Neuron Firing

Single unit of activity; an all-or-none event.

Synapse

Gap between neurons where information passes through the release of neurotransmitters.

Cell Membrane

Cell wall preventing passage of neurotransmitters, fluids, and chemicals; semi-permeable.

Receptors

Located on the outside of the cell membrane and allow neurotransmitters to influence the post-synaptic neuron.

Ion Channels

Type of receptor that acts like a gate for ions, opening when a neurotransmitter binds.

G Protein Coupled Receptors

Type of receptor that works through second messengers.

Ligand-Gated Ion Channels Function

Neurotransmitter binds to the receptor outside the neuron, causes the gate to open and ions to flow through.

Transmembrane Proteins

Open in response to a ligand (Neurotransmitter, Ion, Nucleotide).

Receptor Domain

Part of a ligand for binding.

Transmembrane Pore

Part of a ligand for ions to pass through.

Extracellular Ligands

Acetylcholine, Glutamate.

Intracellular Ligands

Cyclic adenosine monophosphate (cAMP), Ions (calcium).

G Protein-Coupled Receptor Function

Neurotransmitter binds to the receptor and activates a second messenger system that can either open a channel or cause changes within the cell.

GPCRs

Integral membrane protein, extracellular part contains a ligand binding site for a variety of compounds

Neurotransmission

Chemical substance released from a neuron at a synapse affecting a postsynaptic neuron, muscle cell, or effector cell (1:1 correspondence).

Neuromodulation

Chemical substance released from a neuron affecting groups of neurons or effector cells, often through second messengers (longer lasting, diffuse effects).

Neuromodulation Effects

Alters neurotransmitter release (presynaptic) or neurotransmitter action (postsynaptic); can cause changes in neural function or structure.

Norepinephrine (Noradrenaline)(NE) system

Produced in the LE, neuromodulator production system, projections thoughout the brain, long projections.

Histamine System

Generated in the posterior hypothalamus and is Responsible for a lot of your arousal and sleep functions

Psychopharmacology

The study of drug-induced changes in mood, sensation, thinking, and behavior.

Agonist

Drug that activates a receptor like a natural compound.

Antagonist

Drug that blocks a receptor and prevents the natural compound from activating it.

Synthesis

Synthesised neurotransmitters in the cell body and transported into the axon terminals where they are stored.

Vesicles

Cells within cells holding on to different kinds of neurotransmitters

MDMA prevents vessicles

prevents the vessicles from packaging serotonin so it leaks out of the cell.

Hormones

Signalling molecules produced by glands and transported through the blood to regulate physiology (muscles, neurons etc) and behaviour

Synaptic Communication

Transmission of messages from one neuron to another across a synapse, messages carried by neurotransmitters released by presynaptic cells

Binding Site

Receptor molecule which neuron transmitter effect is applied

Ligand

(often neurotransmitter) binding site which chemicals attach on

Synapses

Junctions between the terminal buttons at the ends of axonal branches of one neuron and the membrane of another

Presynaptic Membrane

Located at the end of the terminal button faces the postsynaptic membrane located on the neuron that recives the message

Synaptic Cleft

Gap between synapses containing extra cellular fluid through which the neurotransmitter diffuses

Synaptic Vesicles

Small rounded spheres containing molecules of neurotransmitter, membranes containing lipid molecules which are inserted into protein molecules

Release zone

The region from which the neurotransmitter is released

Golgi Apparatus

Produces mall synaptic vesicles carried by fast axoplasmic transport to the terminal button

Soma

Produces large synaptic vesicles transported through the axoplasm

Neurotransmitter Release

Action potential conducted down an axon causes small synaptic vesciles to fuse with the presynaptic membrane and break open, spilling their contents into the presynaptic cleft

Docking

Clusters of protein molecules attach to other protein molecules located in the presynaptic membrane

Fusion Pore

hole through both membranes which enables them to fuse together produced by calcium ions binding with the terminal button

Release Ready Vesicles

docked against inide of presynaptic membrane, ready to release their contents when action potential arrives (1%)

Recycling Pool

(10-15%): releases contents if axon fires at an increased rate

Reserve Pool

85-90%

Neurotransmitter-dependent ion channels

once binding occurs these channels permit the entrance of particular ions to pass through the membrane

Ionotropic Receptors

ion channel opens when a molecule of neurotransmitter attaches to the binding site

Metabotropic Receptors

molecule of neurotransmitter binds with a receptor a G protein activates an enzyme which produces a second messenger than opens nearby ion channels

Second Messengers

chemicals synthesised from ATP, synaptic and non synaptic communication, can alter functions of cell and methylase genes

Postsynaptic Potential

Excitatory (depolarizing) or Inhibitory (hyperpolarizing)

EPSPs

Excitatory Postsynaptic Potential which means that when socium channels are opended the result is depolarisation

IPSP

Inhibitory Postsynaptic Potentials which means that If potassium channels are open a surplus of posititvley charged potassiums will hyperpolarise the membrane

Reuptake

Removal of neurotransmitter from the synaptic left into the cytoplasm and is then taken back

Enzymatic Deactivation

enzyme destroys molecules of the neurotransmitter

Neural integration

interaction of the effects of excitatory and inhibitory synapses on a particular neuron

Autoreceptors

receptors that respond t othe neurotransmitter the neuron itself releases

Presynaptic Modulation

Inhibition: decreases the release of neurotransmitter
Facilitation: increases the release

Dendrodendric Synapses

Lack axons so don’t transmit info, perform regulatory functions

Neuromodulators

chemicals released by neurons that travel father and are dispered more widely than neurotransmitters

Peptides

chains of amino acids

Target Cells

cells that contain receptors for a particular hormone affecting behaviour

Glutamate

Main excitatory neurotransmitter in the brain (increasing likelihood of the post synaptic neuron firing)

GABA

(gamma amino butyric acid) is the primary inhibitory neurotransmitter- decreasing likelihood of the post synaptic neuron firing

Glutamate synthesis

Glutamate is an amino acid that acts as a neurotransmitter in its original form BUT this amino acid does not pass the blood brain barrier (BBB) so it still needs to be synthesised in the brain

NMDA Receptor

Multiple types of Glutamate receptors

Alcohol

an NMDA antagonist that blocks glutamatergic function, which downregulates excitation which leads to a sort of sedative inhibitory effect, it blocks information processing and memory functioning

Alcohol is a non-competitive antagonist

it antagonises and blocks the NDMA receptor at a site that’s not where glutamate attaches to, doesn’t compete against glutamate -- we don’t know exactly where alcohol binds

Phencyclidine (PCP)

angel dust

Ketamine

special k, k , ket, horse tranquiliser and is an NDMA antagonist-- sensory anaesthetic

Schizoprenia:

1% of population > psychosis is 3% of pop

GABA Overview

GABA (gamma amino butyric acid) is the primary inhibitory neurotransmitter- decreasing likelihood of the post synaptic neuron firing

Epilepsy

is a neurological disorder characterised by seizures

Simple

can cause changes in consciousness (altered sensory, autonomic responses etc) but not loss of consciousness

Complex

lead to a loss of consciousness

Drug

exogenous(produced outside the body) chemical not necessary normal cellular functioning that significantly alters the functions of certain cells of the body when taken in relatively low doses

Drug effect

changes we can observe in an individual's physiological processes and behaviours

Site of action

the points at which molecules of drugs interact with molecules on or in cells of the body affecting biochemical processes of the cells

Pharmacokinetics

How the drug molecule is absorbed, distributed in the blood, metabolised,excreted

Therapeutic Index

drugs margin of safety, ratio of the amount of people with toxic affects to people with nontoxic effect, The lower the therapeutic index the more care is needed when prescribing

Affinity

readiness with which two molecules join together for sites to which they attach Drug with low affinity needs to be administered at higher doeses

Tolerance

diminishing effects of a given dose with repeated uses

Sensitisation

increasing effects of a given dose with repeated uses

Withdrawal

the opposite effects of the drug itself: indicative of physical dependence following repeated use of drug

Withdrawl symptoms

opposite effects of the drug itself caused by the same mechanisms reposible for tolerance

Physical Dependence

when a person has repeatedly used a srug enough to produce withdrawal symptoms when they stop using it

Placebo

an inactive substance that can produce physiological or psychological effects

Placebo effect

occurs when an individual expects that a placebo can have a physiological or psycholigcal effect, and the placebo subsequently produces an effect

Antagonist

drugs that block or inhibit the postsynaptic effects

Agonist

drugs that facilitate post synaptic effects

Reuptake

postsynaptic potentials are terminated When action potential arrives Removal of neurotransmitter from the synaptic left into the cytoplasm and is then taken back

agonist drugs

produce their effects by acting as precursors to increase the amount of neurotransmitter a cell can synthesize and release into the synapse

Antagonist Drugs

inactivate neurotransmitter-synthesizing enzymes to prevent neurotransmitters from being produced

Direct Agonist

mimics the effects of a neurotransmitter as molecules attach to the binding site similarly

Indirect Agonist

drug attaches to one of the alternative sites and fascilitates the opening of the ion chancel

Direct Antagonists

Drugs that bind to presynaptic receptors occupying the site and preventing activation

Non competitive binding

drug binds to a different spot and blocks the receptor without competing with the neurotransmitter

Indirect antagonist

attached to one of the alternative sites and prevents an ion channel from opening

Amino Acids

Glutamate, Gamma aminobutyric acid GABA, Glycine

Glutamate Function

Excitatory; interacts with other neurotransmitter systems

GABA Function

Inhibitory; interacts with other neurotransmitter systems

Acetylcholine (ACh) Function

cns: Learning, memory, REM sleep
Pns: Muscle contraction