BIOPSYC UNIT 3

LTP

a synaptic mechanism for associative memory

what is a silent synapse

• has NMDAR but no AMPAR

• AMPAR are usually embedded in cell and can be vesicular exocytosized

schizophrenia

• positive symptoms; delusions, hallucinations, inappropriate affect, disorganized speech and thought, odd bx

• negative symptoms; affect flattening, avoltion (lack motivation), catatonia (no movement)

• pharmacology; drugs that reduce dopamenergic activity ameliorate schizophrenic symptoms

chlorpromazine

dopamine antagonist (blocks dopamine receptors), good for schizophrenia

haloperidol

• reduce dopamenergic symptoms

• good for schizophrenia

d-serine

• coagonist for NMDAR receptors

• helps with schizophrenia

NMDAR hypofunction hypothesis

• inhibitory neuron with NMDAR does not fire enough inhibition

• excitatory neuron gets too excited

• too much APs and too many NTs

• the DA neuron fires too much dopamine

• there is thinning in cortex

reactive depression

• situational depression

endogenous depression

• biological (gense, postpartum)

Depression pharmacology

• monomine oxidase inhibitors (MAOIs)

  • monoamine oxidase breaks down seretonin (if inhibited, more serotonin is present)

  • last resort, need strict diet

• trcyclic antidepressants (SSRIs, SNRIs)

  • blocks reuptake of seretonin and norepinephrine

Bipolar Disorder

depression and hypomania

• hypomania: reduced need for sleep, energetic, talkative, impulsive, positive affect, delusions

• 80-90% heritablity

• overactive Gq/11 signalling

hormones

• chemical signals secreted by cells of the endocrine system

endocrine cells

• cells that secrete chemical signals such as hormones

target cells

• cells that have receptors for the chemical signals

• circulating hormones diffuse into the blood and can activate target cells far from site of release

endocrine glands

• release hormones to the inside of the body

exocrine cells

• release hormones to the outside of the body

• sweat

neurohormones

• NTs in blood

pheremones

• chemical signals released to the environment

posterior pituitary gland

• only releases hormones from hypothalamus to capillaries to everywhere

• antidiuretic hormones: hormones that target kidneys and tell them to not pee to concentrate urine

• oxyticin: targets pair bonding, targets uterus and brain (causes contractions to get closer and closer)

negative feedback

• fluctuating around a set point for homeostasis (cold —> shiver, hot —> sweat)

positive feedback

• childbirth and action potentials

• get away from set point (more contractions, more birth, non homeostatic)

Thyroid gland physiology

• hypothalamus detects low levels of thyroid hormones so releases TRH

• goes to anterior pituitary gland, then releases TSH to the thyroid

• TSH in blood to capillaries, thyroid cells G-protein coupled in cells

• cells make thyroglobulin

• iodinate thyroglobulin

• splits to T3 and T4 because of number of iodines attached

• T3 and T4 increases metabolism and makes temperature increase

• NORMAL

get a hypothyritic goiter

• hypothalamus releases TRH

• anterior pituitary gland makes TSH

• in thyroid, thyroglobulin is made

• no iodination occurs

• so hypothalamus makes too much TRH

• stimulates too much and thyroid cells duplicate

• goiter occurs

• solve: have iodine tablets

get a hyperthyritic goiter

• immune system is elevated, too many antibodies

• TSH receptors activated by antibodies

• make thyroglobulin

• makes T3 and T4

• low leaves of TRH and TSH

• but antibodies continue and make thyroid enlarged

• goiter

• solve; destroy thyroid and go on HRT

Adrenal gland: chronic stress

• brain interprets situation

• hypothalamus makes CRH

• anterior pituitary gland releases ACTH

• adrenal cortex (middle zone, zone fasciulata)

• releases cortisol (stress response, blocks immune system)

• CALLED THE HPA AXIS

positive incentive hypothesis

• hunger depends on flavor of food, effects of the food, time since last meal, type and quality of food in gut, presence of con specifics (other humans save them), and blood glucose levels

chemical digestion

• digestive enzymes and stomach acid (pepsin)

mechanical digestion

• chewing

pancreas

• insulin, causes blood glucose levels to fall (eat)

• glucogon, blood glucose levels to increase (don’t eat)

gut brain interaction

• know what nutrients they need

• fecal transplant

digestion essay

HUNGRY

• grelin stimulatory to NPY

• causes food intake

FULL

• insulin, leptin, and or CCK

• stimulates CART and inhibits NPY

• feel full

REM sleep

stage of sleep characterized by rapid eye movement

dreaming

memory transfer of info from hippocampus to cortex (dream is brain making sense of it)

circadian rhythms

24 hour cycle of physiological processes that exist for all organisms. generated endogenously and regulated by external cues (sun)

suprachiasmatic nucleus

• rhythms independent of light if optic nerve cut before suprechiasmatic nucleus

• rhythms are light entrained if optic nerve is cut after the SCN

tolerance

• receptor endocytosis (something high, need more receptors

the reward circuit

• ventral tegmental area

• natural reward circuit

• when VTA activated, releases dopamine

• no pleasure (drugs)

• normal state, releases dopamine and makes you want to do something

nicotine

• presynaptic dopaminergic neuron, stimulates nicotine, nicotine agonist for Ach

cocaine

cocaine dopaminergic, dopamine reuptake inhibitor, more dopamine, more wanting

alcohol

• does not increase dopamine

• less addictive

• GABA receptor co-agonist influx Cl-

• alcohol increases inhibition and disinhibition

caffeine

• antagonist for adenosine receptors

• block parasympathetic NS

prove a silent synpase

• stimulate presynaptic neuron at -80mV, there will be no current

• change charge of the cell with voltage clamp

• make charge more positive (+10MV) and see if now the cell will fire an AP.

• positive charge repels the Mg++ block, so if it is truly a silent synapse, the Mg++ will repeal and an AP will fire

• After Mg++ block is repelled, current is outward and the current is positive

unsilence a silent synapse

• you must hold neuron at the perfect positive charge to repel Mg++ blocks while allowing Ca++ to influx into the cell (-10mV)

• stimulate the presynaptic neuron multiple times

• when the Ca++ influxes, it will imitate vesicular exocytosis of AMPAR, which are only ligand gated and do not have Mg++

• then, the neuron will fire APs at any charge like -80mV with the ligand gated AMPAR

• at -80mV, you will see an inward EPSC, which shows you have AMPAR

When there is synaptic plasticity and no new proteins, learning only lasts 24 hours. what are three different ways to get proteins to synapses to ensure LTP?

• proteins are made in cell body and delivered via pathways to the synapse with activity (Fedex)

• proteins already in the synapses, so when activated, proteins are already there (synapse specific capture)

• ribosomes make proteins right at the synapse, translate at activated synapse because mRNA everywhere (local protein synthesis)

LTP in amygdala correlational

• fear conditioning, paired stimuli group and control unpaired stimuli group

• infect with special AMPAR in both groups

• rectified; only inward currents in vesicles

• experimental group: tones and foots shocks, Ca++ comes in and special AMPAR get inserted

• control group: unpaired stimuli, no insertion

LTP in amygdala, causation

• three types of viruses: AMPAR agonists, AMPAR antagonists, and control group

• both groups paired shocks

• one group has c-terminous antagonist of AMPAR, one group gets control

• control group gets scared at sound

• c-terminous group does not get scared at sound

• both groups get influx of Ca++, but antagonist prevents insertion of AMPAR receptors so no LTP

LTP in hippocampus correlation

• mice, dark room, allowed to go to light room. if wants to go back to dark room they get shocked (control no shock)

• stop going to dark room eventually

• put stimtrode in vivo, extracellular

• electrode measures field EPSP

• Na+ goes in, but since recording outside of cell it is a negative charge

• more stimulation, larger fEPSP

• with learning, fEPSP gets bigger, without learning, fEPSP stays the same

LTP in hippocampus causation

saturation; two synapses connected, new firing big change but eventually cna’t add more AMPAR (Max out)

• stimulate experimental group, have less plasticity due to saturation

• control they will have big EPSP change so more plasticity and less saturation

concsious brain waves

big amplitude low freq

unconscious Brain waves

low amplitude high freq

clock gene

genes every cell body has that keeps rhythms

insulin

blood glucose levels down

globulin

increase blood glucose levels

bipolar biology

overactive gq/11 and IP3 signalling

licl inhibits IP3 signalling