Drugs Brain and Behavior Ch 6 + 7

Depression

Presence of sad, empty, or irritable mood, accompaniedby somatic and cognitive changes that significantly affectthe individual's capacity to function

Major Depressive Disorder Time Frame

At least 2 weeks of loss ofinterest and/or depressed mood

Major Depressive Disorder

Feeling of sadness, loss ofpleasure, tearful, sleepdisturbances, guilt,helplessness, suicidal ideation

Bipolar Disorder Time Frame

One or more manic episodecoupled with depressionevents

Bipolar Disorder

Inflated self-esteem, decreasesleep needs, excessivereward behaviors, easilydistracted

Mood Disorder Time Frame

Prominent and persistent mood disturbances

Mood Disorder

Depressed, elevated,expansive, or irritable mood,diminished pleasure

Clinical Depression vs feeling depressed

Normal Depression - depression episodes, short feelings of sadness,

Clinical- long lasting 2+ weeks, puts a "pause" on life,

Antidepressants

Medication targeted at monoamines

Khat

Stiumlant, thought to be the first antidepressant used

Iproniazid

The first antidepressant drug; a monoamine oxidase inhibitor, found when treating tuberculosis

MAO Enzymes

critical role in oxidation ofnorepinephrine, serotonin, anddopamine

List of Antidepressants

Monoamine Oxidase Inhibitors, Selective Norepinephrine Reuptake Inhibitors, Selective Serotonin Reuptake Inhibitors, Tricyclics, Tetracyclics, Neuropeptides, NMDA antagonists

MAOI

monoamine oxidase inhibitor

Tricyclics

inhibit reuptake of dopamine,serotonin & norepinephrine

Lithium Salts

targeted at treating bipolar disorders- no proper reason has to be found why it works

Stimulants

Excites the whole system

cocoaine

stimulant

SSRI/SNRI

targeted at blocking reuptake of monoamines- SSRI - blocks reabsorption of serotonin

How are these different than typical tricyclics we discussed?

SELECTIVE Reuptake Inhibitor

serotonin sydrome

presents when there is an excess of serotonin; often develops when patients are switching anti-depressive medications, or with patients with liver disease

Neuropeptides

small chains of aminoacids that "act" as neurotransmitters

Why don't antidepressants have an immdiate effect

Plasticity takes time to develop- strengethening the neural pathways

How does synaptic plasticity play a role in the development and treatment of depression disorders?

Synpatic plasticity stregnthens the neural pathways built by the antideppressents. Depression is linked to an imbalance in the brain so the antideppressants attempt to rewire those neurons.

What is the exact mechanism of MAOIs? What about lithium?

Monoamino oxidose inhibitors, inhibit reuptake of a monoamines. Block the breakdown of the monoamine and allow the neurotransmitter to be used repeadetly. Don't know why lithium works.

If an individual was clinically diagnosed with depression,how would you explain to them it is different from being generally sad/disinterested at times?

Clinical depression lasts longer than two weeks and tends to interfere with work and school, regular discomfort in life itself

Anxiety

Excessive fear or worry that is persistent and causes significant distress or impairment in dailyfunction

Fear

emotional response to aperceived or real threat

Anxiety- non medical

Fear without a stimulus - anticipation of a future threat

Social Anxiety Disorder

Marked fear or anxiety about one or more socialsituations; fears that they will show anxietysymptoms that will be negatively evaluated

Seperation Anxiety Disorder

Developmentally inappropriate and excessive fear oranxiety concerning separation from the attachedindividual; recurrent and excessive; excessive worryof an event for that person

Specific Disorder

Marked fear or anxiety about a specific object orsituation, which nearly always provokes an anxietyresponse; out of proportion to actual danger; 6+months

Where did Anxiety Originate?

Initially thought to be driven by sympathatic "fight or flight" adrenaline response

Anxiolytics

antianxiety medication, minor tranquilizers, and sedatives

Benzodiazepines ADME

Acids absorbed rapidly from GI tract, Oral works better due to protein binding at injection site, distrubution and elimination are different

Benzodiazepines biobehavior effects

Insomania, Seizures, motor alterations, crosses the placenta border

Addiction to anxiolytics is a big problem because

DISINHIBITION OF DOPAMANERGIC NEURONS, dopamanergic neurons are increased causing addictions, dopamine releases a "feel good" feeling causing addiction

Compare a person experiencing a "fight-or-flight" response to someone who has been diagnosed with a specific phobia?

Fight or flight is a normal response to something in a regular situation like something is on firing so leaving the building possibly screaming, while someone with a specfic phobia will exhibit an absurd reaction and possibly deal with it long term

What options would you have for a pregnant person that has developed a clinical anxiety disorder?

Just therapy since anxiolytics can cross the placenta border giving an addiction to the baby, and when the baby is born they get withdrawl symptoms

How do benzodiazepines become so addictive? Describe the target of these pharmaceuticals

Benzodiapines cause dopaminergic neurons to have an increase in firing which trarget the dopamine pathway which is our reward system causing addiction to the pleasure feeling

Benzodiazepines Process

Binds to the GABA receptors and inhibit them from firing- work as an agonist, and reduce GABA, resulting in the calming effects like reduced anxiety, muscle relaxation, and sedation.

Psychosis

A multitude of symptoms that impact the brain, resulting in some loss of contact with reality

Delusions

fixed beliefs that has no basis in reality. 2 common subtypes, paranoid + grandeur

Hallucinations

Brain percieving something that is not there. Typically auditory, but can occur in any sensory system

Initial treatment with psychosis included...

-cold-water submersion

- bleeding with leeches

- burning at the stake

Last century treatment with psychosis included..

-straight jackets, restraints

- insulin-induced comas

- lobotomies, shock-therapy

1st antipsychotics was targeted at

destroying monoamine vesicles (Reserpine)

Thorazine

reduced psychosis events, and did not alter normative behavior

Most identified, original, and studied psychoses

Schizophrenia

Schizophrenia

Can be acute (sudden onset, full-blown) or chronic(gradual onset, progressive deterioration). Disturbances involving reality tests & concept formation, psychomotor poverty, and disorganization

ADME of antipsychotics

Typically administered orally (rare instances, hospitalization -use injections)

Daily administration is essential to maintain steady bloodconcentrations of the drugs (have a longer half-life to help withthis)

High levels of metabolization = lots of complex metabolite production and interactions occur

Basis of psychotic disorders

Too many dopamine receptors.. postmortem receptor binding studies with controls showed more in diagnosed schizophrenics

Psychogens may be involved

Brains of schizophrenics produce higher levels of phenylethylamine (a dopaminergic agonist)

Enzyme involved with psychotic disorders

Monoamine oxidase levels of activity in the brain are lower in schizophrenic individuals

phenylethylamine

dopaminergic agonist

Typical Antipsychotics

Dopamine antagonism

atypical antipsychotics

Fewer side effects, target serotonin as an antagaonist

Medical consequences of atypical antipsychotics

Endocrine impact: Altered breast formation• Lactation onset• Abnormal menstrual cycles• Infertility

Motor Impact: Substantia nigra dysfunction• Extrapyramidal system side effects- Pseudoparkinsonism- Tardive dyskinesia- Acute dystonic reactions

neuropleptic malignant syndrome

results in severe rigidity, fever,ANS dysregulation

Dopaminergic pathways

Mesolimbic

Mesocortical

Nigrostriatal

Tuberoinfundibular

Nigrostriaial pathway

motor function impacted