PSYC110 - Brain & Behavior (EXAM 2)

Endogenous Rhythm

The body generates its own rhythms (will happen even in a constant environment)

• predict that something is going to change/prepare for it

• e.g., temp, light, food availability

• Too late if the animal has to change AFTER the environment changes

How do we know Circadian Rhythm is Endogenous?

Functions on an internal clock

• persistent in constant conditions

• SCN fires in a rhythmic 24-hour pattern

  • Without it, this rhythm doesn’t happen

Suprachiastmatic Nucleus (SCN) Function

• in the hypothalamus

  • The activity (AP) level in the SCN varies on ~24 h cyle; fire for 12 hrs, stop for 12 hrs

• In diurnal animals (like humans) - high SCN activity during day

  • Low SCN activity during night

•  necessary (causality) for generating circadian rhythm (activity)

• JUST the SCN is sufficient in keeping/changing a rhythm

• SCN adjusts faster than other bodily tissues like liver. Glucose production can be affected longer

Changes in the Expression of Timeless, Period, and Clock proteins and how they Correlate with SCN Firing patterns

Rhythm Genes

• 3 major proteins in SCN neurons; they change during the day and adjust AP firing

  • Names: Period, Timeless, and Clock

    • P and T increase during the day

    • C drives T and P levels up. When they reach a sufficient level, they turn off C.

      • This is called negative feedback regulation

        • Low C (morning) = wake

        • High C (night) = sleep; low SCN firing

      • High C levels are correlated with reduced SCN AP

      • Light sensitive -

        • Pulse of light during sleep can inhibit T and decrease C

      • Main Function of C: Turn off/regulate T and P

Suprachiasmatic Nucleus (SCN) Inputs & Outputs

Environmental (Temp, Light, Food availability) & internal signals (e.g., circadian, circannual (hibernation/migration)) (inputs)

Coordinates daily physiological and behavioral rhythms (sleepy? energy?)(outputs)

How can the EEG monitor brain activity during sleep?

• Electrodes allow researchers to measure electrophysiological activity from the brain and muscles in the face and around the eyes

• When neurons are synchronized (all neurons firing at same time) amplitude of EEG is larger 

• When neurons are de-synchronized, amplitude is lower but EEG has higher frequency

Sleep Stages

• Awake: low amp high freq

• Alpha activity – smooth 8-12 hz (relaxed)

• Beta activity – irregular 13-20 Hz

• Stage 1 (not asleep, tired thinking about sleep)

  • Theta activity 3.5-7.5 Hz activity

• Stage 2 (going to lay down, starting to go into sleep)

  • Sleep spindle – short bursts of 12-14 Hz 

  • K complex – sudden sharp waveforms

• STage 3

  • Delta activity - less than 4 hz 

• Stage 4 mostly occurs during early sleep

  • Delta activity – more than 05%

• REM

  • Theta activity

  • Beta activity

Main Distinction between when you’re awake vs. when ur asleep in deep stage 4: awake = desycnhronized; asleep, deep sleep = synchronized

Arousal Sleep (NT & Flip Flop Circuit)

Ach, Serotonin (5-HT), Norepinephrine (NE), Orexin/Hypocretin, Histamine

• Flip-flop circuit

  • Only one state is active at any given time

  • One inhibits the other

• NE, 5-HT, and Histamine inhibit vlPO; arousal-promoting

• Orexin/Hypocretin stabilizes wake/arousal state to prevent the switch from flipping inappropriately (dysfunction here = narcolepsy)

Acetylcholine Regions

Regions: basal forebrain and pons

Function: contains cholinergic and GABAergic neurons that promote cortical activation and wakefulness (or REM)

Serotonin Region

• raphe nuclei

• Function: cluster of nuclei in brainstem responsible for producing serotonin = wakefulness; modulates sensory reactivity

Norepinephrine Region

Locus Coeruleus

Function: brainstem nucleus that’s the primary source of norepinephrine = overall alertness and physiological arousal

Orexin/Hypocretin Region

• lateral hypothalamus

• Degeneration in orexinergic neuron cause narcolepsy (orexinergic neurons wake on button)

Function: stabilizes the wake-sleep switch and prevents inappropriate transitions into sleep

Histamine Region

• tuberomammillary nucleus (in hypothalamus)

Function: drive cortical arousal and wakefulness

Drugs & Sleep

• Antidepressant drugs like SSRI (selective serotonin reuptake inhibitor) can cause insomnia

• Amphetamine (NE agonist) used to treat ADHD and narcolepsy, promoting arousal/sleeplessness

• Antihistamine drugs cause drowsiness

Adenosine and Sleep/Wake Transition

• Increased ATP breakdown = increased adenosine [DAYTIME]

• Adenosine as a NT  activates neurons in vlPOA

• Increased vlPOA activity = increased inhibition in arousal areas [SLEEPY]

What is vlPO?

Ventrolateral Preoptic Nucleus

in anterior hypothalamus

acts as a primary sleep-promoting center

sends inhib signals to wakefulness centers

REM: Paradoxical Sleep

Person is sleeping but the brain activity looks like they’re awake, but they’re sleeping

REM, non-REM and Synchronization

REM is highly desynchronized, non-REM (stages 3 & 4) is highly synchronized

Caffeine and Sleep

• Blocks Adenosine actions 

  • VlPOA is not activated, arousal is dominated

Possible Circadian Factors

• Biological clock (Suprachiasmatic Nucleus in the hypothalamus) connects indirectly with vlPOA

  • Excites orexin neurons and inhibits vlPOA

• Other factors (motivations):

  • Orexin neurons and motivation to stay awake (food seeking)

Sleep & Memory

• Declarative and non-declarative memories

• REM required for procedural memory (e.g., riding a bike)

• SWS required for declarative (e.g., memorizing facts)

  • Nap with SWS improved with declarative learning

Oscillations

produced by the SCN because its neurons run on an internal, self-sustaining molecular feedback loop linked to rhythmic electrical and chemical activity that roughly spans a 24-hour cycle

Homeostasis

Process by which the body’s substances and characteristics are maintained at their optimal level

System Variable

Variable controlled by a regulatory mechanism

Set Point

• Optimal value of the system variable in a regulatory mechanism

Detector

• Mechanism tha signals when the system variable deviates from the set point

Correctional Mechanism

Mechanism that is capable of changing the value of the system variable

Negative Feedback

effect ends itself

Process whereby the effect produced by an action serves to diminish or terminate that action

Example of Negative Feedback Regulation

• Thermostat (detector)

• Temp. setting (set point)

• Air temp (system variable)

• Electric Heater (correctional mechanism)

• Heat (negative feedback)

• Temp. going up is an effect; action is heating up room, if the room reaches a warm enough temperature, the electric heater will turn off.

Intracellular & Extracellular Fluid

• Intracellular Fluid: fluid contained within cells

• Extracellular Fluid: all body fluids outside cells

Intravascular Fluid

• : fluid found within blood vessels

Interstitial Fluid

• fluid that bathes the cells, filling the space between cells of the body

Solute Concentration

• If Solution A is hypertonic to Solution B; water is drawn out of solution B

• If Solution C is hypotonic to solution B; water is drawn into solution B

• Water goes from more dilute solution to a more concentrated solution

Osmometric thirst (Osmotic)

• Thirst produced  by an increase in the osmotic pressure of the interstitial fluid relative to the intracellular fluid

  • In other words: a lot of salt in the fluid outside cell body

• Osmoreceptor

• Example:

  • Eating a lot of chips/working out heavily

  • Salt accumulation in fluids around the cells (interstitial fluid)

Osmoreceptors

• – neuron that detects changes in the solute concentration of the interstitial fluid that surrounds it

• Stretch receptor; when it shrinks it fires action potentials

• As salt concentration of the interstitial fluid increases (decrease), water leaves (enters) the cell and the cell decreases (increases) in volume. Change in cell volume triggers a change in firing rate, which signals thirst or satiety

Osmometric Thirst: water Loss Thru Evaporation

1. Water is lost thru evaporation

2. Concentration of interstitial fluid increases

3. Capillaries lose water by osmosis

4. Cells lose water by osmosis

Circumventricular Organs

• Specialized regions of the brain with rich blood supply 

  • OVLT (organum vasculosum of the lamina terminalis) – lacks a blood-brain barrier. MOST osmoreceptors are located here

  • SFO – SOME osmoreceptors here

• Damage here = Adipsia (lack of thirst = lack of drinking water)

Hormonal Control of Water Balance (Vasopressin)

Vasopressin is a hormone

released by: posterior pituitary

function: raises blood pressure by constricting blood vessels

why: helps compensate for decreased water volume

Antidiuretic hormone: it enables the kidneys to reabsorb water and excrete highly concentrated urine

Inhibited by alcohol

Volumetric Thirst

THirst produced by hypovolemia

• (reduction in the volume of intravascular fluid – loss of blood, vomiting, diarrhea

• Interactions between the kidney and the brain

• Hypovolemia —> Reduced flow of blood to kidneys —> kidneys secrete Renin —> Angiotensinogen —> Angiotensin I —> Angiotensin II —> Retention of sodium; Retention of water; Increase in blood pressure; Salt appetite; Drinking

Renin: Makes new Angiotensin II (coverting angiotensinogen)

Angiotensin I: a hormone that controls blood pressure

Angiotensin II: increases blood pressure & retains water

Feast or Famine Hypothesis

• Need:

  • Building blocks and fuel

    • Carbohydrates, fats, amino acids, vitamins and minerals

• Need to balance:

  • Food availability, metabolism, body weight and nutrition

• Body needs to store nutrients for use when animal is not filling stomach:

  • So need regulations for food storage

    • Short term (carbs)

    • Long term (fat)

Blood Chemical Control of Eating

• Glucose, insulin, and glucagon levels

1. Most digested food enters the bloodstream as glucose, an important source of energy for the body and nearly the only fuel used by the brain

2. When glucose levels are high, liver cells convert some of the excess into glycogen and fat cells convert it into fat

3. When low, liver converts glycogen back into glucose

4. Insulin levels rise as someone is getting ready for a meal and after a meal

5. High levels of insulin generated during a meal generally decrease appetite

Insulin and Glucagon Feedback

• Glucose (simple sugar) –(insulin)--> Glycogen (complex, insoluble carbohydrate)(animal starch, stores in liver and muscles)

• Reverse: Glucose (Simple sugar) ←Glucagon (pancreatic hormones) – Glycogen (complex, insoluble carbohydrate)(animal starch, stores in liver and muscles)

3 Mechanisms of Stomach Control of Eating

• Mechanism 1:

  • Distension is sensed by stretch receptors

  • Sent as signal to the brain by vagus nerve

  • Satiety (stop eating, slow down eating)

• Mechanism 2:

  • Release of hormone by cells in stomach CCK (cholecsytokinin)

  • Closes muscle between stomach and duodenum

  • Reduces gastric emptying and stomach distends faster

• Mechanism 3

  • Ghrelin secretion – stimulates hunger (Ghrelin levels increase before a meal)

  • Constant high ghrelin levels cause Prade-Willi syndrome (constant eating - obesity)

  • Ghrelin from stomach and digestive track signals the hypothalamus

  • Stimulates hunger/feeding

REM vs. SWS Sleep Disorders

• REM sleep disorders – damage in mechanisms that produce paralysis

• Slow wave sleep disorders (e.g., sleep walking)

What is Cataplexy?

(featured in narcolepsy) sudden muscular paralysis while conscious (about a minute)

SFO Function

contains neurons that detect the presence of angiotensin in the blood and excite neural circuits initiating drinking

MPON

OVLT & SFO and nucleus of solitary tract conect to MPON

output: drives drinking behavior

What starst a meal: Metabolic Signals

• Glucoprivation – dramatic fall in the level of glucose available to cells

• Lipoprivation – dramatic fall in the level of fatty acids available to cells

• Role of the Liver: liver has sensory neurons that sense decreased glucose and send message to brain via the vagus nerve

What are Nutrient Receptors?

• Receptors for glucose and lipids are located in the liver, and convey signals about gluco- and lipoprivation to the brain thru the vagus nerve

LT Satiety: Signals from Adipose Tissue

• Leptin – hormone secreted by adipose tissue that may be involved in long-term satiety (LEptos = THIN)

• More fat = more leptin

• Low levels of leptin increase hunger

Brain-Control: Role of the Hypothalamus

• Hunger motivation center

• The lateral hypothalamus regulates hunger,

• while the arcuate nucleus controls how the LH responds

• Destruction of LH: no hunger or eating until death

• Activity of LH promotes eating and satiety

Feeding Circuits in the Brain MPY & OREXIN

• LH has 2 types of neurons

  • MCH

  • Orexin – regulates feeding

  • Activating these neurons = widespread excitation in brain

    • Motivation for food seeking; hunger

Brain Regions involved in Causing Hunger - AN & VN

• Arcuate nucleus

  • NPY/AGRP neurons: provide excitatory signaling to LH

  • Positive controllers of feeding behaviors (cause hunger)

• When vagus nerve is activated = activation of NPY in ventrolateral medulla

  • NPY: glucose-sensitive neurons in medulla

Brain Regions involved in Satiety

• NPY neurons are excited = hunger

• NPY neurons are inhibited (reduces hunger) and CART neurons are excited

• = Satiety

• Leptin can inhibit NPy and activate CART 

Genetic Sex

• Determined at fertilization

• Produces 50% chance of any pregnancy being male or female

• Depends on: whether the sperm cell that fertilizes the ovum carries an X or Y chromosome

Order of Sex Organ Development

• 3 general categories of sx organs

  • Gonads (testes and ovaries)

  • Internal Sex Organs

  • External Sex Organs

Gonad Development & SRY

• Up to 6 weeks of prenatal development gonads are undifferentiated. Can become ovaries or testes

• Sry gene - sex-determining region of the Y chromosome

  • If SRY protein is present – testes develop

  • If SRY protein is absent – ovaries develop

• Once gonads develop, they begin to release hormones

  • Organizational – develop internal/external sex organs and brain development

  • Activational – later in life – activate certain processes (e.g., mating, aggression)

Internal Sex Organs Development

• Early in development, internal sex organs are bisexual (both male and female precursors are present)

• Mullerian (Internal Female Organ) System – embryonic precursors of the female internal sex organs (develops into fimbria, fallopian tubes, uterus, inside of vagina)

• Wolffian System (Internal Male Organ) – embryonic precursors of the male internal sex organs (develops into epididymis, vas deferens, seminal vesicles; these make & transport sperm)

What is the Default Sex?

 female (no hormones needed – “nature’s impulse is to create female”)

If testes present & secretes 2 types of hormones – then male

• Anti-Mullerian Hormone – peptide secreted by fetal testes that inhibits the Mullerian system Defeminizing Hormone

• Androgens (Masculinizing hormones) – promotes development of Wolffian system

  • Testerone

  • Dihydrotestosterone – androgen derived from testosterone

Genetic Disorders — Androgen Insensitivity Syndrome

 indicate how ‘sex’ and ‘gender’ are not so easily defined…

1. Androgen insensitivity syndrome (XY male, with testes, but female external, develop female’s body at puberty, but cannot become pregnant)

Genetic Disorders — Persistent Mullerian Duct Syndrome

 indicate how ‘sex’ and ‘gender’ are not so easily defined…

1. Persistent Mullerian duct syndrome (XY male, androgens masculinize, but no defeminization, both types of internal sex organs present)

Genetic Disorders — Turner’s Syndrome

 indicate how ‘sex’ and ‘gender’ are not so easily defined…

1. Turner’s syndrome (only one sex chromosome, usually XO) – no gonads at all – but female sex organs – no hormones needed to develop as female

External Sex Organs develop along with the Internal

• Male development occurs due to dihydrotestosterone produced by testes (e.g., penis, scrotum)

• Female development does not need any hormone and is default (e.g., vagina, clitoris) – this is why Turner’s develop female external, but no ovaries…

Organizational vs. Activational Effects

• Organizational Effects – hormonal effects on tissue differentiation and development

  • Ex. Anti-Mullerian hormone and effect on defeminizing

• Activational Effects – effect of a hormone that occurs in the fully developed organism

  • Ex. Progesterone effect on maintaining uterine lining

Onset of Puberty (HPG)

• Hypothalamus Pituitary Gonadal Axis

  • Hypo controls pit which controls gonads, which makes a feedback loop to control hypo

Onset of Puberty (GnRH)

• Gonadotropin-Releasing Hormones (GnRH) – released from the Hypothalamus and stimulate the production and release of 2 gonadotropic hormones by the anterior pituitary gland

  • Follicle-Stimulating Hormone (FSH)

  • LuteinizingHormone (LH)

• GnRH release is regulated by Kisspeptin from the arcuate nucleus

______/______ cause secondary sexual characters to mature

Estradiol/testerone