Exam One Study Guide

What is characterized by periods of irresistible sleep, cataplexy attacks, sleep paralysis, and hypnagogic hallucinations?

Chapter Nine: Sleep and Biological Rhythms

∙ Narcolepsy – characterized by periods of irresistible sleep, cataplexy attacks, sleep  paralysis, and hypnagogic hallucinations

o True narcolepsy – immune system of the body starts to attack its own  orexin/hypocretin; degenerative disorder

o Caused by gene mutation on chromosome six

o Sleep attacks – primary symptom; irresistible urge to sleep during the day, after  which the person awakens feeling refreshed

▪ Occurs under monotonous, boring conditions; last two to five minutes ▪ Diminished by stimulants such as Ritalin

o Cataplexy – narcoleptic symptom; complete paralysis that occurs during waking ▪ Person will sustain muscle weakness, will be fully conscious for a few  seconds to several minutes

What is the meaning of sleep attacks in narcolepsy?

▪ Caused by massive motor neuron inhibition in spinal cord; continue to  breathe and control eye movements Don't forget about the age old question of How many angels does a square have?

▪ Preceded by strong emotional reactions or sudden physical effort,  

especially if person is caught unaware

o Sleep paralysis – paralysis occurring just before falling asleep

▪ Can be snapped out of it by being touched or hearing someone call their  name; person dreams while lying awake, paralyzed

▪ Hypnagogic hallucinations – vivid dreams occurring just before falling  asleep, accompanied by sleep paralysis

∙ EEG oscillatory activity and sleep stages (characteristics)

o Electromyogram – electrical potential recorded from electrode placed on muscle o Electro-oculogram – from eyes, recorded from electrode on skin around them;  detects eye movement

What is the meaning of cataplexy in narcolepsy?

Don't forget about the age old question of How can species evolve through natural selection?

o EEG electrodes record many neurons at once, reporting sum of activity ▪ If messages are synchronized – appear as large, clear waves

▪ If messages are randomly active (desynchronized) – appear as small,  chaotic waves without a clear pattern If you want to learn more check out What is fundamental attribution error in psychology?

o EEG during wakefulness shows two basic activity patterns

▪ Alpha activity – smooth electrical activity of 8-12 Hz; associated with  relaxation state

▪ Beta activity – irregular electrical activity of 13-30 Hz; associated with  arousal state

∙ Shows desynchrony – reflects the many different neural circuits in  

brain are actively processing info

▪ Beta and gamma waves – cognitive thought, 20-80 Hz

o EEG during three non-REM (NREM) stages and REM stage

▪ Stage 1 – alpha waves 8-12 Hz, seen when relaxed with eyes closed;  

hypnic jerks (muscle contractions followed by relaxation)

▪ Stage 2 – EEG is irregular, but shows theta activity

∙ Theta activity – 3.5-7.5 Hz, during early stages of SWS and REM  

sleep

o Indicates neuron firing in neocortex is becoming more  Don't forget about the age old question of What is the meaning of knowledge in intimacy?

synchronized; transition between sleep and wakefulness

o Eyes slowly open and close, eye roll up/down

∙ Sleep spindles – short wave bursts of 12-14 Hz that occur two and  Don't forget about the age old question of What are the factors that determine the quality of microscopy?

five tunes per minute during stages 1 through 3

o Consolidation of memories

∙ K complexes – sudden, sharp waveforms found only in this stage

o Spontaneously occur, but can be triggered by noises

▪ Stage 3 – AKA slow-wave sleep (SWS); regular synchronous electrical  activity of less than 4 Hz (high amplitude, low frequency)

∙ Deepest sleep stage – only loud noises will cause person to  

awaken; when awakened, person acts groggy and confused

∙ Minimal eye movements

▪ REM sleep – desynchronized EEG activity; AKA paradoxical sleep  because the waves look like “awake” sleep We also discuss several other topics like What is the content of presidential reconstruction?

∙ Not resting during REM, brain is very active – dreaming, muscular  paralysis occurs (inhibition of spinal cord motor neurons)

∙ Person may not react to loud noises, but aroused by meaningful  

stimuli; when awakened, appears alert and attentive

∙ Eye movements are in response to visual images that are  

experienced during dreaming

∙ Blood flow and brain activity sleep stages

o Blood flow increases in REM in extrastriate cortex (visual association cortex) ▪ Increased activity reflects visual hallucinations occurring during dreams o Blood flow decreases (REM) striate (1º) visual cortex and prefrontal cortex ▪ Prefrontal cortex reflects lack of organization and planning in dreams ▪ Lack of activity that eyes aren’t receiving visual input

o SWS – decrease in blood flow in cerebral area, thalamus, and cerebellum o Lucid dreaming – realizing you’re dreaming, not actually awake

o Particular brain mechanisms that become active during a dream are those that  would become active if events in dream were actually occurring

∙ Sleep apnea – cessation of breathing while sleeping; inability to sleep and breathe  simultaneously

o During period of sleep apnea, CO2 levels in blood stimulate chemoreceptors and  the person wakes up gasping for air

▪ O2 levels of blood then return to normal, the person falls asleep and the  cycle then restarts

o People feel sleepy and groggy during the day because sleep is disrupted o Many cases are caused by airway obstruction that can be surgically corrected or  relieved by device that continuous positive airway pressure (CPAP)

o Patients often snore and are overweight

∙ REM sleep behavior disorder – patients don’t demonstrate paralysis associated with REM  sleep and, as a result, act out their dreams

o Neurodegenerative disorder with some genetic component; damage to brain stem o alpha-synucleinopathy – involves inclusion of alpha-synuclein protein in  degenerating neurons

o Symptoms are opposite of cataplexy – fail to exhibit paralysis during REM;  treated by clonazepam

∙ Insomnia (sleep deprivation in humans)

o Primary insomnia – characterized as difficulty falling asleep after going to bed or  after awakening during the night

o Secondary insomnia – inability to sleep due to another mental or physical  condition such as pain, substance abuse, or psychological/neural condition o Treatment – pharmacological vs. nonpharmacological

▪ Pharmacological – hypnotic drugs; Ambien and Sonata are agonists at the  GABAα receptor, benzodiazepines, OTC antihistamines

∙ Produce side effects such as sleepiness/difficulty concentrating the  following day

∙ Chronic use of sleep-promoting drugs can lead to tolerance and re

bound insomnia when use is ended

▪ Nonpharmacological – cognitive behavior therapy, progressive relaxation  techniques, changes in sleep hygiene (maintain consistent sleep schedule;  keeping bedrooms dark, quiet, cool)

o Sleep deprivation affects cognitive abilities – causes hallucinations/perceptual  distortion, difficulty with concentration, affects learning and memory

▪ Does not affect body function, ability to exercise, or physiological stress  response

∙ Functions of Sleep/Relationship between cognitive activity during wakefulness and sleep o Function – give body rest, but is not the primary function; necessary for survival o SWS and REM are more important than other stages; brain needs to rest  periodically to recover from adverse side effects of its waking activity

▪ Adenosine (NT) builds up while awake

▪ Among the waste products produced by high metabolic rate associated  with waking activity of brain are free radicals – chemicals that contain one  unpaired electron, are highly reactive oxidizing agents that bind with  

electron from other molecules and damage the cells they’re found in

▪ During SWS, the decrease in metabolic rate permits restorative  

mechanisms in cells to destroy free radicals and prevent damaging effects o Brain may need SWS to recover from day’s physical activities

▪ Any activity that requires cortical arousal (focusing, paying attention,  thinking, planning) increases glucose metabolism in the frontal lobe

▪ SWS activity increases in frontal lobe; SWS seems to be increased in brain  regions that were most active during wakefulness

o REM deprivation results in the rebound phenomenon

▪ Instead of progressively going into REM (stages one to three), you go  straight into REM as soon as you fall asleep

o Sleep aids in consolidation of long-term memories

▪ Declarative (explicit) memory – includes those that people can talk about;  relationships between stimuli/events

∙ SWS facilitates consolidation of declarative memories – brain  

rehearses newly learned info during SWS

▪ Non-declarative (implicit) memory – gained through experience and  practice that doesn’t necessarily involve an attempt to memorize info

∙ REM facilitates consolidation of non-declarative memory

∙ Fatal familial insomnia – characterized by progressive insomnia; results in damage to  thalamus (responsible for sensory information, involved in biological rhythms, endocrine  system control)

o Symptoms – attention/memory deficit followed by dreamlike confused state, loss  of control over autonomic NS and endocrine system, increased body temperature,  insomnia

o First signs – decrease in sleep spindles and K complexes

o As it progresses, SWS disappears completely and only brief periods of REM  (without paralysis) remain

∙ Sleep is controlled by chemicals produced in brain

o Adenosine – neuromodulator released by neurons engaging in high levels of  metabolic activity; play 1º role in sleep initiation

o Astrocytes maintain small nutrient stock of glycogen – in times of increased brain  activity, glycogen is converted into fuel for neurons; thus, prolonged wakefulness  causes a decrease in glycogen in the brain, which then causes an increase in  extracellular adenosine, which has an inhibitory effect on neural activity

▪ Adenosine accumulation serves as sleep-promoting substance – during  SWS, neurons rest and astrocytes renew glycogen stock

o Body produces sleep-promoting substance (adenosine) that accumulates during  wakefulness and is destroyed during sleep; the longer someone is awake, the  longer she has to sleep to deactivate this substance

o If wakefulness is prolonged, even more adenosine accumulates, which inhibits  neural activity and produces cognitive/emotional effects that are seen during sleep  deprivation

∙ Neurotransmitters associated with sleep and waking

o ACh – two groups of ACh neurons (one in pons and one in basal forebrain)  produce activation and cortical desynchrony when stimulated; the third group (in  medial septum) controls hippocampus activity

▪ ACh agonists increase EEG signs of cortical arousal and ACh antagonists  decrease them; ACh levels increase in the hippocampus and neocortex  during waking and REM sleep, but low during SWS

o NE – catecholamine agonists that produces arousal and sleeplessness, which are  mediated by noradrenergic system of the locus coeruleus (LC) – dark-colored  group of somas located in pons, involved in arousal and vigilance

▪ LC neurons give rise to axons that release NE (from axonal varicosities)  throughout neocortex, hippocampus, thalamus, cerebellar cortex, pons,  medulla

o 5-HT – found in raphe nuclei, in which axons project to thalamus, hypothalamus,  basal ganglia, hippocampus, and neocortex

▪ Raphe nuclei stimulation causes locomotion and cortical arousal

o Histamine – NT synthesized from the AA histidine; somas are located in  tuberomammillary nucleus (TMN)

▪ TMN axons project to cerebral cortex, thalamus, BG, basal forebrain,  hypothalamus

∙ Projections to cerebral cortex directly increase cortical arousal

∙ Projections to ACh neurons in basal forebrain do so indirectly by  

increasing ACh release in cerebral cortex

o Orexin – peptide NT; somas that secrete orexin are located in the lateral  hypothalamus; axons project to all regions involved in wakefulness/arousal ▪ Orexinergic neurons are the stabilizing force, pushing the circuit toward  arousal (circuit controls sleep and arousal)

▪ Narcolepsy – caused by degeneration of Orexinergic neurons

Chemical

Brain region  

containing  

somas

Waking  

levels

SWS levels

REM levels

Adenosine

--

Increase  

with longer  periods of  

wake

Decreasing

Decreasing

ACh

Pons, basal  

forebrain,  

medial septum

High

Low

High

NE

Locus coeruleus

High

Low

Low

5-HT

Raphe nuclei

High

Low  

(decreasing)

Low

Histamine

TMN

High

Low

Low

Orexin

Lateral  

hypothalamus

High

Low

Low

∙ Brain regions associated with sleep and pathways for sleep and waking o Preoptic area (POA) – most involved in sleep control; contains neurons whose  axons form inhibitory synaptic connections with the brain’s arousal neurons ▪ When preoptic (sleep) neurons – become active, they suppress the activity  of our arousal neurons and we fall asleep

▪ Majority of sleep neurons located in ventrolateral preoptic area (vlPOA) – GABAergic neurons group whose activity suppresses alertness and  

behavioral arousal, and promotes sleep

∙ Damage suppresses sleep; activity of these neurons then increases  during sleep

▪ Sleep neurons secrete inhibitory GABA and send axons to the five brains  regions involved in arousal, which causes cortical activation and  

behavioral arousal; inhibition is necessary for sleep

o Flip-Flop (FF) circuits for sleep/wake (S/W) transitions

▪ Sleep neurons in POA receive inhibitory inputs from some of the same  regions they inhibit (TMN, raphe nuclei, LC); thus, they’re inhibitory by  histamine, 5-HT, and NE

▪ Mutual inhibition provides bases for establishing periods of S/W; it’s  impossible for neurons in both regions to be active at the same time

▪ Reciprocal inhibition characterizes an electronic circuit known as flip-flop  – can assume one of the two states referred to as on/off

∙ Either the sleep neurons are active and inhibit the wakefulness  

neurons or the wakefulness neurons are active and inhibit sleep  

neurons

▪ FF switches from one state to another quickly (stable)

∙ Orexinergic neurons help stabilize S/W FF through their excitatory  

connections to wakefulness neurons

∙ Active orexinergic neurons tips FF activity toward waking state,  

which promotes wakefulness and inhibits sleep

∙ Orexinergic neurons receive inhibitory input from vlPOA, which  

means that sleep signals that arise from adenosine accumulation  

can eventually overcome excitatory input to orexinergic neurons,  

sleep can occur

▪ FF are unstable – have difficulty remaining awake when nothing  

interesting is happening and they have trouble remaining asleep for an  

extended amount of time; people with narcolepsy exhibit this

∙ FF circuits for transition to REM

o S/W FF determines when we wake/sleep; once we fall asleep, REM FF controls  cycles of REM and SWS

o Dorsal pons region contain REM-on neurons that fire at high rate only during  REM; ventrolateral periaqueductal gray matter (vlPAG) contains REM-off  neurons that suppress REM

o On and off regions are interconnected by inhibitory GABAergic neurons o On stimulation with infusions of glutamate agonists elicits most of the REM sleep  elements; inhibition of this region disrupts REM  

o Off stimulation suppresses REM, whereas damage to this region increases REM o Mutual inhibition – only one region can be active at any given time

o During waking, REM-off receives excitatory input from orexinergic neurons of  lateral hypothalamus, which tips REM FF into off state

o When FF switches into sleep phase, SWS begins; excitatory input to REM-off  region begins to decrease

o Once sleep begins, orexinergic neuron activity ceases, which removes one source  of excitatory input to REM-off region

∙ Suprachiasmatic nucleus (SCN) – neural pathways controlling REM

o SCN located in hypothalamus; controls S/W

o Efferent axons of SCN terminate in supraventricular zone (SPZ)

o SPZ projects to dorsomedial nucleus of hypothalamus (DMH), which projects to  other regions, including vlPOA and the orexinergic neurons of the lateral  hypothalamus;  

▪ Projections to vlPOA are inhibitory, in which they inhibit sleep

▪ Project to lateral hypothalamus are excitatory promoting wakefulness

Chapter Ten: Reproductive Behavior

∙ Sexually dimorphic behaviors include courting, mating, parental and aggressive behavior ∙ Sex refers to the genetic or physiological characteristics of males/females ∙ All cells, except sperm/ova, contain 23 chromosome pair, which contains gene info

∙ Gamete production entails meiosis, which produces cells that contain one set  chromosome pairs

∙ Genetic sex determined by presence of XX (female) or XY (male) chromosomes;  determined at time of fertilization of ovum by the father’s sperm

∙ Exposure to sex hormones, both before and after birth, is responsible for sexual  dimorphism; Y chromosome controls development of male sex hormone glands ∙ Gonads (ovary/testis) are the first to develop

o They have a dual function of producing ova/sperms and secreting hormones o Through the sixth week of prenatal development, male and female fetuses are  identical; both sexes have a pair of identical undifferentiated gonads, which have  the potential of developing into either testes/ovaries

o SRY gene – factor that controls gonad development; gene on Y chromosome  whose product instructs the undifferentiated fetal gonads to develop into testes ▪ If SRY gene is not present, the undifferentiated gonads become ovaries o Once gonads have developed, another series of evets occur, which are directed by  hormones; these hormones have organizational effects during prenatal  development, which are permanent and persist throughout the person’s life ▪ Hormones also have activational effects, in which occurs in fully  

developed organism; depends on organism’s prior exposure to the  

organizational effects

∙ Internal sex organs (ISO) are bisexual in early embryonic development, in which all  embryos contain the precursors for both female and male sex organs

o During the third month of gestation, only one precursor develops

o ISO development of fetus is determined by presence/absence of hormones  secreted by the testes – if these hormones are present, the WS develops; if not,  then the MS develops

o Mullerian system (MS) – embryonic precursor of female ISO; develops into  fimbriae and fallopian tubes, uterus, inner vagina

▪ MS needs no  

additional hormonal  

stimulus from the  

gonads to develop

▪ MS cells contain  

receptors for AMH  

that prevent growth  

and division; thus,  

presence of this  

hormone prevents female ISO development

o Wolffian system (WS) – embryonic precursor of male ISO; develops into  epididymis, vas deferens, seminal vesicles

▪ WS doesn’t develop unless gonads are stimulated to do so by a hormone ▪ Precursors contain androgen receptors that are coupled to cell mechanisms  that promote growth and division – when androgen molecules bind with  these receptors, the epididymis, vas deferens, and seminal vesicles develop  and grow

o Testes secrete two types of hormones:

▪ Anti-Mullerian hormone (AMH) – peptide secreted by the fetal testes that  inhibits Mullerian development; has a defeminizing effect  

(reduces/prevents later development of anatomical/behavioral female  

characteristics)

▪ Androgen – male sex steroid hormone that stimulates WS; has  

masculinizing effect (promotes development of male characteristics)

∙ Masculinization is due to two different hormones:

o Testosterone – secreted by testes, principal androgen

o Dihydrotestosterone – androgen produced from  

testosterone through 5α reductase action (enzyme)

o Androgen insensitivity syndrome – caused by congenital lack of functioning  androgen receptors; in a person with XY sex chromosomes, it causes development  of female with testes but no ISO

▪ The external genitalia are female and at puberty, the person develops a  woman’s body, but without uterus/ovaries (unable to have children)

▪ The primitive gonads of a genetic male fetus become testes and secrete  both AMH and androgens

▪ Lack of androgen receptors prevents androgens receptors from having  masculinizing effect; thus, epididymis, vas deferens, seminal vesicles, and  prostate don’t develop

▪ However, AMH still has defeminizing effect, preventing female ISO  development

∙ At puberty, gonads are stimulated to produce their hormones, which causes person to  mature sexually

o 1º sex characteristics are influenced by organizational effects of hormones and  include gonads, ISO, and external genitalia (EG); present at birth

o 2º characteristics are influenced by activational effects of hormones and include  enlarged breasts, widened hips, beard, deep voice; appear at puberty

▪ Female 2º characteristics (pubic hair) are produced by androgens secreted  by the cortex of the adrenal glands

∙ Onset of puberty occurs when cells in hypothalamus secrete gonadotropin-releasing  hormone (GnRH); GnRH stimulates production and release of two gonadotropic  hormones (gonadotropins) by the anterior pituitary glands, in which these hormones  stimulate gonads to produce their hormones

o Follicle-stimulating hormone (FSH) – causes development of ovarian follicle and  the maturation of an ovum

o Luteinizing hormone (LH) – causes ovulation and development of ovarian follicle  into a corpus luteum (CL)

o GnRH – controlled by kisspeptin, which is a peptide produced by neurons in the  arcuate nucleus of the hypothalamus, under the control of leptin receptors; it’s  essential for the initiation of puberty and maintenance of reproductive ability

o Factors speeding up onset of puberty – girls who remain thin during diet and  exercise tend to reach puberty later, while obese girls reach it earlier

▪ Leptin – peptide hormone secreted by well-nourished fat cells; provides  signal to brain concerning the amount of fat tissue in body (high fat, leptin

level increases and signals brain to suppress appetite); this determines the  onset of puberty in females

o In response to gonadotropins, gonads secrete steroid sex hormones ▪ Ovaries produce estradiol, while testes produce testosterone

Class

Where principal hormone  produced

Examples of effects

Androgens

Testosterone (testes)

WS development, sperm  production, facial/pubic hair

Estrogens

Estradiol (ovaries)

Female genitalia maturation,  breast growth, fat deposit

Gestagens

Progesterone (ovaries)

Maintenance of uterine lining

Hypothalamus

GnRH (hypothalamus)

Gonadotropin secretion

Gonadotropins

FSH and LH (anterior  

pituitary)

Ovarian follicle and CL  

development

Other  

hormones

Prolactin (anterior pituitary) Oxytocin (posterior)

Vasopressin

Milk production

Milk ejection, infant bonding Pair bonding (male)

∙ Coolidge effect – restorative effect of introducing a new female sex partner to a male  that’s in refractory period

∙ Lee-Boot effect – slowing and eventual cessation of estrous cycles in female groups that  are housed together, caused by pheromone in urine

o If exposed to male pheromones, cycle begins again; synchronization ∙ Vandenberg effect – earlier puberty onset in females that are housed with male; caused  by pheromone in male’s urine

∙ Bruce effect – termination of pregnancy caused by odor pheromone in male urine other  than the one that impregnated the female

∙ If rodent’s brain is NOT exposed to androgens during critical development period  (shortly after birth), animal will engage in female sexual behavior as an adult o If exposed to androgens during development:

▪ Behavioral defeminization – organizational androgen effect that prevents  animals from displaying female sex behavior in adulthood (suppression of  neural circuits)

▪ Behavioral masculinization – organization androgen effect that enables  animals to engage in male sexual behavior in adulthood (stimulation of  neural circuits)

o Male sexual behavior is dependent on prenatal organizational androgen exposure o Female behavior is dependent on activational effects of estradiol and progesterone ∙ Sexual behavior and effect of ISO and hormones

o Behavior of female rodents depends on gonadal hormones present during estrus  cycle – small amount of estradiol followed by progesterone

▪ Progesterone alone is ineffective; estradiol is the “primer”

▪ This sequence increases receptivity, proceptivity, and attractiveness o Lordosis response – spinal sexual reflex; arching of back in response to male o Human sexual behavior

▪ Ability to mate is not controlled by ovarian hormones – there are no  physical barriers to intercourse during any part of the menstrual cycle

▪ Sexual activity initiated by women showed distinct peak around time of  ovulation, when estradiol level are at its highest

▪ Women are more likely to initiate sex just before and during LH surge that  stimulates ovulation

▪ Women’s sexual interest can be stimulated by androgens, which amplify  the effects of estradiol

∙ Androgen secreted by ovaries and adrenal glands

∙ 1º ovarian sex steroids are estrogen and progesterone; these glands  also produce testosterone

▪ In both men and women, anticipation of sexual activity stimulates  

testosterone production

▪ In men, without testosterone, sperm production and sexual interest ceases ∙ Neural control of sexual behavior

o In animals – primary and accessory olfactory regions ???? medial nucleus of  amygdala ???? MPA

o For both males and females – medial amygdala receives chemosensory info from  VNO and somatosensory info from genitals and sends efferent axons to MPA o Males – spinal ejaculation generator (SEG)

▪ Lumbar neurons, AKA lumbar spinothalamic (LSt) cells, project to  adjacent neurons in the spinal cord that control sympathetic and  

parasympathetic mechanisms that result in emission and ejaculation

∙ This projection provides input to brain that  

constitutes pleasurable orgasmic sensation

▪ Medial preoptic area (MPA) – sex increases  

neural firing rate in MPA

∙ Copulation activates MPA, which causes an  

increase in glutamate release; infusion of  

glutamate into MPA increases ejaculation  

frequency (destruction abolishes male sexual  

behavior)

∙ Sexually dimorphic nucleus (SDN) –

nucleus in MPA that’s much larger in males  

than females (rodents)

o In humans, a homologous structure is known as the  

uncinated nucleus, which is also larger in males

o Size is determined by the amount of androgen present  

during fetal development

o The masculinization period of the SDN starts on the 18th 

day of gestation and ends once the animal is five days old

∙ The central tegmental field and the medial amygdala, both of  

which are sexually dimorphic, project to the MPA

o Damage to medial amygdala eliminates male sexual  

behavior

∙ Connections between the MPA and SEG – PAG of the midbrain  

and the nucleus paragigantocellularis (nPGi) of medulla

o MPA suppress nPGi directly through inhibition pathway  

and does so indirectly by inhibiting PAG activity, which  

normally excites nPGi

o The inhibitory connections between neurons of the nPGi  

and those of SEG are serotonergic

▪ MPA ???? inhibits PAG of midbrain ???? nPGi in medulla ???? spinal cord  sexual reflexes (nPGI to spinal cord uses 5-HT)

o Females – ventromedial nucleus of the hypothalamus (VMH)

▪ The medial amygdala receives chemosensory info from VNO and  

somatosensory info from genitals and sends  

efferent axons to the MPA

▪ Amygdala neurons also send efferent axons  

to VMH

▪ Estradiol increases progesterone receptor  

production, which increases progesterone  

effectiveness

▪ PAG contains both estrogen and  

progesterone receptors

▪ Medial nucleus of amygdala ???? VMH ????

PAG ???? nPGi ???? motor neurons in ventral horn  

of lumbar spinal cord

∙ Pheromones – chemical released by one animal that affects the behavior/physiology of  another animal; smelled or tasted, sensitive to nonvolatile compounds found in urine and  other substances

o Odor detection accomplished by olfactory bulbs (1º olfactory system) o Effects on the reproductive cycles are mediated by vomeronasal organ (VNO) ,  which is arranged around a pouch connected by a duct to the nasal passage ▪ VNO gives rodents the ability to ID the sex of another individual

o VNO projects to accessory olfactory bulb (AOB) located immediately behind the  olfactory bulb

▪ AOB sends axons to the medial nucleus of the amygdala, which projects  to the preoptic area, the anterior hypothalamus, and the ventromedial  

nucleus of the hypothalamus

o Androgenic chemical androstadienone (AND) is found in men’s sweat – increase  in alertness and positive mood in women, decreases positive mood in men o Estrogenic chemical estratetraene (EST) is found in women’s urine – activates  paraventricular nucleus and dorsomedial hypothalamus in men

o Signals are carried to the glomeruli in the olfactory bulb; from there, they are sent  to the 1º olfactory (piriform) cortex in the temporal lobe ???? 2º olfactory  

(orbitofrontal) cortex in the frontal lobe and the hypothalamus via dorsomedial  nucleus of the thalamus

▪ Amygdala ???? hypothalamus; entorhinal cortex ???? hippocampus (HP)

Chapter Twelve: Ingestive Behavior

∙ Ingestive behaviors are correctional mechanisms (CM) that replenish the body’s depleted  stores of water and nutrients

∙ Because of the delay between ingestion and replenishment of depleted stores, IBs are  controlled by satiety mechanisms (SM), which cause thirst/hunger cessation and are  produced by adequate and available nutrient/water supplies

o SMs monitor CM activity; when sufficient amount of drinking occurs, SMs stop  further drinking in anticipation of replenishment that will occur later

∙ Isotonic – equilibrium

∙ Hypertonic – too much solute (salt) inside, it will pull water from extracellular space ∙ Hypotonic – too little solute inside cell, develop salt appetite

∙ Two-thirds of body’s water is contained in intracellular fluid (IF); the rest is extracellular  fluid (EF), which includes:

o Intravascular fluid (IVF, blood plasma), CSF, and interstitial fluid (ISF, fluid that  bathes cells, filling the space between cells)

∙ IF and IVF must be kept within precise limits (regulation)

o IF – loss of IF water deprives cells of the ability to perform chemical reactions  and a gain of water causes membranes to rupture

o IVF – decrease in blood volume (hypovolemia) deprives the heart of the ability to  pump blood effectively; if volume is not restored, heart failure will result ∙ Volumetric thirst (VT) – thirst produced by hypovolemia; IVF volume decreases o When we lose water through evaporation, we lose it from IF, ISD, and IVF ▪ Evaporation produces VT and OT; loss of blood, vomiting, and diarrhea  all cause hypovolemia without IF depletion

o Leads to salt appetite because hypovolemia involves loss of Na+and water o Detectors in heart and kidney contribute to monitoring blood volume and induce  VT when IVG is low; kidney cells detect decrease in blood flow

o Kidneys are responsible for presence of angiotensin, which initiates drinking and salt appetite; this causes kidneys to conserve water and salt, which increases bp ▪ Reduced flow to kidneys causes water and salt to be retained, which  encourages ingestion of water and salt, which then allows for  

compensation for reduced flow until fluid balance can be restored

o VT signal is provided by angiotensin, which can’t cross BBB so it can’t directly  affect brain neurons, except for OVLT and SFO

∙ Osmotic thirst (OT) – thirst produced by an increase in osmotic pressure on ISF relative  to IF, producing cellular dehydration

o Occurs when [solute] draws water out of cells, so they shrink in volume; solutes  are substances, such as salt, that are dissolved in a solution

o Osmoreceptors – osmotic detector cells that respond to change in [ISF] that  surrounds them; neuron firing rate affected by  

hydration level

▪ Responsible for OT located in the lamina  

terminalis (LT), which contains two  

specialized circumventricular organs

∙ Organum vasculosum of LT (OVLT)  

and subfornical organ (SFO, site at  

which angiotensin acts to produce thirst)

∙ Located outside the BBB; substances dissolved in blood pass  

easily into ISF within these organs

▪ OVLT – located in antero-ventral to third ventricle (AV3V) on blood side  of BBB; increase in firing rate when ISF is hypertonic and decrease when  it’s hypotonic

∙ Lesions reduce OT, damage to AV3V produces lack of thirst,  

infusing NaCl into AV3V induces drinking

▪ Thirst activates the anterior cingulate cortex (ACC, perception of  

unpleasant stimuli); immediate relief upon drinking; LT activity reflects  that blood plasma still contain high [solute]

o When we eat a salty meal, we incur a pure OT

▪ Salt is absorbed into plasma; [salt] of blood draws water from the ISF,  which causes water to leave the cells

∙ Median preoptic nucleus (MPN) – small nucleus wrapped around front of anterior  commissure, which is a fiber bundle that connects amygdala and anterior temporal lobe o Contains A2 receptors inside the BBB; responds to both types of thirst o Neurons in SFO send axons to MPN

o MPN acts as integrating system for OT and VT stimuli; controls drinking through  its efferent connections with other brain parts

o Receives info from OVLT and from nucleus of solitary tract, which receives info  from atrial baroreceptors (detect hypovolemia in atria)

∙ Angiotensin – kidneys; initiates drinking and a salt appetite

o Angiotensin synthesis - renin catalyzes  

angiotensinogen ???? A1 cleaves to A2 ???? Now A2  

is the only one that’s active ???? A2 binds to  

receptors, causing it to communicate with other  

structures in hypothalamus that will release  

hormones

o Biological effects

▪ Copious drinking because  

circumventricular organs have A2 receptors

▪ Vasoconstriction to increase blood pressure

▪ Release of vasopressin, an anti-diuretic  

hormone, by the posterior pituitary

∙ Water reabsorption by kidneys;  

water retention to increase bp

▪ Release of aldosterone from adrenal cortex  

for NaCl reabsorption, which causes an increase in salt appetite; salt  

retention

∙ Role in insulin in the body and brain (short-term carbohydrate reservoir) o Liver cells convert glucose into glycogen and store it

o This conversion is stimulated by insulin,  

a pancreatic hormone that facilitates  

entry of glucose and AA into the cell,  

glucose-glycogen conversion, and  

transport of fats into adipose tissue

o When glucose and insulin are present in the blood, some glucose is used as fuel  and some is stored as glycogen

▪ When all food has been absorbed from tract, glucose level in the blood  begins to fall

o A decrease in glucose is detected by pancreatic cells; the pancreas then responds  by stopping its secretion of insulin and starting to secrete glucagon, a pancreatic  hormone that promotes conversion of liver glycogen into glucose

▪ The liver soaks up excess glucose and stores it as glycogen when plenty of  glucose is available

▪ The liver releases glucose from its reservoir when the tract becomes empty  and glucose levels decreases

o Controls entry of glucose into cells – the cell membrane isn’t permeable to  glucose, so it uses transporters

▪ Glucose transporters have insulin receptors; required in body, not brain ∙ Phases of metabolism and glucose levels

o Fasting phase – metabolic phase during which nutrients aren’t available from the  tract; glucose, AA, and fatty acids are derived from glycogen, protein, and  adipose tissue

▪ A decrease in glucose level causes pancreas to secrete glucagon

▪ Absence of insulin means most of the body’s cell can no longer use  glucose; thus, all glucose present in the blood are reserved for the CNS (brain uses glucose)

▪ Presence of glucagon and absence of insulin instruct the liver to start  drawing on short-term carbohydrate reservoir, meaning to start using  

glycogen-glucose conversion

∙ This also instructs fat cells to start drawing on long-term fat  

reservoir – breaking down triglycerides into fatty acid and glycerol

▪ The body lives on fatty acids and glycerol, which is converted into glucose  by liver, which is used by the brain

∙ Brain uses glucose, body uses fatty acids (no insulin)

▪ Breakdown of triglycerides is controlled by – lack of insulin (pancreas  stops secreting), glucagon (pancreas increases secretion), epinephrine

o Absorptive phase – metabolic phase during which nutrients are absorbed from the  tract; glucose and AA constitute the principal source of energy for cells; excess  nutrients are stored in adipose tissue in triglyceride forms

▪ Glucose – as nutrients are absorbed, glucose level increases

∙ Increase is detected by cells in brain, which causes sympathetic NS  activity to decrease and parasympathetic NS to increase

o This tells pancreas to stop secreting glucagon and to begin  

secreting insulin, which permits ALL cells to use glucose  

as fuel

o Extra glucose is converted into glycogen, which fills the  

short-term reservoir; if some glucose is left over, it’s  

converted into fat

▪ AA – small portion of AA received from the tract used to construct  proteins and peptides; the rest are converted into fat and are stored in  

adipose tissue (emergency storage)

▪ Fat – not used as fuel at this time; stored in adipose tissue (long-term)

o Top is consumption; bottom is due to fasting

∙ Role of ghrelin in feeding behavior

o Ghrelin – peptide hormone released by stomach that increases eating; also produced  by brain neurons

o Released from GI when individuals are in fasting phase and digestive system is  empty; it then binds to receptors in the hypothalamus to help stimulate eating  behavior

o Ghrelin levels increase with fasting and are reduced after a meal

▪ Blocking ghrelin signals inhibits eating and increases food intake, which  decrease fat metabolism

▪ Levels increase shortly before each meal, suggesting that this peptide is  involved in meal initiation

o Ghrelin exerts its effects by stimulating NPY receptor, which stimulates feeding,  insulin and glucocorticoid secretion, and decrease triglyceride breakdown ▪ Glucoprivation (decrease in glucose level available to cells, which stimulates  eating) and ghrelin activate orexinergic NPY neurons

∙ Leptin and obesity

o Leptin has no effect on people who lack leptin receptor

o People who are obese already have a high level of leptin

▪ Increasing this level with injections has little or no effect on their food intake

∙ Brain regions involved in eating/drinking, peptides/hormones involved in feeding behavior

Name

Location of  

somas

Location of  

terminals

Interaction with  other peptides

Physiological or  behavioral effects

Melanin

concentrating  hormone  

(MCH)

Lateral  

hypothalamus

Neocortex, PAG,  reticular formation,  thalamus, LC, scord  neurons that control  sympathetic NS

Activated by  

NPY/AGRP;  

inhibited by  

leptin and  

CART/α-MSH

Eating, decreased  metabolic rate

Orexin

Lateral  

hypothalamus

Similar to those of  MCH neurons

Activated by  

NPY/AGRP;  

inhibited by  

leptin and  

CART/α-MSH

Eating, decreased  metabolic rate

Neuropeptide  Y (NPY)

Arcuate  

nucleus of  

hypothalamus

Paraventricular  

nucleus, MCH, and  orexin neurons of  lateral  

hypothalamus

Activated by  

ghrelin; inhibited  by leptin

Eating, decreased  metabolic rate

Agouti-related  protein  

(AGRP)

Arcuate  

nucleus of  

hypothalamus

Same regions as  

NPY

Inhibited by  

leptin

Eating, decreased  metabolic rate;  

acts as antagonist  at MC4 receptors

CART

Arcuate  

nucleus of  

hypothalamus

Paraventricular  

nucleus, lateral  

hypothalamus,  

PAG, neurons in  scord that control  sympathetic NS

Activated by  

leptin

Suppression of  

eating, increased  metabolic rate

α-melanocyte  stimulating  

hormone (α

MSH)

Arcuate  

nucleus of  

hypothalamus  (co-localized  with cart)

Same regions as  

CART neurons

Activated by  

leptin

Suppression of  

eating, increased  metabolic rate;  

acts as agonist at  MC4 receptors

References: