Description
Exam One Study Guide
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
▪ 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
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