Behavioral neuro exam 3

secretory hypothalamus

releases hormones into the bloodstream that can act all over the body and in the brain

part of the diencephalon that sits below the thalamus - collection of many nuclei (sub-regions)

• thermostat of the body, regulates homeostasis

autonomic nervous system

regulated by the hypothalamus and controls the function of internal organs, blood vessels, etc.

homeostasis

keeping the body in a narrow, optimal, physiological range

maintains temperature, blood pressure, salinity, glucose, stress responses, social behavior, feeding, sleep, etc.

zones of the hypothalamus

lateral, medial, and periventricular zones

periventricular mostly release factors to the blood stream

• composed of many interconnected nuclei (branches of neurons)

• connected to the pituitary gland

pituitary gland

extends below the brain where it is held in a delicate bone cradle

anterior and posterior lobes

“mouthpiece” by which the brain speaks to the body and release to the bloodstream

has 2 modes of communication

posterior pituitary

magnocellular (big) neurosecretory cells in the hypothalamus project to here

• release oxytocin and vasopressin in the bloodstream directly

cells reside in the hypothalamus, by is secreted by this

oxytocin

important for social behavior, labor (parturition), and lactation, projected by hypothalamus

vasopressin

anti-duretic hormone (ADH) (prevents water loss), regulates water balance (important in kidney), and also social behavior

anterior pituitary

parvocellular (small) neurosecretory cells in the hypothalamus project here

• an actual gland itself, secretes hormones in response to hypothalamic inputs

anterior pituitary pathway

1. parvocellular neurosecretory cells - transport hormones in axons

2. hypophysiotropic hormones released (from hypothalamus to anterior), hormone transport in blood

3. stimulation or inhibition of anterior pituitary hormone release - hormone transport in blood

4. action on organs of the body

hypophysiotropic hormones

from the hypothalamus, released into hypothalamic-pituitary portal circulation and stimulate or inhibit anterior pituitary hormone secreting cells

follicle-stimulating hormone (FSH)

Gonads

ovulation, spermatogenesis

luteinizing hormone (LH)

gonads

ovarian and sperm maturation

thyroid-stimulating hormone (TSH), thyrotropin

thyroid

thyroxin secretion (increases metabolic rate)

adrenocorticotropic hormone (ACTH), corticotropin

adrenal cortex

cortisol secretion, mobilizes energy stores, inhibits immune system, etc

growth hormone (GH) prolactin

all cells

mammary glands

stimulation of protein synthesis, growth and milk secretion

hypothalamic-pituitary-adrenal (HPA axis)

controls stress responses, cortisol release

negative feedback loops

thermostat-like function allows for maintenance of homeostasis

neurosecretory cells of the hypothalamus are sensitive to the hormones that are secreted in their pathways

• when high levels get too high they can shut off production

acute physical stressors

physical exertion, acute injury, predator-prey interaction, emergency

chronic physical stressors

illness, starvation/obesity, altitude exposure, heat/cold exposure

fight or flight: down regulation, not necessary for stressful moment

decrease in:

• saliva production

• digestion

• filtration

• food movement

• reproduction

fight or flight: upregulation, necessary for stressful moment

increase in:

• attention and vigilance

• pupil dilation

• breathing

• blood pressure and heart rate

• blood sugar and fat concentrations, vessel constriction

• contraction strength (trembling)

HPA axis pathway

1. stressor is perceived

2. hypothalamus releases corticotropin releasing hormone (CRH) in the capillary beds of the hypophyseal portal system

3. anterior pituitary cells secrete adrenocorticotropic hormone (ACTH) in the bloodstream in response to CRH, goes all over body

4. adrenal cortex releases glucocorticoid hormones (GCs) in the systemic blood circulation

5. systemic GCs stimulate metabolism and suppress immune function

6. GCs circulate back into the brain and stimulate GC receptors, providing negative feedback at multiple levels

prednisone

synthetic steroid/form of cortisol - anti-inflammatory (inhibits immune function)

the body thinks that cortisol levels are very high, so it shuts off its secretion

• if this is stopped too quickly, the body can’t turn on cortisol again fast enough → adrenal insufficiency

adrenal insufficiency

caused by the quick removal of prednisone, low blood pressure, abdominal pain, mood/emotional changes

addison’s disease

degeneration of the adrenal gland

leads to fatigue, skin discoloration, stomach pain, weight loss, mood changes

cushing’s disease

anterior pituitary releases too much ACTH (too much cortisol)

rapid weight gain, sleeplessness, memory impairment, immunosuppression, irritability

eustress

optimal amount of stress, focused attention, emotional regulation, rational thinking

distress (too much with low behavioral performance)

impaired memory, burn out, impaired executive functions

too little stress

impaired attention, boredom, confusion, apathy

psychological chronic stressors

personal conflict

acute frustration

financial

grief and loss

care-giving

school and career

causes of chronic stress

cause the negative feedback loop to break down, chronically high levels of cortisol cause atrophy of the dendrites in places like hippocampus that express glucocorticoid receptors, less responsive to feedback.

low-ranking individuals; high

In primates and animals with social hierarchy, ______ experience chronically ____ levels of stress, leading to ulcers, colitis, memory impairments, immunosuppression, atherosclerosis (hardening of blood vessels), etc.

factors that moderate how stressors impact physiology long term

• when they occur in the lifespan

• how severe they are

• whether you have social support

• genetic

• how much control you have over the situation

susceptibility vs. resilience to stress is a balance of all these

control over stressor

can lessen the negative consequences of a stress exposure

activates the pre-frontal cortex and blocks some of the negative outcomes

learned helplessness

uncontrollable stress can lead to ______ phenotype

autonomic nervous system

controlled by periventricular hypothalamus, automatically carried out without conscious control

sympathetic and parasympathetic

cell bodies outside the CNS in autonomic ganglion

before - preganglionic fibers

after - postganglionic fibers

sympathetic nervous system

part of autonomic nervous system, increases heart rate and blood pressure, mobilizes glucose reserves, suppresses digestion, fight or flight

releases norepinephrine

parasympathetic nervous system

part of autonomic nervous system, decreases heart rate and blood pressure, promotes digestion, “rest and digest”

releases acetylcholine

cause of stress on sympathetic nervous system activation

• dilates pupils and inhibits salivation

• relaxes airways

• increases heart rate

• stimulates glucose production and release

• stimulates release of adrenaline

• inhibits digestion

• inhibits voiding of bladder

• stimulates orgasm

parasympathetic nervous system activation

• constrict pupils and stimulates tear production and salivation

• constricts airways

• slows heart rate

• stimulates digestion

• stimulates voiding of bladder

• stimulates erection of genitals

somatic motor system

controls skeletal muscle, cell bodies in the brainstem or ventral spinal cord

motivation

____ is what drives the voluntary mechanisms to return to homeostasis

1. specialized cells in the brain and body detect internal changes in homeostatic factors

2. sensory signals are integrated in neural control centers, usually located in the hypothalamus or brainstem

3. different effector systems produce a response to maintain homeostasis (change in behavior, hypothalamus-pituitary axis, and autonomic nervous system

homeostasis process

1. change in behavior → neural systems in the brain orchestrate a change in animal behavior and a motivation to correct homeostatic deficit

2. hypothalamus-pituitary axis → the hypothalamus causes the release of hormones from the pituitary that affect target organs throughout the body

3. autonomic nervous system → the autonomic NS changes the activity of organs throughout the body

different effector systems produce a response to maintain homeostasis and how

set point

the physiological process where the body maintains internal conditions (like temperature, pH, or glucose levels) within a narrow, optimal range around a specific target value

prandial state, postabsorpative state

2 states of energy balance in the body

prandial state

state of energy balance in the body, right after we eat a meal, the blood is filled with nutrients.

• energy is stored in glycogen and triglycerides

• anabolism

glycogen

actively using after eating, prandial state, short term and finite

liver and skeletal muscle

triglycerides

in prandial state, long term in adipose (fat) tissue

virtually unlimited

anabolism

prandial state, the assembly of these macromolecules (glycogen + triglycerides) from simple precursors (storing for later use)

• intestines (full) → absorbed nutrients → (immediate) glucose → neurons & all cells, fatty acids→ all cells, ketones → all cells, glycogen → liver and skeletal muscle, triglycerides → fat tissue

postabsorptive state

state of energy balance in the body with energy for cellular metabolism

catabolism

the breakdown of these macromolecules for use

in postabsorptive state

• intestines (empty)

• Adipose fat tissue & liver and glycogen → triglycerides → fatty acids, glucose (neurons), ketones → all cells

1. the size of energy reserves

2. their rate of replenishment

energy balance requires mechanisms to regulate feeding behavior depending on:

lipostatic hypothesis

gordon kennedy (1953), that the brain monitors the amount of body fat and works to protect this energy store

leptin

released from adipocytes and regulates feeding by acting on the neurons in the hypothalamus to decrease feeding and increase energy expenditure

• gene that must encode for something that tells the brain that fat reserves are normal/adequate, if not, they just store more fat

ob gene

• effective for weight loos only in __ deficient individuals

anorexia

lesions of lateral hypothalamus

overeating

lesions of ventromedial hypothalamus

ventromedial hypothalamus, lateral hypothalamus

hunger and satiety centers in the hypothalamus

• too simplistic, more about the precise where and when and what of hormone signaling

1. arcuate nucleus

2. paraventricular nucleus

3. lateral hypothalamic area

3 important nuclei for the control of feeding

1. high circulating leptin activates leptin receptors on neurons in the arcuate nucleus. (these neurons make alphaMSH/CART)

2. few things happen:

   1. these neurons project to the paraventricular nucleus, stimulate ACTH and thyrotropin release from the anterior pituitary gland.

   2. activate sympathetic ANS to increase metabolic rate

   3. project to the lateral hypothalamic area to inhibit feeding

process when leptin levels are too high (after eating a lot)

1. low/falling circulating leptin activates leptin receptors on neurons in the arcuate nucleus, making NPY (neuropeptide Y)/AgRP

2. few things

   1. inhibit ACTH and Thyrotropin release from the anterior pituitary to decrease metabolism

   2. activate parasympathetic ANS to decrease metabolic rate

   3. project to the lateral hypothalamic area to stimulate feeding

process when leptin levels are too low (diet)

NPY/AgRP

orexigenic peptides - ‘appetite’

melanin-concentrating hormone (MCH) neurons in the lateral hypothalamus

has widespread connections throughout the cortex and limbic system and can therefore mediate movement and action towards feeding

rise in the brain as leptin levels fall

prolongs food consumption

orexin neurons in the lateral hypothalamus, also called hypocretin - wakefulness

has widespread connections throughout the cortex and limbic system and can therefore mediate movement and action towards feeding

rise in the brain as leptin levels fall

may promote meal initiation

ghrelin, gastric distension, cholecystokinin, insulin

short term regulation of feeding behavior: feeling full and hungry

ghrelin

short term regulation (throughout the day), the main hunger signal, released by the stomach into the bloodstream when the stomach is empty

activates NPY/AgRP neurons in the arcuate nucleus

Gastric distension

short term regulation, fullness signal, mechanoreceptors sends signals to the nucleus of the solitary tract (ANS control) via the vagus nerve

cholecystokinin

short term regulation, fullness signal, released by the intestine when fatty foods are consumed via the vagus nerve

insulin

short term regulation, a critical regulator of blood sugar, can also act directly on the hypothalamus to regulate feeding

released by beta cells in the pancreas, required for the transport of glucose from the blood to other cells of the body

blood glucose is tightly regulated by it

highest after we have eaten and glucose reaches our blood stream

serves as satiety signal by directly interacting with arcuate neurons

high blood glucose

low insulin

low blood glucose

high insulin

type 1 diabetes

genetic autoimmune disease where the immune system kills beta cells in the pancreas

• leads to high blood glucose/inability to use glucose

• treated with insulin injections

can cause blood sugar to plummet, causing insulin shock, delirium, dizziness, tremors, loss of consciousness since the brain uses so much sugar

too much insulin in type 1 diabetes

type 2 diabetes

acquired insulin resistance, cells stop responding efficiently to insulin, also leading to high blood sugar

1. because it tastes good, pleasurable, hedonic experience (liking)

2. because we are hungry, drive reduction, satisfies a craving (wanting)

*research suggests separate circuits in the brain for each one

2 reasons we eat