Psy 342 Final

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Mescaline

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Found in peyote cactus, Used for thousands of years by Native Americans for religious and healing rituals.

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Psilocybin

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"shrooms"

Converted to Psilocin actual psychoactive ingredient

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Hallucinogens

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Substances that cause perceptual and cognitive distortions in the absence of delirium

Many are natural except LSD

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Hallucinogens: Pharmacokinetics

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Mostly orally taken, except DMT and salvia which are smoked - causes rapid onset / shorter duration

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Hallucinogens: Potency

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Most - LSD

Least - Mescaline

Based on range of dosage

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Hallucinogens: Indolamines

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Related to serotonin,

5-HT 2A receptor agonist

Ex. LSD, psilocybin, DMT, 5-MeO-DMT, and the synthetic tryptamines.

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Hallucinogens: Phenethylamines

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Related to Neuropinephrine

5-HT 2A receptor agonist

Ex. Mescaline / Amphetamine

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Hallucinogens: Adverse effects

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Non dependence forming

Little withdrawal

Tolerance occurs with rapid repeated use

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DMT (Dimethyltryptamine) / 5-MeO-DMT (5-Methoxy-Dimethyltryptamine)

Pharmacokinetics

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found in several plants indigenous to South America.

Mainly smoked

produce alkaloids called β-carbolines known to inhibit MAO

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LSD: History

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Albert Hofmann synthesized LSD-25 in 1938, first tested in 1943

based on fungal alkaloids (ergot)

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LSD: Dosage

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Dose dependent (micrograms)

- Low dose — more cognitive, emotional

- High dose — actual hallucinations

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5-HT 2A

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Common receptor for Indolamines and Phenylethylamines

Critical receptor for hallucinations

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Dissociative Anesthetics

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PCP and Ketamine

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PCP

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More intense than ketamine

Experience: distortion in body image, feelings of depersonalization, sense of timelessness or being dead, could be caused by increased presynaptic glutamate

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Ketamine

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Used as veterinarian tranquilizer

Increasing in popularity

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Ketamine and PCP pharmacology

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PCP - blockade of NMDA receptors

Both act as noncompetitive receptor agonists

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Ketamine and PCP: Abuse potential

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Highly reinforcing,

High

Heavy users show dose escalation and compulsive use, which indicates tolerance and dependence

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Anxiety

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Disturbing feeling of concern accompanied by bodily changes including activation of the Autonomic nervous system that prepares the animal to cope with impending danger

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Anxiety: Brain regions

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Insula, cingulate cortex, hypothalamus, and hippocampus are also involved

Amygdala plays central roll - Forms emotional memories and enhances semantic memory consolidation by the hippocampus

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Anxiety disorders

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May arise from an imbalance between emotion generating brain regions and higher cortical control

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CRF (Cortitropic Releasing Factor)

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Regulates stress hormone secretion and activates neuronal circuits of emotion that produce anxious behaviors in animal models

Released from the hypothalamus in response to stress

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Difference between fear and anxiety

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Fear is an emotional response to clear and current danger, anxiety is apprehension about future events or misfortune and our ability to deal with them.

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BNST (Bed nucleus of the stria terminalis)

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Plays a big role in fear response

Chronic stress can increases the volume and branching of the BNST

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CER (conditioned emotional response)

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makes an association between an environmental stimulus and an aversive stimulus. It is established quickly and is long-lasting.

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Anxiety: CRF: Mechanism of action

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CRF -> ACTH (adrenocorticotropic hormone) -> cortisol

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Anxiety: NE

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Locus Coeruleus - major cluster of noradrenergic cells

Increase in NE increases alert/fear response

Too much NE can cause anxiety

Released during ANS activation

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Anxiety: Yohimbine

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α2-autoreceptor antagonist, (increases NE release) induces alerting and fear responses.

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Anxiety: Clonidine

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α2-autoreceptor agonist, has antianxiety effects.

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Anxiety: GABA

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Main inhibitory NT

GABA A receptor has a chloride (Cl–) channel that opens following GABA binding; Cl– enters cell and causes hyperpolarization

BDZ also binds to this receptor causing further hyperpolarization

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Benzodiazepines (BDZ)

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cause sedation and reduced anxiety by binding to modulatory sites on the GABA receptor complex

Work by enhancing GABA doesn't cause any more influx of Cl-

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BDZ sites

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Attached to GABA receptors

High concentration in the amygdala and cortex frontal lobe

People with less binding sites are more likely to have anxiety disorder

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Anxiety: Serotonin (5-HT)

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Increase 5-HT -> Decrease Anxiety, depending on the receptor subtype involved, Stimulating 5-HT 1A receptors decrease anxiety

neurotrophic effect of 5-HT is necessary for fetal development

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Anxiety: DA

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Modulatory role in anxiety for dopamine (DA) is suggested by the significant DA projections from the Ventral tegmental area to the medial prefrontal cortex and limbic regions including the amygdala.

More stress more dopamine release

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Early exposure to stress/neglect

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Alters the developing brain and can produce a lifelong tendency for enhanced anxiety

Alters the HPA (Hypothalamatic-Pituitary-Adrenal) axis, causing a hyperactive hormonal response to stress that persists throughout adulthood

Early stress can have bad mind altering affects that last into adulthood

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Generalized anxiety disorder (GAD)

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Individuals show signs of constant worry and continuously predict, anticipate, or imagine dreadful events

Increased volume of amygdala and too little inhibitory control by the prefrontal cortex

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Panic attacks

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individual experiences all the effects of a fear reaction without a threatening stimulus, accompanied by strong arousal of the sympathetic ANS.

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Panic disorder

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individual experiences both panic (individual attacks) and anticipatory anxiety over the possibility of having an attack in a place that is not safe.

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Anxiolytics.

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Drugs that relieve anxiety

Reduce neuron excitability

produce a calm and relaxed state, with drowsiness, mental clouding, and incoordination

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Barbiturate side effects

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Reduces REM sleep

Mental clouding, slow reflexes

High doses lead to gross intoxication. Coma and death result from respiratory depression.

Respiratory depression does not show tolerance, as you need more of the drug, the less safe it gets

Barbiturates produce significant physical dependence and potential for abuse. Potentially fatal withdrawal

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chlordiazepoxide (Librium)

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First BDZ

first true anxiolytic that targeted anxiety without producing excessive sedation, had low incidence of tolerance, less severe withdrawal than barbiturates

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Longer-acting BDZs

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Useful hypnotics for Sleep-aid

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Effects of high dose of BDZ

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produce disorientation, cognitive impairment, and amnesia, but no respiratory depression

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BDZ side effects

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Lower risk of dependence and abuse

Much lower reinforcement than barbituates

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Buspirone (BuSpar)

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Second generation BDZ

Advantages: treats depression, no sedation or mental clouding, Does not enhance CNS-depressant effects of alcohol, little to no potential for recreational use, Not withdrawal symptoms

Better then generation one BDZ in most ways, slow onset of anxiolytic effects, doesn't relieve insomnia, lacks muscle-relaxant effects

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Anxiety: Antidepressants

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Can treat both anxiety and depression, which often occur together

SSRI's are the first choice because they have fewer troubling side effects, a high therapeutic index, and low abuse potential.

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Phobias

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Irrational fears of objects or situations that are best treated with behavioral desensitization.

Very mild Psychological Disorder

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PTSD (post traumatic stress disorder)

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Not all trauma victims develop PTSD.

Amygdala shows increased activity

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OCD

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Severe chronic psychiatric problem characterized by recurring, persistent, intrusive, thoughts and repetitive rituals. The irrational acts of OCD must be performed to prevent extreme anxiety.

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Flumazenil

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BDZ receptor competitive antagonist that reduces BDZ effects but has no effect on GABA-induced hyperpolarization

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Barbiturate mechanism of action

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Increase GABA induced Cl- conductance and directly open the Cl- channel without GABA

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Brain Derived Neurotrophic Factor (BDNF)

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May protect your brain from being chewed up by stress,

Increased BDNF increases brain health

Long term antidepressants increase BDNF expression

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Antidepressants: History

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Reserpine -1950s, caused depletion of NE and 5-HT after drug was eliminated that lasted weeks

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Antidepressants: Drugs

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First generation: MAO-inhibitors, tricyclics

Second generation: SSRIs

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Tricyclic antidepressants mechanism of action

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block presynaptic NE and 5-HT reuptake transporter, block postsynaptic histamine receptors (makes you drowsy), block postsynaptic ACh receptors

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SSRIs

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Block 5-HT reuptake transporter, Blocks 5-HT 1-3

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Serotonin syndrome

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cognitive - disorientation, confusion, hypomania behavior - agitation, restlessness

usually occurs when combined with other SSRIs, St. John’s wort or valerian

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SSRI withdrawal symptoms

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Abrupt withdrawal not recommended, anxiety, agitation, crying spells

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DRUGS FOR:

Mania and bipolar disorders

Autism

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Mania and bipolar disorders: Lithium, Depakote (anticonvulsant), Symbyax, Abilify

Autism: Risperdal

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Types of bipolar disorders

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Bipolar I - At least one episode of mania

Bipolar II - Major depressive and hypomanic episodes

Cyclothymia - Less severe

Hard to diagnose

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Lithium

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Drug of choice for BP

Reduces mania,

Can be difficult to be used safely

Enhances 5-HT action

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Anticonvulsant drugs Mechanism of action

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blockade voltage-dependent Na channel

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Weight gain

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Bipolar drugs can cause significant weight gain

"Rather be insane than fat"

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Risperidone (Risperdal)

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Treats: schizophrenia, manic-depression

Adverse effects: significant weight gain, tardive dyskinesia, sedation

Receptor interactions: 5-HT, ACh, DA, and histamine

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Depression in population

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15-20% of population, twice as common in women, comorbid with anxiety and alcohol abuse

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Twin studies with mental disorders

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Shows genetic contribution is high because of concordance rate in identical twins

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Abnormalities of HPA axis

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Associated with depression,

High ACTH/cortisol, hypersecretion of CRF

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Monoamine hypothesis: Depression

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Depression is associated with low levels of monoamines,

Mania = excess levels

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Role of 5-HT in depression

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Low levels of 5-HT is associated with depression

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Third-generation antidepressant mechanism of action

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CRF receptor antagonists enhancers of the cAMP intercellular cascade

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Schizophrenia

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Most severe mental illness

Characterized by hallucinations, delusions, apathy, thinking abnormalities, and “split” between thoughts and emotions

affects about 1 percent of the population

It’s NOT split personality or multiple personality disorder

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The Four Subtypes of Schizophrenia: Disorganized Schizophrenic

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Incoherence, grossly disorganized behavior, bizarre thinking, and flat or inappropriate emotions

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The Four Subtypes of Schizophrenia: Paranoid Schizophrenic

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Preoccupation with delusions of grandeur or persecution; also involves hallucinations that are related to a single theme, especially grandeur or persecution

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The Four Subtypes of Schizophrenia: Catatonic Schizophrenic

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Marked by stupor where victim may hold same position for hours or days; also unresponsive

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The Four Subtypes of Schizophrenia: Undifferentiated Schizophrenic

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Any type of schizophrenia that does not have paranoid, catatonic, or disorganized features or symptoms

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Schizophrenia: Positive Symptoms

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Psychosis, Hallucinations (auditory is most common), Delusions,

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Schizophrenia: Negative Symptoms

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Flat affect, Disturbed vocal communication, Personality Disintegration (Uncoordinated thoughts, actions, and emotions), Lack of voluntary motor behavior, Social withdrawal

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Schizophrenia: Cognitive Symptoms

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impaired working memory, executive functioning, and attention

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Hypofrontality

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Abnormally low activity in the prefrontal cortex

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Chlorpromazine (Thorazine)

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1956 psychosis drug, didn't really treat symptoms as much as it just sedated the patient

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The Odyssean Personality

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It is proposed that the schizoid-paranoid personality (designated as the Odyssean personality) which characterizes so many nonpsychotic relatives of schizophrenics, represents a selective advantage

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Family studies: schizophrenia

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The closer the genetic relationship, the greater the risk

Concordance in identical twins is high indicating significant genetic contribution

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DISC1 gene

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Mutations of this gene increase the probability of developing schizophrenia

Codes for protein necessary for embryonic brain development

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Dopamine hypothesis: Schizophrenia

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Excess DA function results in positive symptoms of schizophrenia.

There is a strong correlation between D2 receptor blockade and reduction of schizophrenic symptoms

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Tardive dyskinesia

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Characterized by stereotyped involuntary movements, particularly of the face and jaw, quick and uncontrolled movements of the arms and legs, and other motor effects.

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Law of thirds

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One third of patients treated with antipsychotics improve and live a normal life

A second third show improvement but experience relapses and need help with day-to-day living

The final third show little improvement and have significant periods of hospitalization

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Antipsychotics: side effects

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Parkinson's like symptoms (lower incidence with second generation drugs)

Anticholinergic effects, effect ANS function

Weight gain

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Clozapine

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Improves negative and cognitive symptoms in schizophrenics without motor side effects

Has other serious side effect which limits its use.