Untitled Flashcards Set

Consciousness

Defining Consciousness

  • Consciousness is the state of being aware of and able to communicate about one's thoughts, perceptions, memories, and feelings. (Page 14)

  • "It's the biggest challenge to science, because all the problems we have tackled and solved so far have to do with the external world, such as DNA, or the Earth not being the center of the universe, or cosmology, or string theory. But we are now finally confronted with, in some ways the biggest problem of all, namely, understanding the very organ that made all those other discoveries possible, turning on itself and asking, ‘Who am I?’” - Vilayanur Ramachandran (Page 2)

  • "There is a lot of confusion about it.... When you try to define consciousness you have to start in the right place, and then your understanding gradually develops. The right place to start for me is the everyday experience that you and I have – in this particular moment..." - Max Velmans (Page 3)

  • "Well, that’s the hard problem. The brain is an excellent information processing system, but there’s no accounting for how and why we have subjective experience, emotional feelings, and ‘inner life’.” - Stuart Hameroff (Page 3)

  • “...there’s nothing in our physical theory of what the universe is like, which says anything about why some things should be conscious and other things not” - Roger Penrose (Page 3)

  • "I think the main problem is that everyone has a consciousness but they have no access whatsoever to anyone else’s. This is the problem of the minds and so far it’s insurmountable: we don’t know what it’s like to be someone else, and we don’t know what it’s like to have another consciousness." - Daniel Wegner (Page 3)

  • "Consciousness is that in which all experience appears with which all experience is known out of which all experience is made" - Rupert Spira (Page 4)

  • "Consciousness is the first-person experience" - Deepak Chopra (Page 4)

Mind-Brain Philosophical Positions

  • Idealism: Nothing exists in the world except our conscious experiences. (Page 6)

    • Present in some Eastern traditions (Advaita Vedanta, Yogacara) (Page 6)

    • Radical form proposed by George Berkeley in the 18th century (Page 6)

    • Influenced thinkers like Hegel, Schopenhauer, Husserl, and Bergson (Page 6)

  • Materialism: Only matter exists. (Page 10)

    • Identity theory: Mental states are identical to physical states in the brain. (Page 5)

    • No problem explaining the causal relationship between mental states and behavior because both are part of the physical world. (Page 10)

    • Subjective consciousness is a product of neuronal interactions in the brain. (Page 10)

  • Dualism: There are two worlds: one of mind and one of matter. (Page 6)

    • Substance dualism: Mind and matter are fundamentally different substances. (Page 5)

      • Interactionism: Mental states interact with physical states. (Page 8)

      • Cartesian dualism: The mind can exist outside the body, and the body cannot think. (Page 7)

    • Property dualism: Mind and matter have different properties. (Page 8)

      • Epiphenomenalism: The brain causes the mind, but the mind does not cause the brain. (Page 8)

  • Emergentism: New properties emerge from complex systems. (Page 9)

    • Emergent dualism: The mind is a fundamentally different substance that emerges from the brain. (Page 9)

    • Emergent materialism: The mind emerges from the brain but is not reducible to it. (Page 9)

  • Dual Aspect Monism: Ultimate reality is one kind but can be perceived from two different perspectives: physical and mental. (Page 11)

    • Your brain appears physical from the outside but mental from the inside. (Page 11)

    • These aspects are distinct but inseparable and irreducible to each other. (Page 11)

  • Neutral Monism: Ultimate reality is neither mental nor physical but a neutral substance. (Page 11)

    • Both mind and matter reduce to an underlying neutral domain. (Page 11)

  • Mysterianism: The hard problem of consciousness may be beyond our cognitive abilities. (Page 12)

    • We may not be able to understand how neural activity produces subjective feelings. (Page 12)

Studying Consciousness

  • Blindsight: Perception can affect behavior without conscious awareness. (Page 15)

    • Lesion in the striate cortex (V1/primary visual cortex) (Page 15)

    • Anton-Babinski syndrome: Reverse situation where people are unaware of their blindness. (Page 15)

  • Split-Brain: A lesion to the corpus callosum can produce two "consciousnesses." (Page 16)

    • We become conscious of something only if it reaches parts of the brain responsible for verbal communication. (Page 16)

  • Hallucinogens: Drugs that distort perception and consciousness. (Page 17)

    • Also called psychedelic ("mind-expanding") drugs. (Page 17)

    • Users often feel transported to a new reality. (Page 17)

    • Examples: Mescaline, Psilocybin, Dimethyltryptamine (DMT), LSD, Salvinorin A, Phencyclidine, Ketamine (Page 18)

    • Psychedelics may provide information about the "easy problems of consciousness" but not the "hard problem." (Page 20)

  • "Easy problem" of consciousness: How the brain works, such as how memories are formed. (Page 21)

  • "Hard problem" of consciousness: Why it feels like something to be conscious. (Page 21)

    • "Something that it is like to be" - Thomas Nagel (Page 21)

  • Neural Correlates of Consciousness (NCCs): Minimal neural mechanisms necessary and sufficient for conscious experience. (Page 22)

  • Theories of Consciousness (ToCs): Attempts to explain how consciousness arises. (Page 22)

    • Higher-order theories (HOTs): Experiences become conscious when they are re-represented at higher levels of the brain, specifically in the prefrontal cortex (PFC). (Page 23)

    • Global workspace theories (GWTs): Perceptions, thoughts, and emotions become conscious when they gain access to a "workspace" distributed across the frontal and parietal regions of the cortex. (Page 23)

    • Integrated information theory (IIT): Consciousness is related to how much information is integrated among different parts of the brain. (Page 24)

    • Re-entry and predictive processing theories: Conscious mental states are associated with top-down signaling, where higher-level brain regions send information to lower-level regions. (Page 24)

The Function and Evolutionary Origins of Consciousness

  • Susan Greenfield: Consciousness emerged gradually. (Page 25)

  • Nicholas Humphrey: Consciousness appeared rapidly as an emergent property that evolved for its social function. (Page 25)

  • Robert Trivers: Deception is central to consciousness, and self-deception may have been an evolutionary advantage. (Page 25)

  • Terrence Deacon: The human brain and language co-evolved, and symbolic representation may have emerged from this process. (Page 26)

  • Patricia Churchland and eliminative materialists: The concept of consciousness will be discarded once we understand how the brain functions. (Page 26)

  • Antonio Damasio: Consciousness of self could be adaptive by increasing our concern for survival. (Page 26)

  • Feinberg & Mallatt: Primary consciousness (sensory consciousness) originated in early vertebrates, cephalopods, and arthropods. (Page 27)

    • Three domains of consciousness:

      • Exteroceptive awareness: Awareness of the external world. (Page 27)

      • Interoceptive awareness: Awareness of the internal state. (Page 27)

      • Affective awareness: Precursor of emotions, "likes" and "dislikes." (Page 27)

  • Dr. Audrey Vanhaudenhuyse: Two types of consciousness: (Page 28)

    • Internal consciousness (self-awareness): Precuneus/posterior cingulate, anterior cingulate/mesiofrontal cortices, and parahippocampal areas ("intrinsic system"). (Page 28)

    • External consciousness (awareness of the environment): Lateral fronto-parietal cortices ("extrinsic system"). (Page 28)

    • These systems are anti-correlated neurophysiologically. (Page 28)

Sleep

Why Do We Sleep?

  • We spend about 1/3 of our lives asleep. (Page 30)

  • Sleep deprivation has dramatic effects on physiological equilibrium. (Page 30)

  • The restorative effects of sleep are more important for the brain than the body. (Page 30)

  • Slow-wave sleep and REM sleep promote different types of learning. (Page 30)

  • REM sleep appears to promote brain development. (Page 30)

Operational Definition of Sleep

  • Sleep is a reversible state of reduced sensory and motor interaction with the environment. (Page 31)

  • Coma: State of lost consciousness with limited response to the environment. (Page 31)

  • Deep non-REM sleep: Comparable to the unconsciousness of anesthesia but with impaired information integration. (Page 31)

  • Hibernation: A state of reduced metabolic activity and lowered body temperature. (Page 31)

Early Sleep Studies

  • Electroencephalography (EEG): Used to differentiate two kinds of sleep: (Page 32)

    • Non-REM (NREM) sleep: Characterized by high-amplitude, low-frequency EEG waves, occasional motor activity, and repetitive thoughts. (Page 32)

    • REM (or paradoxical) sleep: Brain activity similar to wakefulness (low-amplitude, high-frequency waves), vivid internal sensations, no motor activity except REM, and bizarre thoughts. (Page 32)

Non-REM Sleep

  • Divided into 3-4 distinct stages. (Page 33)

  • Parasympathetic nervous system (PNS) becomes predominant, slowing down metabolism. (Page 33)

  • Extensive synchronization of neural activity orchestrated by the thalamus. (Page 33)

  • People awakened from non-REM sleep typically recall only vague thoughts. (Page 33)

REM Sleep

  • "Active, hallucinating brain in a paralyzed body" - William Dement (Page 34)

  • 90-95% of people awakened from REM sleep report dreaming. (Page 34)

  • EEG traces accompanied by pontogeniculooccipital (PGO) spikes. (Page 34)

  • Brain's oxygen consumption is high, often higher than when awake. (Page 34)

  • Body's internal temperature shifts toward the surrounding temperature. (Page 34)

  • Heart and respiratory rates increase irregularly. (Page 34)

Effects of Preventing REM Sleep

  • Few negative effects observed after two weeks of REM sleep deprivation. (Page 35)

  • REM sleep rebound: Increased REM sleep after deprivation. (Page 35)

  • Monoamine oxidase inhibitors (MAOIs): Antidepressants that reduce REM sleep. (Page 35)

  • Total sleep deprivation is harmful to the organism. (Page 35)

  • Increased REM sleep after new or unusual situations. (Page 35)

  • Increased non-REM sleep after heavy physical exercise or hot weather. (Page 35)

Sleep and Memory Consolidation

  • Sleep aids in the consolidation of long-term memories. (Page 36)

  • Slow-wave sleep and REM sleep play different roles in memory consolidation. (Page 36)

Thinking About Past Experiences While Asleep

  • Participants who reported thinking about a virtual reality navigation task during sleep showed superior performance. (Page 38)

Sleep Physiology

  • EEG traces during REM sleep and Stage 1 NREM sleep are similar, so other devices are used to distinguish them: (Page 39)

    • Electromyograph (EMG): Records muscle contraction and detects muscle atonia in REM sleep. (Page 39)

    • Electro-oculograph (EOG): Records eye movements, including REM. (Page 39)

  • In some animals, the EEG trace during REM sleep is similar to wakefulness. (Page 39)

  • Paradoxical sleep: Another name for REM sleep, coined by Michel Jouvet. (Page 39)

EEG Frequency Ranges

Wave Type

Frequency (Hz)

Amplitude (μV)

Location

State

Beta

13-15 to 30-60

30

Frontal/Central

Awake, alert, actively processing information

Gamma

30-60+

Related to consciousness, making connections among brain regions

Alpha

8 to 12

30 to 50

Frontal/Central

Awake, eyes closed, relaxed, meditating

Theta

4 to 8

50 to 100

Limbic/Cortical

Drowsy, meditative, hypnotic, sleeping (Stage 1 & 2)

Delta

0.5 to 4

100 to 200

Deep sleep, coma

Flat-line

0

Brain death

Four Stages of Non-REM Sleep

  • Stage 1: Begins when you close your eyes, with alpha waves replaced by slower theta waves. (Page 43)

    • People awakened from Stage 1 report falling asleep or being in the process. (Page 43)

    • Each period lasts about 3-12 minutes. (Page 43)

  • Stage 2: Light sleep with predominant theta waves, sleep spindles, and K-complexes. (Page 44)

    • Sleep spindles: 8 to 14 Hz, 50 to 150 μV, may be involved in memory consolidation. (Page 44)

    • K-complex: Associated with brief awakenings, often in response to stimuli. (Page 44)

    • Lasts about 10 to 20 minutes in the early sleep cycle and accounts for nearly 50% of total sleep. (Page 44)

  • Stage 3: Transition to deep sleep with delta waves appearing. (Page 45)

    • Sleep spindles and K-complexes occur less often. (Page 45)

    • Lasts about 10 minutes during the first sleep cycle and accounts for about 7% of total sleep. (Page 45)

    • Muscles still have some tonus. (Page 45)

    • Sleepers show little response to external stimuli unless they are very strong or have personal meaning. (Page 45)

  • Stage 4: Predominant delta waves, lowest neuronal activity and brain temperature, reduced breathing, heart rate, and blood pressure. (Page 46)

    • Lasts about 35 to 40 minutes during the first sleep cycle and accounts for 15 to 20% of total sleep. (Page 46)

    • Most of the body's repair work takes place. (Page 46)

    • Most difficult to wake someone up. (Page 46)

REM Sleep Across the Lifespan

  • REM sleep in infants is about 50%. (Page 49)

  • Stabilizes in children at 20-25% of total sleep. (Page 49)

  • Declines significantly after age 60, to about 10-15% per night by 70 years old. (Page 49)

  • The large amount of REM sleep in infants is believed to assist neurodevelopment. (Page 49)

Dream Theories

  • Activation-synthesis model (Hobson & McCarley, 1977): The first neurobiological model of dream origin. (Page 50)

    • Rejected Freudian interpretations. (Page 50)

    • Images in dreams are random nerve impulses triggered by acetylcholine (ACh) release. (Page 50)

    • Dreams are the brain's attempt to extract coherent images from confusing signals. (Page 50)

  • Theory of active unlearning (Crick & Mitchinson, 1983): The brain examines stimuli and discards meaningless information during sleep. (Page 51)

    • Random neuronal activation plays a role in this "unlearning" process. (Page 51)

    • Obsessive ideas may be the main information eliminated through dreams. (Page 51)

  • Dreams as custodians of the memory of a species (Michel Jouvet): REM sleep preserves and modifies an individual's personality. (Page 52)

  • Cortical origin of dreams (Mark Solms): Dreams may arise in the cortex, not just the brainstem. (Page 53)

    • Damage to the occipito-temporo-parietal junction and frontal cortex can cause loss of dreaming. (Page 53)

    • Dreams may reprocess subjective events experienced previously. (Page 54)

  • Dreams during micro-awakenings (Jean-Pol Tassin): We may dream only as we are awakening. (Page 55)

    • Consciousness vanishes during sleep, and dreams require consciousness. (Page 55)

    • Dreams may be constructed from subliminal images generated during sleep. (Page 56)

Sleep Deprivation and Insomnia

  • Sleep deprivation: Diminished alertness, concentration, thinking ability, muscle fatigue, slowed reflexes, memory problems, mood swings, time and space disorientation, hallucinations, and long-term health problems. (Page 57)

  • Transitory insomnia: Affects 15-25% of Canadians. (Page 57)

  • Chronic insomnia: Affects about 10% of Canadians. (Page 57)

Sleep Problems and Disorders

  • Causes of chronic insomnia: Excessive noise, heat, or cold, internal or psychological factors. (Page 58)

  • Restless legs syndrome: Unpleasant sensations in the legs with an urge to move them. (Page 58)

  • Periodic limb movement disorder: Involuntary leg movements during deep sleep. (Page 58)

  • Sleep apnea: Collapse of the respiratory tract blocking airflow, leading to snoring and repeated awakenings. (Page 59)

    • Can cause cardiovascular problems and shorten life expectancy. (Page 59)

  • Depression and anxiety: Can disrupt sleep. (Page 59)

    • Depression: Waking up too early. (Page 59)

    • Anxiety: Difficulty falling asleep and waking during the night. (Page 59)

  • Fatal familial insomnia: Rare genetic degenerative condition affecting the thalamus. (Page 60)

    • Symptoms: Progressive insomnia, memory loss, cognitive deficits, dementia, high blood pressure, increased heart rate, anxiety, hallucinations, involuntary muscle twitching. (Page 60)

    • Onset: 20-70 years old. (Page 60)

    • Duration: 18 months, leading to death. (Page 60)

    • Treatment: Symptomatic relief and palliative care. (Page 60)

  • Narcolepsy: Hypersomnia characterized by excessive daytime sleepiness and sudden irresistible bouts of sleep. (Page 61)

    • Intrusion of REM sleep into waking life. (Page 61)

    • Hypocretins (orexins): Neuropeptides reduced in people with narcolepsy. (Page 62)

    • Cataplexy: Sudden decrease in muscle tonus, usually triggered by strong emotions. (Page 62)

    • Sleep paralysis: Temporary inability to speak or move while falling asleep or waking up. (Page 62)

    • Sleep hallucinations: Strange experiences resembling waking dreams. (Page 62)

    • Narcolepsy is often a genetic autoimmune condition. (Page 63)

    • Treatment: Stimulants like methylphenidate for sleep attacks and antidepressants for REM sleep phenomena. (Page 63)

Sleep Disorders - Parasomnias

  • Night terrors: Occur mainly in children 3-6 years old, characterized by screaming, crying, open eyes, incoherent speech, and confusion upon awakening. (Page 64)

    • No recall of elaborate dream imagery. (Page 64)

    • Occur during deep non-REM sleep (Stage 3 and 4). (Page 64)

    • Overactivation of the sympathetic nervous system. (Page 64)

  • Somnambulism (sleepwalking): Occurs in about 30% of children, 3% monthly, and 1-4% of adults. (Page 65)

    • Episodes last about 10 minutes and occur during deep non-REM sleep (Stage 4). (Page 65)

    • Not caused or accompanied by dreams. (Page 65)

    • Genetic component. (Page 65)

    • Triggered by noise, need to urinate, etc., waking the body but not the brain. (Page 65)

    • Gently guide sleepwalkers back to bed. (Page 65)

  • Somniloquy (talking in one's sleep): Can happen during REM or non-REM sleep, with poorly articulated and meaningless sentences. (Page 66)

  • Bruxism (teeth grinding): Repetitive, involuntary grinding of teeth, causing wear and tear and jaw muscle discomfort. (Page 66)

    • About half of people move their jaws in their sleep, but only 6% display bruxism. (Page 66)

  • REM sleep behavior disorder: Rare but sometimes seen in older people, characterized by acting out dreams during REM sleep. (Page 67)

    • People may injure themselves while externalizing their dreams. (Page 67)

    • Responds to benzodiazepine (clonazepam). (Page 67)

    • Often associated with Parkinson's Disease (PD). (Page 67)

Neuroanatomy of Sleep

  • Regulation of wakefulness involves several redundant brain structures. (Page 69)

  • Three structures that project to the cortex maintain the desynchronized EEG pattern of wakefulness: (Page 69)

    • Posterior hypothalamus: Produces wakefulness comparable to stimulating the reticular formation. (Page 70)

      • Releases less histamine during sleep. (Page 70)

    • Intralaminar nuclei of the thalamus: Contain thalamocortical neurons that project to the cortex and release excitatory amino acids. (Page 71)

      • These neurons fire in bursts during sleep, causing synchronized EEG patterns. (Page 71)

    • Basal forebrain (basal telencephalon): Composed of neurons that synthesize acetylcholine and/or GABA. (Page 72)

      • Stimulation causes wakefulness, but destruction causes a short-term decline in wakefulness. (Page 72)

  • The "executive network for wakefulness" is influenced by other brainstem systems. (Page 72)

  • The thalamus serves as a gatekeeper to the cortex, interrupting wakefulness signals at the onset of non-REM sleep. (Page 72)

Structures Influencing the "Executive Network for Wakefulness"

  • Anterior hypothalamus and preoptic area: Sensitive to serotonin released during waking periods. (Page 73)

    • Serotonin stimulation inhibits the posterior hypothalamus, promoting sleep. (Page 73)

    • Damage to GABAergic neurons in this area causes insomnia, while stimulation causes rapid sleep onset. (Page 73)

  • Reticular formation: Projects to the thalamic nuclei, influencing the cortex. (Page 74)

    • Desynchronizes the cortex, facilitating wakefulness and REM sleep. (Page 74)

  • Cholinergic mesopontine nuclei: Project to the thalamus. (Page 75)

    • Acetylcholine (ACh) reduces thalamic nucleus activity (part of the sleep system) and activates thalamocortical neurons involved in wakefulness. (Page 75)

  • Locus coeruleus: Noradrenergic, projects to the thalamus, hippocampus, and cortex. (Page 76)

    • Most active during wakefulness. (Page 76)

    • Less active during non-REM sleep. (Page 76)

    • Completely quiescent during REM sleep. (Page 76)

  • Anterior (superior) raphe: Serotonergic, projects to the hypothalamus and cortex. (Page 76)

    • Active during wakefulness. (Page 76)

The Brain During REM Sleep

  • Deactivation of the primary visual cortex (striate cortex): No external input. (Page 78)

  • Activation of the extrastriate cortex: Decodes complex visual scenes, leading to visual dreams. (Page 78)

  • Activation of the hippocampus: Learning and memory, contributing to memory consolidation after sleep. (Page 78)

  • Deactivation of the inferior parietal lobule: Conveys experiences to memory, explaining difficulty remembering dreams. (Page 78)

  • Activation of the limbic system: Amygdala and hippocampal region, contributing to the emotional aspect of dreams. (Page 80)

  • Deactivation of the prefrontal cortex (PFC): Suppression of reasoning, logical thinking, and judgment. (Page 80)

  • Activation of the anterior cingulate cortex (ACC): Governs attention and motivation, contributing to dream vividness. (Page 80)

  • Activation of the pons: REM sleep is triggered by nuclei in the pons, such as the nucleus reticularis pontis oralis (RPO). (Page 80)

  • Microinjection of ACh agonists into RPO induces REM sleep. (Page 81)

  • Simultaneous reduction in activity of the dorsal raphe nucleus and locus coeruleus (5-HT and NE) is necessary for REM sleep onset. (Page 81)

Molecules That Build Up and Make You Sleep

  • Henri Piéron and his dogs: CSF injections suggested that sleep is triggered by hypnogenic substances. (Page 82)

  • Two processes involved in sleep onset: (Page 82)

    • Production and build-up of hypnogenic substances while awake. (Page 82)

    • Cyclical fluctuations in substances like melatonin associated with the biological clock. (Page 82)

  • Adenosine: A hypnogenic substance studied extensively since the 1980s. (Page 82)

Adenosine

  • Blocking adenosine effects makes animals more alert. (Page 83)

  • Injecting adenosine agonists causes animals to fall asleep. (Page 83)

  • Adenosine concentration increases during the day and decreases at night, but stays high if animals are forced to stay awake. (Page 83)

Neural Control of Arousal

Neurotransmitter

Brain Region

Function

State

Acetylcholine

Pons, basal forebrain, medial septum

Increases cortical activation and arousal

High during waking

Norepinephrine

Locus coeruleus

Increases alertness and vigilance

High during waking

Serotonin

Raphe nuclei

Regulates mood, sleep, and appetite

High during waking

Histamine

Tuberomammillary nucleus (TMN) of posterior hypothalamus

Directly increases cortical activation and arousal, indirectly increases acetylcholine release

High during waking

Orexin

Lateral hypothalamus

Projects to almost every part of the brain with an excitatory effect, promotes wakefulness, especially during exploratory activity

High during alert or active waking

Circadian Rhythms and Zeitgebers

  • Circadian rhythms: Daily rhythms in behavior and physiological processes, approximately 24 hours. (Page 88)

    • Some are passive responses to changes in illumination. (Page 88)

    • Others are controlled by internal mechanisms. (Page 88)

  • Internal clocks: Endogenous rhythms synchronized by zeitgebers (time givers). (Page 88)

    • Light serves as a zeitgeber and resets the internal clock. (Page 88)

The Suprachiasmatic Nucleus (SCN)

  • Receives light information from the environment and entrains behaviors to a 24-hour cycle. (Page 89)

  • Provides primary control over the timing of sleep cycles. (Page 89)

  • Retinohypothalamic pathway: Visual system projects from the retina to the SCN. (Page 89)

  • Melanopsin: A special photoreceptor that provides information about ambient light levels. (Page 89)

SCN Control of Sleep and Waking

  • Subparaventricular zone (SPZ): Efferent axons of the SCN terminate here. (Page 91)

  • Projections to the ventrolateral preoptic area (vlPOA): Inhibitory, inhibit sleep. (Page 91)

  • Projections to orexinergic neurons: Excitatory, promote wakefulness. (Page 91)

  • The SCN can also control rhythms by secreting chemicals that diffuse through the brain. (Page 91)

Control of Seasonal Rhythms: The Pineal Gland and Melatonin

  • Melatonin: A hormone secreted by the pineal gland at night in response to input from the SCN. (Page 92)

    • Controls hormones, physiological processes, and behaviors that show seasonal variations. (Page 92)

Sexual Development

Terminology

  • Sex: Refers to the genetic or physiological characteristics of males and females. (Page 95)

  • Gender: Refers to the socially influenced identity, roles, and/or behavior of an individual. (Page 95)

  • Intersex: Broad term describing a variety of combinations of biologically male and female characteristics. (Page 95)

  • Transgender: Describes a gender identity that does not necessarily correspond to biological sex at birth. (Page 95)

Production of Gametes and Fertilization

  • Gametes: Produced during meiosis, a cell division process that produces cells with one set of each chromosome pair. (Page 96)

  • Fertilization: Genetic sex is determined at fertilization. (Page 96)

    • Genetic females: XX (Page 96)

    • Genetic males: XY (Page 96)

Determination of Genetic Sex

  • Genetic sex is determined by whether the sperm cell carries an X or Y chromosome. (Page 97)

    • X chromosome sperm produces females. (Page 97)

    • Y chromosome sperm produces males. (Page 97)

Development of the Sex Organs

  • Exposure to sex hormones before (organizational effects) and after birth (activational effects) contributes to sexual development. (Page 98)

  • Gonads: The first sex organs to develop, producing ova or sperm and secreting hormones. (Page 98)

  • Three categories of sex organs: Gonads, internal sex organs, and external genitalia. (Page 98)

Early Embryonic Development

  • Internal sex organs are bisexual in early embryos, containing precursors for both female and male organs. (Page 99)

  • Müllerian system: Embryonic precursors of the female internal sex organs. (Page 99)

  • Wolffian system: Embryonic precursors of the male internal sex organs. (Page 99)

  • Only one precursor develops during the third month of gestation. (Page 99)

  • Sry (sex determining region Y): Gene on the Y chromosome that instructs the gonads to develop into testes. (Page 99)

    • Leydig cells: Produce testosterone. (Page 99)

    • Sertoli cells: Produce anti-Müllerian hormone. (Page 99)

Anti-Müllerian Hormone

  • A peptide secreted by the fetal testes that inhibits the development of the Müllerian system. (Page 100)

  • Defeminizing effect: Reduces or prevents the development of female characteristics. (Page 100)

Testosterone and Dihydrotestosterone (DHT)

  • Testosterone: Principal androgen in males. (Page 101)

  • Dihydrotestosterone (DHT): Another androgen produced from testosterone. (Page 101)

  • Masculinizing effect: Promotes the development of male characteristics. (Page 101)

Genetic Conditions Illustrating Bisexual Embryonic Development

  • Androgen insensitivity syndrome: Lack of functioning androgen receptors, causing female external characteristics with testes but no internal sex organs in XY individuals. (Page 102)

  • Persistent Müllerian duct syndrome: Lack of anti-Müllerian hormone or receptors, causing development of both male and female internal sex organs in males. (Page 103)

Other Genetic Conditions Affecting Sexual Development

  • Turner's syndrome: Only one X chromosome, lack of ovaries, typical female sex organs and genitalia, no puberty without hormone therapy, most infertile. (Page 104)

  • Klinefelter's syndrome: Extra X chromosome (XXY), may affect testicular growth and testosterone production, reduced muscle mass, reduced body and facial hair, enlarged breast tissue, some men can father children with assisted reproductive procedures. (Page 105)

Hormonal Control of Development of the Internal Sex Organs

  • Gonadotropin-releasing hormones (GnRH): Hypothalamic hormone that stimulates the anterior pituitary to secrete gonadotropic hormones. (Page 107)

  • Gonadotropic hormones: Anterior pituitary hormones that stimulate the gonads. (Page 107)

    • Follicle-stimulating hormone (FSH): Causes development of an ovarian follicle and maturation of an ovum. (Page 108)

    • Luteinizing hormone (LH): Causes ovulation and development of the corpus luteum. (Page 108)

  • Estrogen: A class of sex hormones that cause maturation of female genitalia, breast growth, and other female characteristics. (Page 108)

    • Estradiol (E2): Principal estrogen in many mammals, including humans. (Page 108)

    • Estrone (E1): Most prominent after menopause. (Page 108)

    • Estriol (E3): Most prominent during pregnancy. (Page 108)

Hormonal Control of Sexual Behavior

Female Reproductive Cycles

  • Menstrual cycle: The female reproductive cycle of most primates, including humans, characterized by growth of the uterine lining, ovulation, development of a corpus luteum, and menstruation if pregnancy does not occur. (Page 110)

  • Estrous cycle: The female reproductive cycle of mammals other than primates. (Page 11

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