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Psych 275 > Chapter 6 > Flashcards

Chapter 6 Flashcards

1
Q

Psychopharmacology

A

Study of the ways drugs affect the nervous system and behavior

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2
Q

Psychoactive Drug

A

Substance that acts to alter mood, thought, or behavior, used to manage neuropsychological illness

Often used recreationally

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3
Q

Drugs

A

Chemical compounds administered to produce a desired change

Improvement of physical/mental symptomatology

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4
Q

Routes of Drug administration

A

Orally → safest and most convenient: ingestion » absorption by stomach/small intestine » then enters bloodstream (water-soluble)

Inhaled → encounter few barriers enroute to the brain » absorbed into bloodstream almost immediately

Injected into bloodstream → fewest barriers to brain but must be HYDROPHILIC » dosage can be reduced by factor of 10

Injected into muscle → encounter more barriers than inhaled drugs

Injected into brain → acts quickly and in LOW doses

Absorbed through skin → adhesive patches into bloodstream » small-molecule drugs can penetrate

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5
Q

Weak acid drugs

A

Pass from stomach into bloodstream

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6
Q

Weak base drugs

A

Pass from intestines to bloodstream

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7
Q

Factor of 10 rule

A

1 milligram of amphetamine produces noticeable behavior change orally

If inhaled into lungs or injected into blood, a dose of 100 ug yields the same results

If amphetamine is injected into CSF, 10 ug is enough for identical outcome

1 ug if drug directly applied to target neurons

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8
Q

Blood-brain barrier

A

Cell membranes, capillary walls, and placenta → all barriers to internal movement of drugs

Blood-brain barrier prevents most substances from entering brain via the bloodstream

Protects brains ionic balance

Denies neurochemicals that can disrupt neural communication

Protects brain from circulating hormones and from toxins/infectious diseases

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9
Q

Endothelial cells → blood-brain barrier

A

Form a cell layer that lines blood vessels → regulates exchanges between bloodstream and surrounding tissues

Endothelial cells in capillaries throughout the body are not tightly joined: easy for substances to move in and out of the bloodstream

Endothelial cell walls in brain are fused to form fight junctions → most substances cannot squeeze between them

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10
Q

Barrier-free Brain sites

A

Pineal gland → entry of chemicals that affect day-night cycles

Pituitary gland → entry of chemicals that influence pituitary hormones

Area postrema → entry of toxic substances that induce vomiting

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11
Q

What helps access and support brain function?

A

Brain needs oxygen and glucose for fuel and amino acids to build proteins

Fuel molecules reach brain cells from blood, carbon dioxide + other waste products are excreted from brain cells and carried away by the blood

Molecules of these vital substances cross the blood-brain barrier in 2 ways:
↳small, uncharged molecules (ex. Oxygen and carbon dioxide) are fat soluble and can freely pass through the endothelial membranes
↳complex molecules of glucose, amino acids, and other food components are carried across the membrane by active transport systems or ion pumps

SOME psychoactive drugs (must be small or have correct chemical structure) DO gain access to the CNS

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12
Q

How body eliminates drugs

A

Drugs are catabolized in the kidneys, liver, and intestines → then excreted in urine, feces, sweat, breast milk, and exhaled air

Liver is active in catabolizing drugs: houses a family of enzymes involved in drug catabolism

The cytochrome P450 enzyme is involved in drug catabolism → some of which are also present in gastrointestinal tract microbiome

Liver is capable of turning drugs into other forms that are more easily excreted from body

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13
Q

Agonist vs. Antagonist drugs

A

Agonist → drugs that increase neurotransmission

Antagonist→ drugs that block; decrease neurotransmission

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14
Q

Drugs and Major steps in neurotransmission

A

Drugs can influence synthesis of NT, packaging and storage of NT, release of NT, receptor interaction with the NT, and reuptake/degradation of the NT

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15
Q

Tolerance to drugs → 3 types

A

Decreased response to a drug with repeated exposure → 3 types

Metabolic tolerance: increase in number of enzymes in liver, blood, or brain used to break down a substance → metabolized faster = blood levels decrease

Cellular tolerance: activities of brain cells adjust to minimize effects of substance → accounts for low signs of intoxication with high blood-alcohol levels

Learned tolerance: People learn to cope with being intoxicated so they may no longer appear intoxicated

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16
Q

Sensitization relative to drugs

A

Sensitization more likely to develop with periodic use → occasional drug taker may have an increased responsiveness to successive, equal doses

Related to dependence→ before a person becomes dependent they must be sensitized by numerous experiences with the drug

Life experiences (stress) can produce effects resembling sensitization that prime nervous system for addiction

Sensitization to SSRI’s causes them to work → must be taken for several weeks first

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17
Q

Psychoactive drugs

A

Psychoactive drugs can be grouped based on the primary neurotransmitter system that they are known to effect

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18
Q

Priming

A

Synapse first receives chemical then becomes more ready to fire after first dose

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19
Q

Main psychoactive drugs → 9 types

A

Adenosinergic antagonist → caffeine

Cholinergic agonist → nicotine or diazepam, alprazolam, clonazepam

Glutamatergic antagonists → ketamine/PCP or memantine

Dopaminergic antagonists → Thorazine, Haldol, clozaril

Dopaminergic agonists → cocaine, amphetamine, methamphetamine, or aderall, Ritalin etc.

Serotonergic agonists → DMT, ecstasy, LSD or Zoloft, Prozac, tofranil

Opiodergic agonists → opium, morphine, heroin, or codeine, oxycodone,fentanyl

Cannabinergic agonists → THC

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20
Q

Adenosinergic antagonist

A

Most widely consumed psychoactive drug: caffeine

Binds to adenosine receptors without activating them → suppresses endogenous adenosine which includes drowsiness → leads to alertness

Also inhibits enzyme that usually breaks down the second messenger; cyclic adenosine monophosphate (cAMP): resulting increase in cAMP leads to increased glucose production→ resulting in more available energy and higher rates of cellular activity

Promotes release of dopamine and acetylcholine

Repeated daily use: mild form of drug dependence → fade within a week of abstinence

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21
Q

Cholinergic agonist

A

Nicotine→ feelings of relaxation, sharpness, calmness, and alertness

Within a few seconds from inhalation, nicotine stimulates acetylcholine nicotinic receptors

Acetylcholine nicotinic receptors cause the release of acetylcholine, norepinephrine, epinephrine, serotonin, endorphins, and dopamine

At low doses can act as a stimulant→ very high doses: dampens neuronal activity

Dependence involves both psychological and physical aspects

Potentially lethal poison → smoking can be a risk factor for Alzheimer’s disease

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22
Q

GABAergic agonists

A

Alcohol

At low doses: reduce anxiety, medium doses: sedate, at high doses: they anesthetize or induce coma → death

GABAa receptor contains a binding site for GABA, one for alcohol, and one for benzodiazepines and a Cl-

Excitation of the GABAa receptor produces an influx of Cl- through its pore → influx of Cl- increases concentration of negative charges inside the cell membrane, hyperpolarizing it (less likely to propagate an AP) → widespread reduction of neuronal firing underlies the behavioral effects of drugs that affect GABAa synapse

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23
Q

Summation in GABAergic agonists

A

Sedative-hypnotic drugs (alcohol) increase GABA binding, thereby maximizing the time the pore is open

Antianxiety drugs (benzodiazepines) influence the frequency of pore opening

Because actions summate, they should not be taken together

Cross tolerance for benzos and alcohol→ act on NS in similar ways

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24
Q

GABAergic Receptors

A

Alcohol consumption has short-term psychological and physiological effects that depend on: alcohol volume, body mass, food intake, genetics, etc.

Small amounts improve mood, sociability, fine muscle coordination, etc.

Medium doses result in lethargy, sedation, lack of balance, etc.

Long-term and frequent consumption can lead to increased risk of alcoholism → results in damage to central and peripheral nervous systems, as well as nearly every other system and organ in the body

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25
Glutamatergic antagonists
Glutamatergic system has several receptors: NMDA, AMPA, and kainite Antagonists for NMDA receptor such as phencyclidine (angel dust) and ketamine can produce hallucinations Both PCP and ketamine are known as dissociative anesthetics → compounds that produce feelings of detachment and dissociation from environment and self (distort perceptions of sight and sound) Ketamine is currently medically prescribed for starting and maintaining anesthesia
26
Dopaminergic Antagonist vs. Agonist uses
DA agonists used recreationally→ cocaine, amphetamine, methamphetamine DA agonists used medically → dextroamphetamine (Adderall), methylphenidate (Ritalin) , L-dopa DA antagonists used medically → for treatment of schizophrenia: chlorpromazine (Thorazine)
27
Dopamine agonists
Cocaine→ from coca plant Amphetamine increases dopamine in the synaptic cleft by reversing the dopamine transporter→ also reverse transporter that packages DA in vesicles (instead takes packaged dopamine and releases it into terminal)→ reverses transport to presynaptic cell = more DA Cocaine ALSO blocks the Reuptake (more DA in synapse) Amphetamine (Adderall) and methylphenidate (Ritalin) medically prescribed to treat ADHD → recreational dose is 5OX stronger than clinical dose
28
Dopamine antagonists
Use of dopamine antagonist drugs that preferentially bind to D2 receptors improved functioning of people with schizophrenia Schizophrenia hypothesis: excessive frontal lobe DA activity → therapeutic actions of D2 antagonists are not fully understood
29
Serotonergic agonists
Natural recreationally used serotonergics: mescaline (peyote), DMT, and psilocybin Synthetic rec serotonergics: LSD, and MDMA (ecstasy/Molly) Some serotonergic agonists prescribed to treat major depression: Monoamine oxidase (MAO) inhibitor → drug that blocks MAO enzyme from degrading NT such as: 5-HT, NE, and DA Tricyclic antidepressants → Drug characterized by its 3-ring chemical structure which blocks 5-HT reuptake transporter proteins Selective-serotonin reuptake inhibitor (SSRI)→ drug that blocks 5-HT Reuptake into the presynaptic terminal and is MOST commonly used to treat depression
30
Drug effects at 5-HT receptors
MAO inhibitor (agonist) inhibits the breakdown of serotonin = more serotonin available for release SSRI (agonist) and tricyclics (agonist) block transporter protein for serotonin Reuptake = serotonin stays in synaptic cleft for longer Both increase availability of 5-HT differently
31
Opioids
Opioid: any endogenous or exogenous compound that binds to opioid receptors to produce morphine-like effects → narcotic (sleep inducing) and analgesic (pain-relieving) properties 3 sources of opioids Isolated → morphine, codeine Altered → heroin, oxycodone Synthetic →fentanyl and methadone
32
Opiodergic agonists
Semi-synthetic: heroin and oxycodone → heroin is much more potent than morphine and penetrates blood-brain barrier faster Alter pain perception, relaxation, and can lead to euphoria Can lead to respiratory depression: high tolerance = higher dosage = resp. dep. → chest cavity stops breathing + coughing functions → suffocation Repeated opioid use produces a tolerance that effective dosage may increase tenfold within few weeks → brutal withdrawl symptoms
33
Naloxone (Narcan) → opiodergic overdose
Opioid use results in both tolerance and sensitization, an opioid user is at constant risk of overdosing Narcan/naloxone act as antagonists at opioid receptors Competitive inhibitor → acts quickly to block opioid action by competing with the opioid for binding sites → reverses AP
34
Cannabinergic agonist
Tetrahydrocannabinol (THC) is one of 84 cannabinoids and is main psychoactive constituent in cannabis THC alters mood by interacting with cannabidiol 1 (CB1) receptor found on neurons, and also binds with CB2 receptors found on glial cells and in other body tissues Cannabis has extremely LOW toxicity (no OD) May cause physiological and psychological dependence
35
Cannabinergic uses
Usefulness of THC and CBD as therapeutic agents: Substitute for opioids Treat glaucoma Eating disorder treatment Chronic pain treatment
36
Disinhibition Theory
Alcohol has a selective depressant effect on the cortex → region that controls judgment Limitation: behavior under influence of alcohol often differs with context→ behavior under influence of alcohol is learned (specific to culture, group, and setting)
37
Behavioral myopia
Under influence of alcohol people respond to a restricted set of immediate and prominent cues and ignore more remote cues and potential consequences Not see past immediate reward/urge → lack of foresight
38
Substance abuse
Pattern of drug use in which people rely on a drug chronically and excessively allowing it to occupy a central place in their life Drug pattern is well established
39
Addiction
Brain disorder characterized by escalation, compulsive drug taking, and relapse Called substance use disorder per the DSM-5
40
Psychomotor activation
Increased behavioral and cognitive activity so that at certain levels of consumption, the drug user feels energetic and in control Abused drugs act on the same target: dopaminergic pathway ↳ from ventral tegmental area to nucleus accumbens Drugs increase dopamine activity in the nucleus accumbens (directly or not) Drugs that decrease abuse → decrease dopamine activity in the nucleus accumbens
41
Risk factors in addiction
Adverse childhood experiences (ACE’s) are associated with an increased risk of drug initiation and addiction Can include emotional, physical and sexual abuse or neglect among other experiences
42
Wanting-and-liking theory
Aka incentive sensitization theory Wanting (craving) and liking (pleasure) may be produced in different parts of the brain Wanting: sensitized with repeated drug use; craving increases → mesolimbic dopamine system Liking: tolerance develops with repeated drug use; pleasure decreases
43
Cue reactivity
Increased use leads to an association of cues→ any instruments associated with drug use can cause desire to increase: relapse Paraphernalia increases feelings associated with drug use → classical conditioning
44
Neural basis of addiction
Decision to take drug → frontal cortex Drug then activates endogenous opioid systems (related to pleasurable experiences) Wanting drugs → from activity in nucleus accumbens in dopaminergic system
45
Mesolimbic pathways → addiction
Axons of dopamine neurons in midbrain project to the basal ganglia, frontal cortex, and allocortex Drug cues release DA in this system → triggering a wanting response and repetitive benaviors Cue + drug taking creates neural associations in the dorsal striatum (basal ganglia)→ leads to loss of voluntary control and increased craving
46
Drugs + Brain damage → general
Natural substances such as glutamate can be neurotoxins → become toxic over time due to excess buildup in brain Hard to determine whether recreational drugs are harmful: Drug itself? Or factors associated with drug use? Do drugs initiate problems? Or just aggravate preexisting conditions? Hard to isolate cause-and-effect
47
Brain damage + Alcohol
Chronic alcohol use can be associated with damage to the thalamus and limbic system Alcoholics typically obtain low amounts of thiamine (vitamin B1) Thiamine plays a vital role in maintaining cell membrane structure → can lead to severe memory loss problems and pathological lying
48
Brain damage + cocaine
Related to the blockage of cerebral blood flow and other changes in blood circulation Brain imaging studies suggest that cocaine use can be toxic to neurons
49
Brain damage + marijuana
Plant contains at least 400 chemicals Determining whether a psychotic attack is related to THC or to some other chemical in marijuana is almost impossible
50
Hormones
Secreted by glands in body and by brain Brain + body hormones that interact form feedback loops that regulate their activity Hormonal influences change across lifespan → influences development and body/brain function Hormone systems are like NT activating systems: use bloodstream as a conveyance→ epinephrine is used in hormone form in fight-or-flight response
51
Hierarchical Control of hormones
Hypothalamus → produces neurohormones to stimulate pituitary gland Pituitary gland → secretes releasing hormones to influence target endocrine glands Target endocrine glands → release appropriate hormones into the blood to act on target organs and tissues
52
Steroid hormone
Fat-soluble chemical messenger synthesized from cholesterol Bind to steroid receptors on the cell membrane and influence DNA transcription Examples: gonadal (sex) hormones, thyroid, cortisol
53
Peptide hormone
Chemical messenger synthesized by cellular DNA ' that acts to affect the target cells physiology Binds to metabotropic receptors → leads to cascade effects Examples: insulin, growth hormone
54
Functional groups of hormones → 3
Homeostatic hormones: maintain internal metabolic balance and regulation of physiological systems Gonadal (sex) hormones: control reproductive functions, sexual development, and behavior Glucocorticoids: secreted in times of stress; important in protein and carbohydrate metabolism
55
Homeostatic hormones
Homeostasis of intra and extracellular environments is essential → body must stay within certain biological parameters for effective functioning Diabetes mellitus → failure of pancreas to secrete enough insulin which leads to impaired functioning
56
Anabolic-androgenic steroids
Class of synthetic hormones related to the male sex hormone testosterone that have both muscle-building (anabolic) and masculinizing (androgenic) effects Health risks: Body reduces production of testosterone, reducing male fertility Increased aggression Increased risk of heart attack + stroke Compromised liver and kidney function Masculinization of female users
57
Glucocorticoids + stress
Stressor: a stimulus that challenges the body's homeostasis and triggers arousal Stress response: physiological and behavioral arousal to handle stress Activating stress response: Fast acting → primes body immediately for fight-or-flight (epinephrine) Slow-acting → both mobilizes the body's resources to confront a stressor and repairs a stress-related damage (cortisol)
58
Activating stress response → fast-acting pathway
Hypothalamus sends neural message through spinal cord Sympathetic division of ANS Is activated to stimulate the medulla of the adrenal gland Adrenal medulla releases epinephrine into circulatory system Epinephrine activates body's cells, endocrine glands, and the brain
59
Activating stress response → slow-acting pathway
In brain, the hypothalamus releases CRH into pituitary gland Pituitary gland releases ACTH, which acts on the cortex of the adrenal gland Adrenal cortex releases cortisol into circulatory system Cortisol activates the body's cells, endocrine glands, and the brain
60
Ending a stress response
Normally, stress responses are brief and turned on/off in the brain Hippocampus is well suited to detecting cortisol in the blood and instructing the hypothalamus to reduce blood cortisol levels → too much cortisol will damage neurons in hippocampus Cycle involving prolonged stress: increased cortisol → triggers brain damage in hippocampus → this increases release of more cortisol
61
Glucocorticoid receptors in relation to childhood abuse
Glucocorticoid receptor density in hippocampus of suicide victims and childhood abuse victims was lower than that of control subjects Decrease in receptors and glucocorticoid mRNA suggests that childhood abuse induces epigenetic changes in the expression of glucocorticoid genes Decrease in glucocorticoid receptors presumably renders the hippocampus less able to end stress responses

Psych 275 (6 decks)

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