BioPsychology - PT Notes PDF
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University of Pittsburgh
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This document provides notes on sleep, circadian rhythms, and various theories of sleep. The content covers aspects like the biological clock, sleep cycles, and the different functions of sleep stages, along with explanations on restorative and elimination theories.
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Sleep Circadian rhythm (general) ○ 14:30 - best coordination ○ 15:30 - fastest reaction time ○ 17:00 - greatest cardiovascular deficiency and muscle strength ○ 18:30 - highest blood pressure...
Sleep Circadian rhythm (general) ○ 14:30 - best coordination ○ 15:30 - fastest reaction time ○ 17:00 - greatest cardiovascular deficiency and muscle strength ○ 18:30 - highest blood pressure ○ 19:00 - highest temperature ○ 21:00 - melatonin secretion starts ○ 22:30 - bowel movements suppressed ○ 2:00 - deepest sleep ○ 4:30 - lowest body temperature ○ 6:45 - sharpest rise in blood pressure ○ 7:30 - melatonin secretion stops ○ 8:30 - bowel movement likely ○ 9:00 - highest testosterone secretion ○ 10:00 - high alertness Suprachiasmatic nucleus = “biological clock” Light stimulates the SCN and results in decreased melatonin production by the pineal gland in the morning ○ Through retinal ganglion cells releasing melanopsin Melanopsin stimulates the SCN Low light leads to increased melatonin production by the pineal gland Chronotype - a person's natural inclination with regard to the times of day when they prefer to sleep or when they are most alert or energetic ○ Alters with age ○ Young - night owls Performance is worst in the morning ○ Older - morning larks Performance is best in the morning Process C - circadian/wake drive ○ ○ Process S - sleep drive Recuperation theories of sleep ○ Restorative theory Repair and regeneration of the body? Muscle repair, tissue growth, protein synthesis, growth hormone release Necessary for optimal functioning of physiological systems ○ Elimination theory R id the brain of excess sensory information? Certain synaptic connections are strengthened, and others are weakened or not established during sleep Synaptic pruning ○ Brain plasticity theory Neural reorganization, growth of neurons & brain structures Adaptation theories of sleep ○ Immobilization therapy Innate response with species specific patterns Keeps one inactive and safe during least efficient part of day/night cycle ○ Energy conservation theory Following survival activities, periods of inactivity are a good way to conserve energy Activation synthesis theory ○ The synthesis and activation of specific brain regions are what cause dreams Functions of Slow-Wave sleep ○ Seems essential for survival i.e. fatal familial insomnia ○ Lack of SWS correlated with disorders i.e. cardiovascular, diabetes, obesity, Alzheimer’s ○ Consolidation of declarative (explicit) memory Functions of REM sleep ○ Promote brain development ○ Facilitate learning ○ Consolidation of nondeclarative (implicit) memory (muscle memory) ○ REM rebound phenomenon - indicates that REM is a bit more important than slow wake ○ REM sleep behavior disorder Patient acts out dreams by the movement of limbs and talking Malfunctions of the nerve pathways that control movement during REM sleep Atonia—normal temporary muscle paralysis during sleep—is absent After 17 hours of wakefulness, cognitive psychomotor performance decreases to a level equivalent to the performance impairments observed at a blood alcohol concentration of 0.05% ○ Driving sleepy is just as bad as driving drunk After 24 hours of wakefulness, cognitive psychomotor performance decreases to a level equal to the performance deficit observed at a blood concentration of 0.1% Large sleep differences found between species ○ Bat ~20 hours ○ Horse ~3 hours ○ In some species, only half of the brain sleeps at a time Physiological measures of Arousal & Sleep ○ Electroencephalogram (EEG) E lectrical potential recorded from electrodes placed on the scalp (brain waves) ○ Electrooculogram (EOG) Measure of eye movements seen during sleep ○ Electromyogram (EMG) Electrical potential recorded from an electrode placed on muscles Measures changes in muscle tension particularly in facial and neck muscles Mentalis muscle When it stops firing, you're asleep and vice versa Theories of sleep ○ Passive theory of sleep Bremer (1936) Cerveau isole Transection cut in the midbrain - separates the forebrain from the brainstem and spinal cord Animal remains in a state similar to constant sleep with predominantly synchronized EEG patterns - similar to patterns in SWS Showed the forebrain can’t maintain wakefulness and input from the lower brain regions is needed for arousal - importance of brainstem structures in regulating wakefulness and consciousness Encephale isolé Transection between the spinal cord and medulla - isolates the entire brain from the spinal cord Animal can show cyclic EEG patterns associated with wakefulness - brainstem is capable of maintaining a level of arousal and regulating sleep-wake cycles Showed that reticular formation in the brainstem plays a critical role in arousal and wakefulness - structures in the upper brainstem are essential for maintaining these functions → influence EEG patterns associated with different states of consciousness ○ Active theory of sleep Moruzzi and Magoun (1949) Discovered the reticular formation Reticular activating system’s involvement in sleep ○ Cats with a mid collicular transection (i.e. a cerveau isolé preparation) displayed a pattern of continuous slow-wave sleep in their cortical EEGs ○ Lesions at the mid collicular level that damaged the core of the reticular formation, but left the sensory fibers intact, produced a cortical EEG indicative of continuous slow-wave sleep ○ Electrical stimulation of the pontine reticular formation desynchronized the cortical EEG and awakened sleeping cats ○ C ats with a transection of the caudal brainstem (i.e. an encéphale isolé preparation) displayed a normal sleep-wake cycle of cortical EEG ○ All four findings suggests that a wakefulness-producing area was located in the reticular formation between the cerveau isolé and the encéphale isolé transections ○ Stage 1 - just falling asleep - people normally stay in it for 1-7 minutes NREM Alpha waves to theta waves Muscle activity slows ○ Stage 2 - the feeling of not being in deep sleep - the middle of sleep and awake - can last about 10-20 minutes - about 50% of sleep time NREM Theta waves, sleep spindles, & k-complexes ○ Stage 3 - slow wave sleep - deep sleep - can last 20-40 minutes (calling a person’s name could get them out of this stage) - spend more time in it earlier in the sleep cycle - nightmares and sleepwalking tend to occur at this stage NREM Delta waves ○ Transitory stage 1 = REM sleep ○ Stage 4 - REM sleep - dream - more time in this stage as the sleep cycle progresses - takes up about 20-25% of the night Beta waves “Paradoxical sleep” To remember dreams, you have to wake up right when the dream ends ○ On average, about 1.5 hours is one sleep cycle S leep stages & brain waves ○ ○ Gamma wave Irregular, low amplitude, highest frequency about 30-120 Hz Flo - hyper focused & concentrated ○ Beta wave Irregular, low amplitude, high frequency about 13-30 Hz ○ Alpha wave Fairly regular, low amplitude, high frequency about 8-13 Hz Seen during meditation ○ Theta wave Low amplitude, moderate frequency about 4-8 Hz Indicator of sleep ○ Sleep spindles Short bursts of about 12-14 Hz Play a role in inhibiting external stimuli from waking the sleeper by reducing sensory perception Helps prevent the transition from light to wakefulness Helps with memory consolidation and learning - transfers info from working memory in the hippocampus to long-term memory in the cortex ○ K complexes Sudden sharp waveforms Responds to external stimuli–prevents sleeper from waking Sleep-preserving reactions - help the brain determine if a stimulus requires waking or not Contribute to memory consolidation ○ Delta wave High amplitude, low frequency about 1-4 Hz Synchronized neuronal activity - associated with body’s restorative processes Arousal & neurotransmitters ○ Acetylcholine Dorsal pons and basal forebrain Plays a role in arousal of cerebral cortex Levels high during wakefulness and REM Project to medial pons, thalamus, cortex Involved in cortex and hippocampus arousal Primarily involved in promoting wakefulness in the pons ○ Norepinephrine Locus coeruleus (in pons) Plays a role in attention and vigilance Possible role in ‘behavioral’ arousal Levels high only during wakefulness (lower levels during SWS and lowest during REM) Project to and impact the cortex, thalamus, hippocampus, cerebellum, pons, and medulla ○ Serotonin (5-HT) Raphe nuclei (medial pons; near caudal end of reticular formation) Levels high during wakefulness Levels lowering as descending towards REM Cortical and behavioral arousal Plays a role in activating behavior (pacing, chewing, grooming in rodents) Project to and impact the thalamus, hypothalamus, cortex, hippocampus, basal ganglia ○ Histamine Tuberomammillary nucleus (in hypothalamus) Levels high during wakefulness Levels low during SWS and REM Implicated in control of wakefulness and arousal Projects to and impacts the cortex, thalamus, hypothalamus, basal ganglia, and basal forebrain ○ Orexin From lateral hypothalamus Levels high during wakefulness Ensures the brain remains alert and active (particularly under stimulating/demanding conditions Low during rest and all sleep stages Increases activity in the brainstem and forebrain arousal systems Slow wave sleep and neurotransmitters ○ GABA From ventrolateral preoptic area (vlPOA) Suppress alertness and behavioral arousal and promote sleep High levels are associated with sleep - inhibits wake-promoting neurons to maintain sleep state (contributes to the paralysis characteristic of REM sleep) Low levels associated with wakefulness ○ Adenosine Peptide released by neurons during high levels of metabolic activity throughout the day Increases activity in the vlPOA The sleep/waking flip-flop ○ When the flip-flop is in the ‘wake’ state, the arousal systems (cholinergic (ACh), noradrenergic (NE), serotonergic (5-HT), and histaminergic) are active and the vlPOA is inhibited by the brainstem and forebrain arousal systems When the flip-flop is in the ‘sleep’ state, the vlPOA is active and the arousal ○ systems are inhibited v lPOA sends inhibitory signals (GABA) to the arousal systems and prevents the release of the neurotransmitters Results in slow-wave sleep - deep stage of sleep crucial for rest and recovery ○ ○ Narcolepsy ○ Symptoms Sleep attack Cataplexy Sleep paralysis Hallucinations - hypnagogic and hypnopompic Difficulty staying awake during the day Difficulty falling asleep during the night - fragmented sleep REM sleep intrudes into waking state Seem to skip SWS and enter REM sleep quickly ○ Prevalence - 1 in 2000 ○ Cause Seems to be related to deficiency of peptide neurotransmitter orexin Mutation in orexin B receptor - causes canine narcolepsy In humans - complete absence of orexin in 7 out of 9 people with narcolepsy Most are born with orexin, but during adolescence, the immune system may attack these neurons and start the symptoms ○ Treatment Stimulants Ritalin ○ Methylphenidate - dopamine and norepinephrine agonist (reuptake inhibitor) Amphetamine ○ Dopamine and norepinephrine agonist (reuptake inhibitor) Provigil ○ Modafinil - orexin agonist Typically taken in the morning Helps reduce daytime sleepiness - decrease sleep attacks SSRIs and SNRIs Fluoxetine - Prozac, Sarafem, others (SSRI) Venlafaxine - Effexor (SSRI) Atomoxetine - Strattera (SNRI) Typically taken later in the day H elps reduce episodes of REM sleep components - cataplexy, sleep paralysis, hallucinations Tricyclic antidepressants Norepinephrine, serotonin, dopamine agonist (reuptake inhibitor) Protriptyline - Vivactil Imipramine - Tofranil Typically taken later in the day Helps reduce episodes of REM sleep components - cataplexy, sleep paralysis, hallucinations Sodium oxybate (Xyrem) CNS depressant that reduces excessive daytime sleepiness and cataplexy GABA-B receptor agonist Taken at night, immediately before bed Second dose = 3-4 hours later - middle of the night 0/17/24 1 Sexual Development & Behavior Chromosomes ○ Male testes produce sperm cells 23 chromosomes ○ Female ovaries produce ova (eggs) 23 chromosomes ○ Fertilization Sperm cell + ovum = zygote ○ X & Y chromosomes XX = Female XY = Male Testis determining factor (TDF) aka SRY protein ○ T DF initiates the development of testes If TDF were introduced to a genetic female fetus at 6 weeks, it would trigger the development of testes instead of ovaries The presence of testes would lead to the production of male hormones, influencing the development of male secondary sex characteristics S wyer syndrome ○ 46, XY genotype Prevalence approx. 1 in 80,000 ○ ○ 15-20% SRY gene mutations of missing segment containing SRY gene 46, XX testicular disorder ○ Translocation of genetic material between chromosomes ○ SRY gene is misplaced onto X chromosome ○ Prevalence approximately 1 in 25,000 At 6 weeks after conception, the primordial gonads of XX and XY individuals are identical ○ Differentiation occurs in the second and third prenatal months ○ Female (XX) If no Y chromosome is present, the cortex of the primordial gonad develops into an ovary ○ Male (XY) Under the influence of the Y chromosome, the medulla of the primordial gonad develops into a testis ○ Wolffian ducts Male reproductive structures Regression trigger in females - lack of much testosterone Testosterone Presence of Y chromosome → development of testes → production of testosterone & AMH → wolffian ducts develop, mullerian ducts regress ○ Mullerian ducts Female reproductive structures Regression trigger in males - presence of anti-mullerian hormone Anti-mullerian hormone (AMH) or MIS Absence of Y chromosome → mullerian ducts develop, wolffian ducts regress ○ Sperm is held and matures in the epididymis ○ Testes develops first A s testis develops ○ M ullerian inhibiting substance (MIS) and testosterone are synthesized and released MIS - stops the development of the Mullerian system ○ 5-alpha reductase converts testosterone to dihydrotestosterone 5-alpha reductase is necessary for the conversion 5-alpha reductase deficiency syndrome ○ Lack of sufficient levels of 5-alpha reductase ○ Without dihydrotestosterone - male genitals (external) cannot grow ○ Once puberty hits, high levels of testosterone are released which would cause people with 5-alpha reductase deficiency syndrome to develop their genitals John Money & John/Joan ○ Money argued for the socialization theory of gender identity A child’s gender identity is primarily shaped by socialization and environmental influences rather than biological factors ○ David Reimer was born male, but lost his private in a botched circumcision as an infant His parents decided to raise him as a girl, following Money’s advice He was subjected to hormone treatments and psychological therapy (to reinforce a female gender identity) David struggled with his female identity, experiencing distress and rejecting the role as he grew up He eventually transitioned to a male and went through surgeries to reverse the assignment ○ Case led to re-evaluations of theories surrounding gender identity development It does have a biological factor Primary sex characteristics ○ Organizational effects of hormones (or lack of) Occur during development and lay foundation for future behavior and physiological responses ○ Ex. development of male & female reproductive organs Secondary sex characteristics ○ Activational effects of hormones ○ Ex. breasts growing, facial hair, voice deepening, pelvis widening Phenotype: physical observable traits determined by the genotype Genotype: genetic constitution of an organism Female brains ○ Higher percentage of gray matter ○ Larger hippocampus ○ Larger ventral prefrontal cortex Involved in social cognition and interpersonal judgment ○ Higher levels of serotonin, dopamine, and GABA Male brains ○ 10% larger cerebral hemisphere ○ Higher percentage of white matter & cerebral spinal fluid L ○ arger and more reactive amygdala ○ Larger hypothalamus ○ Differences may occur as a result of higher androgen levels in males, rather than in females, during fetal development? Masculinization of the (rodent) brain ○ Aromatase Converts testosterone into estradiol In cytoplasm, dendrites, & soma Aromatization hypothesis Certain effects of testosterone in the brain are mediated by its conversion to estrogen ○ Alpha fetoprotein Produced by placenta and fetal liver cells during fetal development Binds to circulating estradiol and prevents its entry into brain Does not bind to testosterone Hypothalamic-Pituitary-Gonadal (HPG) Axis ○ Hypothalamus Paraventricular nucleus & supraoptic nucleus directly release hormones through posterior pituitary portal I.e. oxytocin ○ “The love hormone” - helps trigger the bonding between mother and infant ○ Stimulates lactation ○ Levels stay high for long after birth ○ Levels rise during sexual interaction Pitocin ○ Given to women in labor if contractions stalls Releases hormones that stimulate anterior pituitary gonadotropin-releasing hormone Anterior pituitary ○ Releases gonadotropins Follicle-stimulating hormone (FSH) Ova development perm development S Increase estradiol production Secreted by the anterior pituitary gland Promotes the maturation of ovarian follicles Starts high at the beginning of the cycle then decreases as the dominant follicle matures Luteinizing hormone (LH) Stimulates testosterone secretion ○ From Leydig cells in testes ○ From Theca cells in ovaries LH surges mid-cycle (around day 14) and triggers ovulation Gonadal hormones Gestagens i.e. progesterone ○ Referred to as pregnancy hormone ○ Helps prepare for and maintain pregnancy - high levels are needed ○ Enables a zygote to implant ○ Keeps placenta attached to uterine wall ○ If progesterone drops below a certain level, the placenta detaches and a miscarriage occurs—or labor initiation ○ Possible role in sperm generation ○ Produced mainly by the corpus luteum in the ovary after ovulation ○ Rises and peaks in the postovulatory phase after ovulation to maintain the endometrial lining Androgens (i.e. testosterone (responsible for bone growth, body hair growth and sex drive (in females), hydrotestosterone) ○ Leydig cells in testes ○ Theca cells in ovaries Estrogens (i.e. estradiol) ○ Converted from testosterone by aromatase ○ In males - erection ○ Females - thickens the uterine wall (endometrium), plays a modulating effect with sex drives ○ Produced by developing follicles ○ Rises during follicular phase & peaks just before ovulation Has a second, smaller increase in the postovulatory phase “____-releasing” - likely to come from the hypothalamus P ○ reovulatory (follicular) phase - about days 1-14 ○ Postovulatory (luteal) phase - about days 14-28 ○ Ovarian cycle Start with the primary follicle Early stages of follicle development in the ovary during the follicular phase Secondary follicle Further maturation of the follicle Matured but unable to be fertilized Graafian The fully mature follicle that will rupture and release an egg during ovulation Can be fertilized Ovulation Around day 14 The mature follicle ruptures to release the oocyte (egg) Corpus luteum After ovulation, the empty follicle transforms into this Secretes progesterone and some estrogen Corpus albicans If fertilization does not occur, the corpus luteum degenerates into this Can no longer stimulate hormones ○ Uterine (endometrial) cycle Menstruation - lasts avg. 5 days Uterine wall sheds Low levels of estrogen & progesterone (end of luteal phase) B leeding occurs when hormone levels drop, indicating no pregnancy Proliferative phase As estrogen levels rise in the preovulatory phase, the endometrium begins to thicken (proliferate) in prep for possible implantation Secretory phase After ovulation, progesterone from the corpus luteum causes the endometrium to further thicken secrete nutrients, preparing the uterus for potential pregnancy Menstruation repeats If pregnancy does not occur, the corpus luteum degenerates, progesterone levels drop, and the cycle restarts Birth control pills ○ Utilizes the negative feedback loop between ovaries, and the hypothalamus and pituitary ○ Most effective is the “combination pill” Delivers both estrogen and progestin for 3 weeks Estrogen decreases secretion of FSH Progestin prevents secretion of LH ○ Plan B Levonorgestrel (progestin) Taken within 72 hours (3 days) of unprotected sex Stops release of ovum If ovum is already released - may stop implantation? Will not if fertilized ovum has implanted ○ Mifepristone Progesterone receptor blocker Stop pregnancy from continuing Used to end early pregnancy (within 70 days or less since last menstrual period) Followed by Misoprostol (24-48 hours) Softens and dilates cervix Stimulates uterine contractions Medial preoptic area in the hypothalamus ○ Involved in regulation of male sexual behavior in rodents Ventromedial nucleus in the hypothalamus ○ Involved in female sexual behavior in rodents ○ Stimulate arousal ○ Lordosis: posture of female rodent sexual receptivity Castration + estrogen = female behaviors exhibited ○ ○ Testosterone on day 1 + testosterone = male behaviors exhibited Lee-boot effect ○ Occurs when female mice are housed together without any males ○ Reproductive cycles become synchronized and often lengthened, and some of the females may even stop cycling together ○ Thought to be driven by pheromones released by females that inhibit each other’s reproductive cycles in the absence of male stimuli Whitten effect ○ Occurs when a group of female mice exposed to scent of a male mouse or his pheromones after being isolated from males for some time ○ Reproductive cycles of the females synchronize and they enter the period of fertility at the same time ○ Male pheromones act as a stimulant, reactivating and synchronizing the reproductive cycles of females who have previously been in reproductive suppression asynchrony Bruce effect ○ Occurs when a recently mated female mouse is exposed to the scent of a new, unfamiliar male (one who is not the father of her current pregnancy) ○ The female will often terminate the pregnancy through reabsorption of embryos or spontaneous abortion ○ Phenomenon is thought to be an evolutionary strategy - the new male might be more likely to kill offspring sired by another male By terminating the pregnancy, the female can quickly become receptive to the new male and potentially mate with him, ensuring the survival of future offspring under his protection Vandenberg effect ○ Involves the acceleration or delay of sexual maturation in young female mice depending on the presence of adult males or females ○ When young females are exposed to adult males or their pheromones, they reach puberty faster ○ When exposed to only adult females or kept isolated from males, their puberty may be delayed ○ M ale pheromones promote the onset of puberty in young females possibly as a means of increasing reproductive opportunities for the male
