psy 456 exam 4

learning

process by which experiences produce long-lasting change in our nervous system and behavior

habituation

decrement in reflexive response due to repeated stimulus presentation

pavlovian conditioning

Classical conditioning
-unconditioned stimulus
-unconditioned response
whistle > puff of air > eye blink

instrumental conditioning

a learning procedure where the effects of a particular behavior in a particular situation increase or decrease probability of behavior; also called operant conditioning

reinforcing stimulus

a stimulus that strengthens or weakens the behavior that produced it

punishing stimulus

aversive stimulus that follows a particular behavior and thus makes the behavior become less fequent

long-term potentiation

long-term increase in excitability of a neuron caused by repeated high-frequency activity of input

short-term memory (working memory)

immediate memory for events, which may or may not be consolidated into long-term memory

long-term memory

relatively stable memory of events that occurred in the more distant past

consolidation

process by which short-term memories are converted into long-term memories

re-consolidation

process by which a previously consolidated memory is retrieved into working memory and updated

declarative memory (explicit)

memory that can be verbally expressed, such as memory for events in a person’s past

nondeclarative memory (implicit)

memory whose formation does not depend on the hippocampal formation; a collective term for perceptual, stimulus-response, and motor memory

episodic memories

memory of a collection of perceptions of events organized in time and identified by a particular context

semantic memories

memory of facts and general information

spatial memories

functional imaging studies have shown that the right hippocampus formation becomes active when a person remembering or performing a navigational task

place cell

a neuron that becomes active when the animal is in a particular location in the environment; most typically found in the hippocampal formation

Frontal-striata-thalami circuit

frontal cortex suppresses prepotent responses, and deficits in this circuit may underlie ADHD, Tourette’s, and/or OCD. D1 DA receptor agonists may restore function

anterograde amnesia

loss of memory for events immediately following a trauma; sometimes in effect for events during and for a long time following the trauma

retrograde amnesia

loss of memory for events immediately prior to a trauma

korsakoff’s syndrome

permanent anterograde amnesia caused by brain damage resulting from chronic alcoholism

confabulation

reporting of memories of events that did not take place without intention to deceive, seen in people with Korsakoff’s

morris water maze

learning
-rat goes in one side of tank every time with hidden platform on other side
-rat learns to swim straight
-destroyed hippocampus does not affect this learning process or memory of platform location
-stimulus response learning (dont need hippocampus)

fear

-innate vs. learned
-fearful events have both a cognitive and emotional component
-cognitive-hippocampus
-emotional-amygdala

anxiety

unlike fear, there is no specific event or object that evokes anxiety (BNST)

mood

general emotional state that has either a positive or negative valence (happy or sad)

animal model: fear

conditioned suppression test

animal model: anxiety

elevated plus maze

animal model: mood

no valid animal model to differentiate happy vs. sad

conditioned emotional response

a classically conditioned response that occurs when a neutral stimulus is followed by an aversive sitmulus

unipolar depression

can be modeled by learned helplessness or Porsolt swim test

fear circuitry

stimulus > thalamus > amygdala or sensory cortex > from sensory cortex to hippocampus/amygdala

central amygdala

output nucleus
-freezing, blood pressure, stress hormones, startle reflex

basolateral amygdala

input nucleus
-goes to central gray, pons, and amygdala
-activates regions that stimulate cortex

output: lateral hypothalamus

sympathetic arousal

output: paraventricular n. hypothalamus

corticotropin releasing hormone (CRH)

output: periaqueductal gray

descending pain inhibition

output: locus coeruleus

arousal and vigilance

Bed nucleus of stria terminalis (BNST)

amygdala=fear
BNST=anxiety

Subgenual cingulate cortex (brodman area 25)

-involved in mood regulation
-activated by pain and frustrating experiences
-overactive in depression
-target for deep brain stimulation to treat depression

mPFC

medial prefrontal cortex
underactive in anxiety disorders

OFC

orbitofrontal cortex
underactive in anxiety disorders

affective disorders

-sleep disturbance
-appetite disturbance
-depressed mood
-axiety

sleep disturbance brain regions

pontine tegmentum and suprachiasmatic nucleus

appetite disturbance bain region

hypothalamic nuclei

depressed mood brian region

nucleus accumbens, medial prefrontal cortex, amygdala, subgenual cingulate cortex

anxiety brain regions

BNST and paraventricular nucleus of hypothalamus (CRH)

anxiety disorders

phobia
OCD
Panic
generalized

phobia

specific irrational fear
responsive to behavioral treatment

OCD

repetitive intrusive thoughts or actions
SSRI treatment

Panic disorder

episodes of intense anxiety
benzodiazepine treatment

generalized anxiety disorder

free-floating anxiety
benzodiazepine treatment

major anti anxiety medications

benzodiazepines

Xanax

panic, generalized, phobias, social anxiety, OCD

Klonopin

panic, generalized, phobias, social anxiety

Valium and Ativan

generalized, panic, phobias

Serax and Librium

generalized, phobias

Side effects of benzodiazepines

-drowsiness, lack of energy
-clumsiness, slow reflexes
-slurred speech
-confusion and disorientation
-depression
-dizziness, lightheadedness
-impaired thinking
-memory loss, forgetfulness
-nausea, stomach upset
-blurred or double vision
-addiction

nonbenzodiazepine GABAa allosteric modulators

zolpidem

beta blockers

propranolol

tricyclic antidepressants

doxepin

SSRIs

fluoxetine, sertraline

nonbenzodiazepine anxiolytic

buspirone

anticonvolsants

gabapentin

Cognitive-Behavioral Therapies

therapeutic approach emphasizes modification of dysfunctional thoughts, emotions, and behaviors. in contrast to analytic approaches, CBT focuses on solutions rather than analysis of cause of problem

proven efficacy for generalized anxiety, panic disorder and PTSD

most useful when combined with SSRIs

symptoms of depression

change in body weight and appetite
change in normal sleep pattern
loss of libido
feelings of hopelessness
thoughts of suicide
internalizing of negative outcomes
often co-morbid with anxiety (BNST)

unipolar depression

episodes of depression only
30-40% heritable

bipolar disorder

episodes of mania and depression
80% heritable
type 1 (full manic episode) vs. type 2 (hypo mania)

Seasonal Affective Disorder

specific to winter
more common in countries far from equator
disrupted circadian rhythm, suprachiasmatic nucleus

monoamine hypothesis

depressed patients have less monoamine activity
supported by evidence showing:
reserpine-induced depletion of monoamine stores leading to depression
clinical evidence showing efficacy of SSRIs and SNRIs

treatment of depression

antidepressant medication
ECT
sleep deprivation
light therapy
CBT
DBS
TMS

first generational antidepressants

-tricyclic antidepressants
-other antidepressants
-monoamine oxidase inhibitors

second generation antidepressants

SSRIs
SNRIs

side effects of antidepressant medications

sedation
insomnia
body weight change
anticholinergic side effects
hypotension
agranulocytosis
cheese effect with MAO inhibitors

Ketamine

-in 2019, approved for use in individuals with treatment-resistant depression
-no delay in efficacy
-first delivered i.v. or intranasal by primary care health provider. then transitioned to oral classical antidepressant
-is a dissociative anesthetic similar to NMDA noncompetitive antagonist PCP
-implicates glutamatergic dysfunction in depression

tolerance

decrease in the effect of a drug when given repeatedly at a constant does. can be due to either pharmacokinetic or pharmacodynamic changes

sensitization

increase in the effect of a drug when given repeatedly at a constant does

dependence

an adaptive state that develops in response to repeated drug administration

positive reinforcement

add rewarding stimulus to increase or maintain behavior

positive punishment

add aversive stimulus to decrease behavior

negative reinforcement

remove aversive stimulus to increase or maintain behavior

negative punishment

remove rewarding stimulus to decrease behavior

cycle of addiction

intoxication>positive reinforcement>withdrawal>negative reinforcement>pre-occupation>relapse>and cycles again

classical conditioning

CS + US = CR
add a neutral stimulus that creates a CR

animal models: self administration

measures reinforcing effects of drugs
can predict abuse liability of drugs
useful in developing treatments

Psychostimulants

catecholamines mimetics: cocaine, amphetamine, methamphetamine
antidepressants: tricyclics, MAO inhibitors, SSRIs
nicotine
caffeine

opiods

natural: morphine, the wine, codeine
synthetic: methadone, heroin, oxycodone, hydrocodone, fentanyl

sedative hypnotics

barbiturate
nonbarbiturates
benzodiazepines
alcohol
antipsychotics

hallucinogens

natural
synthetic
miscellaneous

3 dopamine reward pathways

meso-cortic
meso-limbic
nigrostriatal (movement/goes into striatum)

mesocorticol pathway

vita to nuc accumbens

mesolimbic pathway

vta to prefrontal cortex

nucleus accumbens has what kind of neurons

-GABAergic medium spiny neurons

cocaine and meth on DA pathways

they block monoamine transporters DAT
meth also increases release of DA from vesicles in pre-synaptic nerve terminals

nicotine on DA pathway

activates mesolimbic system in 3 ways:
1. activates DA neurons in VTA directly via stimulation of cholinergic receptors on the neurons
2. activates DA neurons in VTA indirectly via stimulation of cholinergic receptors on GLU nerve terminals
3. activates endogenous opioid pathways

opiods on DA pathway

1. inhibition of GABA neurons lead to disinhibition of the VTA which results in DA release in NAc
2. dopamine-independent activity in the NAc

direct actions on the mu and delta opioid receptor in NAc neurons

alcohol on DA pathway

1. promotes GABAa receptor function that leads to inhibition of GABA nerve terminals and disinhibition of the VTA which results in DA release in NAc
2. activate endogenous opioid pathways
3. acts as an antagonist by inhibiting NMDA GLU receptors

cellular effects of Repeated drug exposure

1. up-regulation of cAMP pathway
2. increased phosphorylation of CREB
3. increased FosB

up-regulation of cAMP pathway

induction of adenylyl cyclase enzyme
increases protein kinase A to phosphorylation ion channels

increased phosphorylation of CREB

-transcriptional factor in the nucleus which alters gene expression
-may mediate tolerance and dependence