Physiological Psychology Exam #2

neurotransmitters

-created in and sent by the presynaptic neuron
-received by and has some effect on the postsynaptic neuron
-types: monoamines, amino acids, and peptides

monoamines

one amine group, ex: dopamine, norepinephrine, serotonin, epinephrine

amino acids

compounds with amino and carboxyl groups, ex: glutamate, GABA, glycine

glutamate

-excitatory pathways, synaptogenesis, strengthening connections
-2 receptors: NMDA and AMPA

GABA

primary inhibitory neurotransmitter (inhibition can lead to seizures)

glycine

inhibitory neurotransmitter involved in sensory/motor pathways, brainstem and spinal cord

peptides

3-40 amino acids, ex: endorphins, oxytocin, vasopressin

endorphins

mood enhancers, pain/reward

oxytocin and vasopressin

social relationships/bonding

acetylcholine (ACh)

motor function, memory/cognition, parasympathetic function

retrograde neurotransmitters

ex: endocannabinoids, nitric oxide

agonist

a drug that influences neurotransmitter function in some way/imitates or enhances the effect of specific neurotransmitters (ex: alcohol - GABA)

antagonists

blocks or decreases the effect of specific neurotransmitters (ex: curare - ACh)

agonists and antagonists

-bind to postsynaptic receptors
-influence amount of neurotransmitter release
-influence how long neurotransmitter stays in the synapse
-influence production of new neurotransmitter

stimulants

drugs that facilitate arousal

caffeine

-most widely used psychoactive drug in the world
-psychological effects: increased energy, self-confidence, alertness, and focus

adenosine

-inhibitory neurotransmitter (inhibits release of excitatory neurotransmitters)
-hippocampus, cerebral cortex, cerebellum
-caffeine: adenosine antagonist, blocks adenosine receptors

nicotine

-psychological effects: heightened tensions/arousal, increased heart rate/blood pressure, sustained attention, stimulates metabolism
-acetylcholine agonist
-nicotenic endinergic receptors
-smoking is neurally rewarding (activates dopamine's "reward system" in the nucleus accumbens)

nicotenic endinergic receptors

-usually bind to ACh
-mostly presynaptic, can effect other neurotransmitter systems
-cerebral cortex, striatum, hippocampus, thalamus, etc.

cocaine

-from the coca plant
-psychological effects: euphoria, increased energy/alertness, feeling competent/powerful
-agonist (blocks reuptake, dopamine/norepinephrine/serotonin)

amphetamine

-1930's
-anti-asthmatic
-boost alertness, well-being, reduces fatigue
-treatment for ADHD and narcolepsy
-agonist (blocks catecholamine reuptake, boosts presynaptic catecholamine release)

MDMA (ecstasy)

-"designer drug"
-enhances social connection, sensory perception, well-being, similar to cocaine
-monoamine agonist (stored serotonin and dopamine release)

depressants

inhibits neural firing

alcohol

-psychological effects: improved mood, drowsiness, increased self-confidence, impaired judgement, impaired muscle coordination
-glutamate: primary excitatory neurotransmitter

alcohol as glutamate antagonist

-binds to NMDA receptor (blocks action): found in hippocampus
-long-term use: create more NMDA receptors, increase glutamate release

alcohol as GABA agonist

-primary inhibitory neurotransmitter
-binds to GABA receptors (mimics their effects)

analgesics

-opium
-often injected for quick delivery to brain
-psychological effects: euphoria, pain relief
-physiological effects: mu, delta, kappa receptors
-endogenous opioids

opium

-from the poppy plant
-morphine, codeine, heroin

mu receptors

-found in many locations in brain/spinal cord
-dense in areas related to pain and reward

delta receptors

-found in the forebrain
-relate to reward, cognitive effects

kappa receptors

-striatum, amygdala, hypothalamus, pituitary
-dysphoria, hallucinations, pain, stress response

endogenous opioids

-endorphins, enkephalin, all variations on morphine
-role: GABA antagonist (leads to increased secretion of dopamine)

hallucinogens

LSD and cannabis

LSD (lysergic acid diethylamide)

-semisynthetic and extracted form rye fungus and made in a lab
-properties discovered in 1943: 40s and 50s (enhance effects of psychotherapy), 60s (spiritual/recreational use), 1966 (becomes schedule 1 drug)
-psychological effects: hallucinations/illusions, changing perception of time and space, synesthesia
-physiological effects: serotonin agonist, found in thalamus, indirectly inhibits GABA neurons, cognitive effects

cannabis

-THC (tetrahydrocannabinol): psychoactive ingredient in cannabis
-psychological effects: altered sensation, appetite, euphoria, disinhibition, relaxation, impaired memory/motor ability
-long term: lack of motivation, more cognitive decline in adulthood (if adolescent use)
-cannabinoid receptors: basal ganglia, substantia nigra, cerebellum, hippocampus, cerebral cortex
-act on presynaptic receptors: inhibit dopamine, norepinephrine, ACh, glutamate, GABA
-anandamide: endogenous cannabinoid (modulates dopamine: similar to opioids)
-GABA: normally inhibits dopamine neurons, without inhibition -> more dopamine

mesolimbic dopaminergic pathway

-activation can motivate/sustain drug use
-drugs alter this pathway, leading to addiction
-drug dependence: need for the drug to maintain physiological function
-tolerance: body's reaction to the drug decreases, decreasing receptor sensitivity, increasing metabolic ability to break down drug, environment component

drug addiction cycle

binge -> withdrawal -> craving

binge

-acute drug effects
-influence on dopaminergic pathway
-leads to reward/feelings of pleasure
-only for quick increases of dopamine activity

withdrawal

-heightened stress response
-activation of extended amygdala region: perceived threat
-increased anxiety

craving

-can occur for months or years after discontinued use
-leads to relapse
-psychological and physiological components: acute stress, exposure to drug, conditioned cues

treatment

detoxification, physiological recovery, drug replacements (e.g., methadone), behavioral therapies, incentivizing abstinence, rehabilitation, targets conditioned cues, vaccine? (block nicotine from crossing the blood-brain barrier)

Wilder Penfield

-mapped the motor and somatosensory cortices
-discovered the "motor homunculus"

map of the body

-large size = more sensitive/more fine motor control
-sends signals to muscles to contract

corticospinal tracts

-axons from motor cortex travel down spinal column (aka "upper motor neurons")
-send movement signals to the body
-synapse in the spinal cord

lateral corticospinal tract

-contralateral control (decussate at the medulla)
-send info to arms/legs

anterior/ventral corticospinal tract

-stay ipsilateral
-send info to trunk

the spinal cord

-31 spinal nerves
-send signals to and from the body

lower motor neurons

-cell bodies in the spinal cord gray matter
-axons leave through the ventral root

dorsal root

afferent sensory information

ventral root

efferent motor information

Interneurons

connect the dorsal root (sensation) to the lower motor neurons

reflex arc

sensory neuron -> interneuron -> lower motor neurons

smooth muscle (and cardiac)

-involuntary control (mostly): biofeedback
-autonomic system

skeletal muscle

-voluntary control (mostly): posture
-extrafusal fibers (contract)
-intrafusal fibers (detect muscle length)

neuromuscular junction

-synapse
-lower motor neurons -> extrafusal muscle fiber (at motor end plate)

antagonistic muscle pairs

actions oppose one another

intrafusal fibers

-sensory receptors monitor stretching
-corrected by inhibition or antagonist contraction

golgi tendon organ

-in tendon
-senses excessive contraction
-prevents damage

knee-jerk response

-tap the patellar tendon = excessive stretch of quad
-compensatory contraction of quad = lower leg kick

complex movements

behaviors that are more complex than reflexes/movement patterns like walking

complex movements: the cortex

-supplementary motor cortex: SMA and pre-SMA
-premotor cortex
-DLPFC
-primary motor cortex (homunculus)

the cortex

-imagining a complex task
-using executive control: e.g., response inhibition, switching tasks/performing in changing conditions
-monitoring performance during skill learning

complex movements: the basal ganglia

-caudate and putamen: the striatum
-putamen
-globus pallidus
-substantia nigra

the basal ganglia

-movement control: inhibit unwanted movements (globus pallidus)
-motor memory: complex skill learning, requires little if any sensory feedback
-habit formation (striatum and frontal cortex): OCD, addiction, superstition

the cerebellum

-flocculonodular lobe: oldest region, balance posture
-vermis: muscle tone
-cerebellar peduncles: communication with other brain regions
-movement coordination: modification of current movements
-timing and rhythm
-cerebellar cognitive affective syndrome: cerebellar lesions and executive function, language, sequencing events, visuospatial abilities all affected

getting tickled

-fMRI study: expected vs. unexpected touch
-result: more activity in 3 areas (ACC, somatosensory cortex, cerebellum)

what it takes to become an expert

-10,000 hours of distributed practice: intentional repetitive practicing of skills
-about 10 years
-trial and error
-reinforcing movements that lead to better skills: refining technique over time

consequences of expertise

-automaticity: less attention needed to perform action
-efficiency: less neural activation required to do well

choking under pressure

-addition under attentional focus
-adds uncertainty/interference with the task
-recruits other brain regions not needed for the task
-leads to mistakes

exercise

-improves intelligence scores
-prevents cognitive decline
-enhances learning
-rodents: enhances new blood vessels, neurogenesis, BDNF

Parkinson's disease

-neurodegenerative disease
-often found in older adults (50s+)
-physical changes: akinesia (lack of voluntary movement), muscle tremors (shaking at rest, goes away with movement), rigidity of movement, fewer automatic movements (arm swings)
-progressive degeneration of substantia nigra: dopamine-producing region, presence of Lewy bodies (protein deposits)

treatments for Parkinson's disease

-L-DOPA: becomes less effective over time
-transplanting dopaminergic neurons to substantia nigra: variable success rates
-leisoning the basal ganglia: decreases tremors/unwanted movements, blocks habitual motor message that compete with goal-directed movement

spinal cord injury

-damage to neurons in the spinal column: swelling in area of damage
-paraplegia: inability to move lower extremities
-quadriplegia: inability to move lower and upper extremities, torso

treatments for spinal cord injuries

-transplants can lead to some regeneration: autologous transplants (your own cultured tissue)
-neurorehabilitation: stimulation/agonist drugs/harness training
-robotic control: electrode implants in motor cortex

circadian rhythms

-anything on a daily cycle of change
-suprachiasmatic nucleus (SCN): within the hypothalamus, input from retina, damage -> stress hormone disruption
-pineal gland: retinal input, produces melatonin (promotes temp. drop)

disruption of cycle

shift work and jet lag

awake at night

-high melatonin levels, response time suffers, accident prone

polysomnography

-EEG measures brain activity
-EOG measures eye movements
-EMG measures muscle tension

awake stage

beta waves (13-30 Hz)

sleepy stage

alpha waves (8-12 Hz)

stage 1 sleep

theta waves: 4 - 5 % pf sleep cycle (3-7 Hz)

stage 2 sleep

sleep spindles and k-complexes (45 - 55% of sleep cycle)

slow wave sleep (SWS)

delta waves: 16 - 21% of sleep cycle (-0.5-3 Hz)

REM sleep (dreams)

faster waves that resemble waking: 20 - 25% of sleep cycle

reticular formation

ascending reticular activating system (ARAS): nuclei within the brainstem, project to forebrain

raphe nuclei

within the brainstem, produce serotonin

acetylcholine (ACh): sleep

contributes to sustaining beta waves

serotonin

contributes to both wake and sleep

slow wave sleep

-cortex and thalamus are in synchrony
-occurs locally, not globally
-ventrolateral preoptic area (VLPO): activity increase, projects to TMN, diminishes wakefulness
-tuberomammilary nucleus (TMN)

REM sleep

-rapid eye movements
-atonia (relaxed muscles)
-pontogeniculoocciptial (PGO) spikes: pons -> LGN of thalamus -> occipital cortex, correlated with eye movements
-subcoeruleus region (pons): damage -> less REM sleep

homeostatic theory of sleep

provides rest and recovery

sleep rebound effect

-lost sleep is made up later
-only about 30%

deprivation and stress

may contribute to cognitive deficits, motor performance, emotional regulation, hallucinations

adaptive theory of sleep

-sleep = adaptive inactivity
-hiding protects form predation
-food is scarce = time to sleep

memories and sleep

-hippocampal neurons fire in SWS
-rehearsal of learned information
-memory consolidation
-task (study): location of objects (odor during SWS, enhanced recall)

synaptic homeostasis hypothesis

-sleep prunes weaker synapses
-thus strengthening stronger synapses
-production of synapses decreases during sleep
-REM sleep: consolidate procedural learning, deprivation leads to memory deficits, after learning difficult tasks we spend increased time in REM, processing survival-related information

improving the immune system

-vaccines are less effective when people have interrupted sleep
-sleep efficiency: percentage of time in bed that you are actually asleep
-study: 2 weeks of sleep reporting, then: exposed to cold virus, next 5 days: 3x more likely to get a cold if previously slept for less then 7 hours/night and 5.5x more likely to get a cold if efficiency is less than 92%

interleukin 1

-tumer necrosis factor: both immune system chemicals, presence increases SWS
-sleep regulation areas respond to these factors: brainstem, hippocampus, hypothalamus
-sickness can disrupt REM and SWS: may help maintain fever (REM: atonia prevents shivering, SWS: temp. drops naturally during this phase)

insomnia

-difficulty falling or staying asleep
-sleepiness during waking hours
-35% of Americans (adults) experience nightly
-58% experience a few days/nights a week

treatments for insomnia

-medications (GABA agonists): long-term effects = fatigue, nightmares
-cognitive behavioral therapy (CBT)
-exercise (late afternoon)
-dim the lights before bed
-limit caffeine and alcohol
-bedroom hygiene (temp, light control)