PSYC 425 Chapter 4

psychopharmacology

the study of the effects of drugs on the nervous system and behavior

drug effects

the changes a drug produces in an animal's physiological processes and behavior

sites of action

location at which molecules of drugs interact with molecules located on or in cells of the body, thus affecting some biochemical processes of these cells

5 routes of administration

ingestion, injection, inhalation, absorption, intracerebral administration

ingestion

oral route

pros of ingestion

easy and relatively safe

cons of ingestion

absorption via digestive tract is unpredictable

types of injection

intravenous, intramuscular, subcutaneous, and intraperitonal,

subcutaneous

SC

intramuscular

IM

Intravenous

IV

Intraperitonal

IP

subcutaneous

under the skin

intramuscular

into large muscle

intravaneous

into veins, drug delivered directly to brain

intraperitonal

to abdominal cavity

inhalation

Absorbed through capillaries in lungs

pros of inhalataion

very rapid effects

absorption through mucous membranes

nose mouth rectum, topical administration

intracerebral administration

directly into brain

intracerebral administration use

some drugs cannot get through the blood brain barrier so drug Injected into brain or CSF

Intracerbral Administration

solubility of blood brain barrier

fat soluble molecules

why heroin more effective than morphine

heroin more fat soluble so it acts more quickly on the brain

normal blood vessel

brain blood vessel

dose response curve

dose response curve

A graph of the magnitude of an effect of a drug as a function of the amount of the drug administered

best way to measure drug effectiveness

does response curve

how dose response curve is measured

subjects given various doses of a drugs based on mg per kg of body weight; effect are plotted

analgesia

inability to feel pain

margin of safety (therapeutic index)

Dose that produces desired effect 50%, dose that produces toxic effect 50%

margin of safety

low index

more risk for adverse reactions and toxic effects

low affinity

more drug needed

high affinity

less drug needed

affinity

the readiness with which two molecules join together (binding sites)

tolerance

decrease in the effectiveness of a drug that is repeatedly administered

sensitization

increase in the effectiveness of a drug that is administered repeatedly

high tolerance

need more drug to get the effects

low tolerance

need less drug to get the effects

withdrawal symptoms

Appearance of symptoms opposite to those produced by the drug

why tolerance occurs

Result of the body's attempt to compensate for the effects of the drug

compensatory mechanisms

body's attempt to compensate for loss or alteration, fight back, make up for the change

upregulation

prolonged expose to drug

the coupling (ion channels/ second messengers) does not work

sensitization example

cocaine will more likely develop movement disorders, convulsions, and psychosis

sensitization likelihood

less common than tolerance because of compensatory mechanisms

antagonist drugs

a drug that inhibits the effects of a particular NT on the postsynaptic cell

agonist drugs

drug that facilitates the effects of a particular NT on the postsynaptic cell

synthesis of NTs

controlled by NT-specific enzymes

metopirone

blocks cortisol synthesis by inhibiting 11ß-hydroxylase

metopirone treatment

Cushing's disease

transporter molecules

help move NTs into the vesicle

transporter molecules location

in the membrane of synaptic vesicles and the terminal

antagonist drug effects

prevent release of NTs into synapse; deactivate proteins that cause the vesicle's fusion to the membrane

presynaptic and postsynaptic receptors

most common and most complex sites of action

direct agonist

Molecules of drug attach to the binding site that the NTs normally connect with

direct agonist image

effect of direct agonist

causes ion channels controlled by the receptor to open

action fo direct agonist

MIMICS the effects of the NT

indirect agonist image

indirect agonist

a drug that attaches to a binding site on a receptor and facilitates the action of the receptor; does not interfere with the binding site for the principal ligand

effects of indirect agonist

Facilitates the opening of the ion channel

direct antagonists

receptor blockers; block binding by NTs

indirect antagonist

noncompetitive binding; prevents ion channel from opening

Trucyclics

Drug molecules attach to transporter molecules and deactivate them; Stop reuptake.

exmaple of trycyclics

Elavil, SERT andNET

drugs that target acetylcholinesterase

Drug molecules bind to enzymes and deactivate them; Stops enzymatic degradation.

example of drug that targets acetylcholinesterase

donepezil

acetylcholine NT type

excitatory

Acetylcholine location

CNS and PNS

Acetylcholine action

muscle action (PNS), learning (basal forebrain), memory (medial septum), & REM sleep (pons)

Increase in ACh effeects

muscle spasm

increase in ACh example

black widow venom

decrease in ACh

reduced muscle activity

decrease in ACh example

botulinum toxin; botox; alzheimer's

acetylcholine abreviation

ACh

ACh synthesis enzyme

Acetyl-CoA (coenzyme A)

mechanism of production of ACh and CoA

When in the presence of choline acetyltransferase (ChAT), acetate ion is transferred from acetyl CoA to the choline molecule

Nicotic receptors

Ionotropic receptor site stimulated by nicotine and blocked by curare

curare

blocks nicotinic receptors located near muscles. Causes paralysis; found in plants- poison darts

muscarnic receptors

metabotropic receptor site stimulated by muscarine and blocked by atropine

muscarine example

poisonous mushrooms

atropine example

found in belladonna

monoamines

catacholamines and indolamines

example of catecholamines

dopamine, norepinephrine, epinephrine

synthesis of catecholamines (precursor)

tyrosine

indolamine example

serotonin

synthesis of indolamines (precursor)

tryptophan

dopamine NT type

excitatory and inhibitory

dopamine controls

¡oluntary movement, attention, learning, and the ability to recognize opportunities for rewarding experiences.

origin of dopamine in the brain

mostly originate in the midbrain

Nigrostriatal Pathway of dopamine

Substantia nigra to the neostriatum (basal ganglia) ---> movement

Mesolimbic Pathway of dopamine

Ventral Tegmental Area (VTA) to the nucleus accumbens (NA) and other parts of the limbic system---> reinforcing behavior

mesocortical pathway of dopamine

¡VTA to the prefrontal cortex---> short term memory, planning, problem solving

mesostrial pathway

mesocortical pathway

mesolimbic pathway

parkinsons treatment

L-DOPA