Chapter 6 Flashcards
Psychoactive Drugs
substances that act to alter mood, thought or behavior, are used to manage neuropsychological illness and may be abused
Route of Administration
way in which a drug enters and passes through the body to reach its target
Oral Administration
Easy and convenient; most complex route. Must be absorbed through the stomach lining or small intestine to enter the blood stream
In order to pass into the blood stream a drug must be….
soluble in water because blood has a high concentration of water
Gas or Aerosol Administration
penetrate the cell linings of the respiratory tract; are easily absorbed across these membranes into the bloodstream
Skin Administration
small molecule drugs penetrate the skin’s barrier (nicotine)
When obstacles are eliminated en route to the brain
the dosage of a drug can be reduced by a factor of 10
Blood-brain barrier
tight junctions between the cells of blood vessels in the brain that prevent the passage of most substances; protects the brain from many circulating hormones, toxic and infectious substances
Brain Capillaries–> Tight Junctions
Capillaries are formed by a single layer of endothelial cells; not fused in most parts of the body but ARE fused in the brain–> causing tight junctions
Where does the blood-brain barrier not exist?
postrema of the lower brainstem allows toxic substances in the blood to trigger a vomiting response; Pineal gland enables hormones to reach it to modulate day-night cycle; Pituitary is triggered in part by other hormones
What does the brain need to work?
oxygen, glucose, amino acids
How do essential molecules cross the BBB?
small molecules (oxygen and carbon dioxide) pass through the endothelial membrane; glucose, amino acids and other food components are carried across by active-transport systems (Ion-pumps-transporter proteins)
Catabolize
breaking down and removal of drugs by the body
What part of the body is especially important in catabolizing drugs?
Liver.
Drug neurotransmission at a synapse
- Synthesis of the neurotransmitter can take place in the cell body, axon or terminal 2. Storage of the neurotransmitter in granules, vesicles or both 3. Release of the transmitter from the terminal’s presynaptic membrane into the synapse 4. Receptor Interaction in the post synaptic membrane, transmitter acts on an embedded receptor 5. Inactivation of excess neutransmitter at the synapse 6. Reuptake into the presynaptic terminal for reuse 7. Degradation of excess neurotransmitter by synaptic mechanisms and removal of unneeded by-products from the synapse
Agonists
Drugs that increase neurotransmission
Antagonists
Drugs that decrease neurotransmission
Acetylcholine
agonists that excite muscles
Acetycholine Antagonists
Botulin Toxin (blocks release) Curare (blocks receptors)
Acetycholine Agonists
Choline-rich diets Black widow spider venom (promotes release) Nicotine (stimulates receptors) Physostigmmine (blocks inactivation) Organophosphates (blocks inactivation)
Tolerance
decrease in response to a drug with the passage of time
Three kinds of tolerance
metabolic, cellular, learned
Metabolic toelrance
number of enzymes needed to break down alcohol in the liver, blood and brain increases. As a result, any alcohol that is consumed is metabolized more quickly, so blood-alcohol levels are reduced
Cellular Tolerance
activities of brain cells adjust to minimize the effects of alcohol present in the blood
Learned Tolerance
can help explain a drop in the outward signs of intoxication. Learn how to cope with influences of alcohol
When are people most likely to experience drug sensitization?
when they are occasional users.
Drug sensitization
increased responsiveness to successive equal doses; may manifest as a progressive increase OR decrease in emitted behavior
Neural basis of sensitization
occurs a number of ways: increase of neurotransmitter at presynaptic terminal, changes in # of receptors on the postsynaptic membrane, changes in the rate of transmitter metabolism in the synaptic space, changes in transmitter reuptake by the presynaptic membrances, changes in the size and # of synapses
Sensitization and environment
showing a change in learned responses to cues in the environment as sensitization progresses. Before someone becomes addicted they must have a number of experiences with the drug away from the home environment
Classes of Drugs
I Antianxiety agents and sedative hypnotics II antipsychotic agents III antidepressant and mood stabilizers IV opioid analgesics V psychotropics
Antianxiety Agents
drugs that reduce anxiety; minor tranquilizers (benzodiazepines) are to aid in sleep; sedative hypnotic agents (barbiturates and alcohol) are sedatives and sleep agents
Characteristic of sedative hypnotics
user develops a tolerance
Cross-Tolerance
tolerance developed for one drug is carried over to a different member of the drug group
Target for sedative hypnotic and antianxiety drugs
GABA (GABAa contains a chloride ion channel), Inhibitory effect of GABA–reduce neuronal firing. Also responds to PCP, GHB and special K
Antipsychotic Agents
first-generation= phenothiazines (chlorpromazine, thorazine) and butyrophenones (haloperidol, haldol)–> work by blocking D2 receptor (reduces motor activity and alleviates excessive agitation)
Dopamine Hypothesis of Schizophrenia
idea that excess activity of the neurotransmitter dopamine causes symptoms of schizophrenia
LSD
produces symptoms similiar to schizophrenia; serotonin agonist that acts on the 5-HT2 receptor
PCP and Special K
produce schizophrenia-like symptoms; formerly used as anesthetics; block glutamate receptors
Antidepressants and Mood stabilizers
Used for Major Depression and bipolar disorder
Antidepressant medications
include: Monoamine oxidase (MAO) inhibitors, tricyclic antidepressants, and second-generation antidepressants. Improve chemical neurotransmission at serotonin, noradrenaline, histamine, acetylcholine, and dopamine synapses. All are AGONISTS
MAO Inhibitor
provides for more serotonin release with each action potential by inhibiting monoamine oxidase (enzyme that breaks down serotonin within the axon terminal)
Tricyclices and Second generation antidepressants
block the reuptake transporter that takes serotonin back into the axon terminal
Selective Serotonin Reuptake Inhibitors
tricyclic antidepressant drug that blocks the reuptake of serotonin into the presynaptic terminal
Second Generation Antidepressant
drug whose action is similar to that of tricyclics but more selective in its action on the serotonin reuptake transporter proteins
Antidepressants take how long to work?
weeks. May be because they stimulate second messengers in neurons to activate repair of those damaged by stress
Mood stabilizers
(lithium) mute the intensity of one pole of bipolar disorder, thus making the other less likely to occur. Does not directly affect mood–> may stimulate neuronal repair.
Opioid Analgesics
Drug like morphine, with sleep-inducing (narcotic) and pain-relieving (analgesic) properties
Sources of Opioids
Opium can be synthesized into: codeine (pain reliever that is transformed into morphine by the liver) and morphine (pain reliever) Brain- peptides in the body have opioid-like effects (endorphines)
Endorphin
peptide hormone that acts as a neurotransmitter and may be associated with feelings of pain or pleasure; mimicked by opioid drugs such as morphine, heroine, opium and codeine
Classes of endorphins
Endomorphins enkephalins dynorphins
Endorphin receptors
mu kappa delta
Morphine
most closely mimics endomorphins and binds most selectively at mu
Heroin
affects mu receptors; is synthesized from morphine; more fat-soluble and penetrates the BBB more quickly
Competitive inhibitor
drugs such as nalorphine and naloxone that acts quickly to block the actions of opioids by competing with them for binding sites; used to treat opioid addictions
Effects of opioids
pain relief, relaxation, sleep, euphoria, constipation, respiratory depression, decreased blood pressure, pupil constriction, hypothermia, drying of secretions, reduced sex drive, flushed warm skin
Psychotropics
stimulants that mainly affect mental activity, motor activity, arousal, perception and mood
Behavioral stimulants
affect motor activity and mood
Psychedelic and Hallucinogenic Stimulants
affect perception and produce hallucinations
General Stimulants
Affect mood
Amphetamine
behavioral stimulant; synthetic compound (attempts to synthesize epinephrine); dopamine agonist that acts frist by blocking the dopamine reuptake transporter; also stimulates DA from presynaptic membranes
Cocaine
Behavioral stimulant; dopamine agonist that acts frist by blocking the dopamine reuptake transporter; extracted from Peruvian coca shrub
Methamphetamine
amphetamine derivative
Psychedelic and Hallucinogenic Stimulants
alter sensory perception and cognitive processes and can produce hallucinations
Types of psychedelicss
Acetylcholine, anandamide, glutamate, norepinephrine, serotonin
Acetylcholine Psychedelics
either both (atropine) or facilitate (nicotine) transmission at acetylcholine synapses
Anandamide Psychedelics
endogenous neurotransmitter that enhances forgetting; prevents brain’s memory systems from being overwhelmed; THC acts on receptors for anandamide (CB1 and CB2)
Glutamate Psychedelics
PCP and Ketamine –block glutamate NMDA receptors (receptors involved in learning)
Norepinephrine Psychedelics
Mescaline (peyote cactus) produces a sense of spatial boundlessness and visual hallucinations
Serotonin Psychedelics
LSD and psilocybin (obtained from shrooms) stimulate serotonin receptors and block the activity of other serotonergic neurons through serotonin autoreceptors. May stimulate other transmitter systems (such as norepinenrine –> ecstasy)
General Stimulants
drugs that cause an overall increase in the metabolic activity of the cells. Ex. Caffeine
Disinhibition Theory
explanation holding that alcohol has a selective depressant effect on the cortex, the region of the brain that controls judgment, while sparing subcortical structures responsible for more primitive instincts, such as desire
Alcohol Myopia
“nearsighted” behavior displayed under the influence of alcohol: local and immediate cues become prominent, and remote cues and consequences are ignored
Substance Abuse
Use of a drug for the psychological and behavioral changes it produces aside from its therapeutic effects
Addiction
Desire for a drug manifested by frequent use of the drug, leading to the development of physical dependence in addition to abuse; often associated with tolerance and unpleasant, sometimes dangerous, withdrawal symptoms on cessation of drug use
Withdrawal Symptom
physical and psychological behavior displayed by an addict when drug use ends; includes muscle aches, cramps, anxiety, sweating, nausea, convulsions, death
Psychomotor Activation
increased behavioral and cognitive activity; at certain levels of consumption, the drug user feels energetic and in control
Abused Drugs
may act on the same target in the brain: dopamine in the mesolimbic pathways of the dopaminergic activating system; abused drugs increase DA directly or indirectly
Sex and Addiction
females are twice as sensitive to drugs as males; females are more likely to abuse nicotine, alcohol, cocaine, amphetamine, opioids, cannabinoids, caffeine, and PCP
Wanting-and-Liking-Theory
AKA incentive-sensitization theory; Wanting = cravings, Liking= pleasure from drug taking; with repeated use, tolerance for liking develops and pleasure decreased BUT wanting sensitizes
Where the decision to take a drug takes place
Frontal cortex
Where liking takes place
opioid systems in the brainstem–> pleasurable experiences
Where wanting takes place
activity in the mesolimbic pathways of the dopaminergic activating system
Learning and Drug Use
repeated pairings of drug-related cues to drug taking forms neural associations in the dorsal striatum (basal ganglia); cues associated with drug taking influence decisions to take or continue to take drugs
Epigenetics and Addiction
addictive drugs can influence gene regulation by determining which genes are expressed
Brain Damage and Glutamate
MSG and glutamate–results in influx of Ca2+ into the cell–>second messenger–>suicide gene–> cell death
Apoptosis
cell death
Brain damage and Alcohol
thalamus and limbic system damage, may be due to a lack of thiamine (B1)
MDMA and Brain Damage
degeneration of fine serotonergic nerve terminals
Cocaine and Brain Damage
blocks cerebral blood blow; brain regions reduce in size
THC and Brain Damage
may cause psychosis, but has neuroprotective properties; aids in healing after TBI and slows progression of Alzheimer’s and Huntington’s
Testosterone
sex hormone secretes by the testes and responsible for distinguishing characteristics of the male
