psyc 306 - exam 2

homeostasis (single-point tuning)

set points are constant

allostasis (multi-point tuning)

set points vary on multiple factors (like environment, activity, etc.)

mechanisms that allow us to produce heat

increased metabolic rate, shivering

mechanisms that allow us to conserve heat

vasoconstriction, huddling

mechanisms that allow us to lose heat

vasodilation, panting, sweating, splaying

fever vs hyperpyrexia

fever: 99-103 degrees F; heat is internally generated

hyperpyrexia: higher than 104 degrees F

where do temperature signals go to in the brain?

preoptic area of the hypothalamus (POA); receives temperature information from free nervse endings in skin, spinal cord, mucous membranes

when we are too hot…

sweat glands activated, blood vessels close to body surface dilate, seek shade

when we are too cold…

piloerection (hairs on skin stand up to trap air and provide insulation), blood vessels constrict, muscles begin to involuntarily contract (shivering), brown fat cells activated (produce heat), seek shelter (behavior)

regulatory system components

system variable, set point, detector, correctional mechanism

system variable

a variable that is controlled by a regulatory mechanisms (air temperature in a heating system)

set point

the optimal value of the system variable (the temperature to which you set the thermostat)

detector

mechanism that signals when the system variable deviates from its set point (thermostat)

correctional mechanism

the mechanisms that is capable of changing the value of the system variable (heater or air conditioner)

negative feedback system

a process in which the effect produced by the response of the correctional mechanism serves to terminate the activity of the correctional mechanism

• only the system variable is being monitored

• better for system variables that change quickly (temp, BP, hormone concentration)

satiety system

a process that causes cessation of a signal is produced by adequate and available supplies to restore the system variable to the set point

• the activity of the correctional mechanism is being monitored

• better for system variables that change slowly (fluid balance, digestion)

physiological effects of exercise increases/decreases

increases — blood flow (more oxygen and glucose), neutrotrophic factors and synaptic plasticity, immune function, endorphins, analgesia

decreases — depression, anxiety, neurodegeneration, negative impact of stress on brain function (reduces cortisol and cortisol receptors in hippocampus)

physiological effects of exercise

insulin regulation, cortisol reduction, dopamine and serotonin production, BDNF production, endorphin production, increased blood flow

how many minutes of moderate exercise do you need to experience benefits?

150-300 minutes every week (20-40 per day)

how many minutes of intense exercise do you need to experience benefits?

75-150 minutes (10-20 per day)

how does exercise promote brain health? what are the neurochemical factors involved in this process?

what are the four states of water?

gaseous, liquid, solid, liquid chrystalline

what is the renin-angiotensin pathway? what does it do?

• osmotic or hypovolemic thirst causes the posterior pituitary gland to release antidiuretic hormone (ADH)

• ADH causes kidneys to reduce urine output and release renin

• renin converts angiotensonigen into angiotensin II

  • blood vessels constrict

  • adrenal glands release aldosterone (kidneys retain sodium)

where do thirst signals originate in the brain? where do they all converge?

OVLT (organum vasculosum laminae terminalis)

what is tonicity? why does it matter?

refers to the concentration of solute in a given volume of water

• hypertonic = too much solute

• hypotonic = too little solute

• isotonic = concentration of solute is the same in both compartments

osmotic thirst

• signals a decrease in the intracellular fluid

• caused by increased tonicity of the interstitial fluid

  • too many solutes for the level of fluid, water is pulled out of cells to balance the solution

hypovolemic thirst

• signals a decrease in total fluid volume

• caused by a loss of total fluid

  • serious blood loss, vomiting, diarrhea

mechanisms of osmotic thirst

• blood becomes hypertonic

  • eating a salty meal; perspiration or urination

• water leaves cells in an effort to regain the isotonic state

• osmoreceptors in the brain detect cell dehydration

the organum vasculosum of the lamina terminalis (OVLT)

located near the third ventricle; OVLT cells change firing rates in response to their intracellular fluid levels and stimulate posterior pituitary cells to release anti-diuretic hormone (ADH)

mechanisms of hypovolemic thirst

• usually occurs due to loss of interstitual fluid and/or blood; because both water and salt are lost it produces thirst and salt appetite

• drops in blood volume are accompanied by drops in blood pressure

• baroreceptors in the kidneys detect decreased blood flow

• baroreceptors in the heart assess blood pressure

  • send information to the NST via glossopharyngeal and vagus nerves

• if blood pressure is low, thirst is initiated and the kidneys conserve fluid

baroreceptors

located in the atria and vessels of the heart; the atria receive blood from the body passively; they contain stretch receptors which serve to measure the volume of blood

how are the different types of thirst monitored? what are the detectors? where are they located?

once thirst is detected, what happens in the brain? what are the chemical signals involved?

what is the best way to treat each type of thirst?

osmotic thirst: drink water

hypovolemic thirst: drink water + solutes

what is fascia and what does it do?

a water delivery system; allows water to slide along filaments from place to place

how much of our body is water? where is it kept? what are the main fluid compartments?

60%!

• intracellular fluid (67%)

• extracellular fluid (33%)

  • cerebrospinal fluid (<1%)

  • blood (7%)

  • interstitial fluid (26%)

what is osmosis and how does it work?

osmosis is the process by which water will move from a compartment of low solute concentration to a compartment of high solute concentration

• equalize the solute concentrations between the two compartments

what is the function of aldosterone? where is it produced?

signals the kidneys to retain sodium; released by adrenal glands

how do you know if you are dehydrated? what is the most common symptom?

low blood pressure, impaired cell function

metabolism — fasting phase

how can we feed our cells when our gut is empty?

• short-term reservoir

• long-term reservoir

• glucagon (which converts stored glycerol into glucose)

metabolism — absorptive phase

what happens to the food we eat?

• carbohydrates

• proteins

• fats

• insulin (opens glucose transporters in cells; converts excess glucose into glycogen for storage)

short-term reservoir

• located in liver and muscles

• contains glycogen (a complex, insoluble carbohydrate)

• glycogen is synthesized from glucose by insulin

• glycogen is converted back into glucose by glucagon

long-term reservoir

• adipose tissue

• contains triglycerides (a soluble carbohydrate combination of fatty acids and glycerol)

• fatty acids are used by body cells; glycerol is converted to glucose by the liver to feed the brain

why does the brain get all the glucose?

• cells take in glucose through glucose transporters

• in body cells glucose transporters are only open when insulin is bound to them

• glucose transporters in brain cells do not require insulin to open, thus the brain can use glucose in the absence of insulin (during the fasting phase)

carbohydrates

• used for energy

• broken down into glucose

• increase in blood glucose causes pancreas to release insulin

• body cells can use glucose; excess is converted into glycogen by liver

• if short-term reservoir is filled, excess glucose converted to fats

what are the two eating-related pathways in the hypothalamus? what are the specific nuclei involved? what chemical signals do they make?

what nerve connects the brain and the gut/ENS?

vagus nerve

what is the BMI? who invented it?

Adolphe Quetelet; Body Mass Index

what are the macronutrients? what are each of them broken down into?

carbohydrates, fats, protein

where do signals from the nucleus of the solitary tract (NST) go?

hunger signals coming from the liver and brain project to the acruate nucleus; signals then sent out to the lateral hypothalamus (LH)

what happens when we consistently make too much insulin?

type II diabetes

CCK (where is it made? what does it do?)

consumption of fats stimulates the release of CCK from the duodenum

• promotes release of insulin

• contracts gallbladder, releasing bile (to break down fats)

• may be brain NT signaling satiety

• CCK antagonists initiate eating

NPY/AGRP (where is it made? what does it do?)

released by the arcuate nuclease neurons in response to stimulation

• NPY: increases insulin release; infusion in hypothalamus induces ravenous eating

• AGRP: antagonist at MC4 receptors in LH; very potent eating stimulant

MCH/Orexin (where is it made? what does it do?)

AN NPY/AGRP neurons stimulate LH MCH/orexin neurons

• increases in eating behavior

• decreases in metabolic rate

alpha-MSH/CART (where is it made? what does it do?)

high leptin levels stimulate the release of alpha-MSH and CART by the arcuate nucleus

• stimulate the release of TSH and ACTH by the pituitary gland, raising metabolic rates

• sympathetic nervous system activity is initiated

• feeding is inhibited

PYY (where is it made? what does it do?)

satiety signal; indicates amount of macronutrients consumed

how do LPL and HPL govern triglyceride storage in the long-term reservoir? how does insulin effect them?

how does insulin get glucose out of the circulatory system? why is it considered cardioprotective?

where does insulin put glucose? how does it change glucose in order to store it in various places?

why do we sleep and what are the advantages?

beta waves

13-30 Hz; alert, active

alpha waves

8-12 Hz; quiet, restive

what are the phases of sleep?

• awake

• non-REM sleep

  • stage 1, stage 2, stage 3, stage 4

• REM sleep

(be able to describe each phase in terms of EEG, EOG, and EMG

activity, as well as behavioral characterizations)

awake (stages of sleep)

• beta waves, alpha waves

• small, spikes, desynchronous waves

non-REM sleep

• stage 1:

  • theta waves

  • transition between waking and sleeping

• stage 2:

  • theta waves, sleep spindles, K complexes

  • asleep, but will claim was not sleeping if awoken

• stage 3:

  • theta waves

  • delta waves (20-50%)

  • slow-wave sleep (SWS)

• stage 4:

  • delta waves (>50%)

  • SWS

  • if awakened, groggy and confused

REM sleep

• first episode after about 90 minutes

• EEG resembles waking (beta and alpha waves; paradoxical sleep)

• EOG becomes active

• EMG becomes flat (loss of muscle tone)

• increased CBF and O2 consumption

  • high levels of activity in occipital lobe, low levels in frontal lobe

slow-wave sleep

stage 3 and 4; human growth hormone is released

how long does a “complete” sleep cycle take?

90-120 minutes

how do sleep cycles early in the sleep period differ from cycles later in the period?

the first four hours contain more SWS (especially stage 3 and 4); the second four hours contain more REM (REM episodes occur ~90-120 minutes

when do we get most of our REM sleep?

during the second 4 hours of sleep; more prevalent in infancy

when do we get most of our SW sleep?

during the first 4 hours of sleep; around puberty, sleep phase shifts ahead a bit

why is SW sleep important?

• “rests” the brain

• rest and repair the body

• cool the brain

  • brain maintenance! transfer of short-term memory to long-term

why is REM sleep important?

• brain development

• learning

  • memory problems associated with lack of REM sleep

what happens to the sleep periods of adolescents? how do they differ from children and older adults?

• REM sleep is more prevalent in infancy

• around puberty, sleep phase shifts ahead a bit

how does sleep change as we age?

• aging is associated with drops in overall sleep and proportion of SWS.

what determines which part of the sleep circuit is inhibited?

hypocretin

activation of hypocretin neurons would…

kick the circuit into “awake” mode

• send excitatory projections to the areas involved in arousal, which in turn inhibit the VLPA when we are awake

sleep is controlled by which two factors?

time of day; length of time we have spent awake

what part of the brain marks time? how does it do it? how does light affect this process?

the suprachiasmatic nucleus is the body’s “master clock”

• SCN is entrained to the day-night by zeitgebers (“time-givers”; external cues to help set circadian rhythms), light being the most important one

SCN regulates the pineal gland’s secretion of melatonin

• light information reaches the SCN by way of the retinohypothalamic pathway

what chemicals control sleep/arousal?

GABA, adenosine

when the brain is awake, the VPLA is _____ and arousal systems are _____

inhibited; activated

when the brain is asleep, the VPLA is _____ and arousal systems are _____

activated; inhibited

what are the “awake” areas in the brain?

what is the “asleep” area in the brain?

how are the “awake” and “asleep” areas connected to each other? how do they influence each other? how does light affect this relationship?

what is the flip-flop circuit?

activity in the VLPA is associated with sleep; activity in the ACTIVATION areas is associated with wakefulness

• hypocretin is the switch

  • it stimulates activation areas

  • no input from VLPA

  • adenosine inhibits

what is adenosine? where is it made and how does it affect waking/sleeping?

• adenosine inhibits neurons in basal forebrain (reduces arousal)

• adenosine accumulates during waking in the basal forebrain area

  (produced during the metabolism of glycogen; levels build while we are

  awake) and inhibits arousal neurons there

• also stimulates sleep in the preoptic area

what is the most common sleep disorder?

insomnia

what causes narcolepsy?

degeneration of hypocretin neurons produces narcolepsy in humans and animals

• people with narcolepsy don’t have clear boundaries between sleep and waking, probably due to abnormalities in the hypocretin (orexin) system

You normally go to bed at 11pm and wake up at 7am. However, one night you go out with friends and stay up until 2am. But you still need to wake up at 7am to go to work. How will this affect your sleep cycles that night? What problems might you expect the next day? How will this impact your sleep the following night?

how do the gonads develop for an XY individual?

up to the 6th week following conception, makes and females have undifferentiated primordial gonads; at the 6th week, the sex-determining region of the Y chromosome (SRY) gene is expressed in males

• the SRY gene encodes testis-determining factor, turning the primordial gonads into testes

how do the gonads develop for an XX individual?

up to the 6th week following conception, makes and females have undifferentiated primordial gonads; in the absence of testis-determining factor, the primordial gonads develop into ovaries

how do the internal sex organs develop for an XY individual?

the developing embryo contains both precursor systems

• in XY (male) individuals, the Wolffian system must be stimulated to develop

  • if the embryo has testes, testosterone and anti-Mullerian hormones will be secreted

how do the internal sex organs develop for an XX individual?

the developing embryo contains both precursor systems

• in XX (female) individuals, the Mullerian system will develop automatically unless it is supressed

  • if the embryo has ovaries, no hormones will be secreted

  • the Mullerian system will develop without stimulation and the Wolffian system will degenerate if not stimulated

how do the external sex organs develop for an XY individual?

• masculinization of external genitalia requires stimulation by 5-alpha-dihydrotestosterone from the testes

• 5-alpha-dihydrotestosterone results when testosterone is acted on by the enzyme 5-alpha-reductase

how do the external sex organs develop for an XX individual?

the labia majora, labia minora, clitoris, and vaginal orifice do not require hormonal stimulation to develop

what are the genotypes for Klinefelter’s syndrome?

XXY

what are the genotypes for Turner’s syndrome?

XO

what are the genotypes for Jacob’s syndrome?

XYY

what are the prenatal effects of testosterone and estradiol?