Zool 343 Final Exam Notes PDF

Mammalian Reproduction 1. The Hypothalamic-Pituitary-Gonadal (HPG) Axis: Hypothalamus: Releases GnRH in a pulsatile fashion, which controls pituitary function. Anterior Pituitary: Secretes FSH and LH in response to GnRH. Gonad...

Mammalian Reproduction 1. The Hypothalamic-Pituitary-Gonadal (HPG) Axis: Hypothalamus: Releases GnRH in a pulsatile fashion, which controls pituitary function. Anterior Pituitary: Secretes FSH and LH in response to GnRH. Gonads: Males: Testes produce testosterone (androgens). Females: Ovaries produce estrogen and progesterone. 2. Hormonal Feedback: Negative feedback by testosterone (males) or estrogen/progesterone (females) regulates GnRH, FSH, and LH levels. Positive feedback in females during ovulation: High estrogen stimulates an LH surge, causing ovulation. 3. Differences in Males and Females: Males: Continuous production of sperm and testosterone. Females: Cyclic ovarian activity regulated by estrous or menstrual cycles. Sex vs. Gender 1. Biological Sex: Defined by physical traits: Chromosomal sex (XX or XY). Gonadal sex (testes or ovaries). Phenotypic sex (external genitalia, secondary sex characteristics). Determined during embryonic development by the SRY gene and hormonal signaling. 2. Gender: Psychological and social identity, not necessarily aligned with biological sex. Influenced by societal norms and individual experience. 3. Intersex Variations: Occur when chromosomal, gonadal, or phenotypic sex do not align. Examples: Androgen Insensitivity Syndrome (AIS): XY individuals develop female characteristics due to lack of androgen receptor response. Congenital Adrenal Hyperplasia (CAH): Excess androgen production causes masculinized genitalia in XX individuals. Gametogenesis: Spermatogenesis and Oogenesis 1. Spermatogenesis: Location: Seminiferous tubules in the testes. Process:  Spermatogonia (diploid stem cells) divide mitotically. Primary spermatocytes undergo meiosis I, producing two haploid secondary spermatocytes. Secondary spermatocytes undergo meiosis II, producing four haploid spermatids. Spermatids mature into spermatozoa via spermiogenesis. Regulation: FSH: Stimulates Sertoli cells to support spermatogenesis. Testosterone: Produced by Leydig cells under LH stimulation, essential for sperm production. 2. Oogenesis: Location: Ovarian follicles. Process: Oogonia divide mitotically during fetal development. Primary oocytes are arrested in prophase I until puberty. During ovulation, meiosis I completes, forming a secondary oocyte (arrested in metaphase II) and a polar body. Meiosis II completes only upon fertilization. Regulation: FSH: Stimulates follicular growth. LH: Triggers ovulation and corpus luteum formation. Ovary and Testes Development 1. Testes Development: SRY Gene: Located on the Y chromosome, encodes Testis-Determining Factor (TDF). TDF induces differentiation of Sertoli cells and Leydig cells. Hormonal Signals: Sertoli cells secrete anti-Müllerian hormone (AMH), causing regression of Müllerian ducts. Leydig cells produce testosterone, promoting Wolffian duct development into internal male reproductive structures (e.g., epididymis, vas deferens). 2. Ovary Development: In the absence of the SRY gene, the gonadal ridge differentiates into ovaries. Müllerian ducts persist and develop into the uterus, fallopian tubes, and upper vagina. Lack of testosterone results in the regression of Wolffian ducts. Sexual Differentiation  1. Stages of Differentiation: Chromosomal Sex: Determined at fertilization (XX or XY). Gonadal Sex: Presence of SRY results in testes; absence results in ovaries. Phenotypic Sex: Determined by hormones: Testosterone and DHT drive male genital development. Absence of testosterone results in female genital development. 2. Critical Hormones: Testosterone: Stimulates Wolffian duct differentiation into male internal genitalia. DHT (dihydrotestosterone): Promotes external male genitalia development (e.g., penis, scrotum). AMH: Causes Müllerian duct regression in males. Puberty: Hypotheses 1. Hypothalamic Maturation Hypothesis: Puberty begins when the hypothalamus increases GnRH secretion. Triggered by changes in sensitivity to steroid negative feedback. 2. Gonadostat Hypothesis: Puberty occurs when hypothalamic and pituitary sensitivity to gonadal steroid inhibition decreases, leading to increased LH and FSH secretion. 3. Energy Availability: Puberty may be influenced by metabolic signals like leptin, which signals adequate energy reserves for reproduction. Two-Cell Model 1. Ovarian Steroidogenesis: Theca Cells: Stimulated by LH to produce androgens (e.g., androstenedione). Granulosa Cells: Stimulated by FSH to convert androgens into estrogens (e.g., estradiol) via aromatase. 2. Male Equivalent: Leydig cells (stimulated by LH) produce testosterone. Sertoli cells (stimulated by FSH) support spermatogenesis and androgen-binding protein secretion. LH Signaling Events (Lectures 23/24)  1. Mechanism of Action: LH binds to G-protein-coupled receptors (GPCRs) on target cells. Activates adenylate cyclase, increasing intracellular cAMP. cAMP activates protein kinase A (PKA), leading to gene transcription and steroid production. 2. Ovarian Effects: LH Surge: Triggers ovulation by promoting follicle rupture. Stimulates luteinization of granulosa and theca cells, forming the corpus luteum. 3. Testicular Effects: LH stimulates Leydig cells to produce testosterone, critical for spermatogenesis and male secondary sexual characteristics. Luteolysis 1. Definition: Luteolysis is the breakdown of the corpus luteum (a temporary endocrine structure formed after ovulation) when pregnancy does not occur. 2. Mechanism: Triggered by prostaglandin F2α (PGF2α), produced by the uterus. PGF2α reduces luteal blood flow and suppresses progesterone production. 3. Purpose: Ensures that progesterone levels fall, allowing the next estrous or menstrual cycle to begin. 4. Pregnancy Exception: If pregnancy occurs, signals like human chorionic gonadotropin (hCG) in humans or interferon tau in ruminants prevent luteolysis, maintaining progesterone to support the pregnancy.m Uterine Cycle 1. Phases of the Uterine Cycle: Menstrual Phase: Shedding of the uterine lining if no implantation occurs. Triggered by falling progesterone and estrogen levels. Proliferative Phase: Estrogen from developing follicles stimulates the regrowth of the endometrium. Secretory Phase: After ovulation, progesterone from the corpus luteum prepares the endometrium for implantation. If no implantation occurs, luteolysis leads to endometrial shedding.  2. Hormonal Regulation: FSH and LH stimulate follicular development and ovulation. Estrogen promotes endometrial regrowth. Progesterone maintains the endometrium during the secretory phase. Parturition (Childbirth) 1. Stages: Stage 1: Cervical Dilation: Begins with uterine contractions. Oxytocin and prostaglandins stimulate stronger contractions. Stage 2: Delivery of Fetus: Coordinated uterine and abdominal contractions expel the baby. Stage 3: Delivery of Placenta: Placenta detaches and is expelled. 2. Hormonal Control: Estrogen: Increases uterine sensitivity to oxytocin. Oxytocin: Triggers uterine contractions, creating a positive feedback loop. Prostaglandins: Amplify contractions and soften the cervix. 3. Fetal Role: The fetus secretes cortisol, which enhances placental estrogen production, initiating labor. Lactation 1. Preparation During Pregnancy: Estrogen: Promotes ductal growth. Progesterone: Stimulates lobular-alveolar development. Prolactin: Prepares mammary glands for milk synthesis. 2. Milk Production: After parturition, progesterone and estrogen levels fall, removing their inhibitory effects on prolactin. Prolactin: Stimulates milk production in alveolar cells. Oxytocin: Promotes milk ejection by contracting myoepithelial cells around alveoli. 3. Lactational Amenorrhea: Suckling suppresses GnRH release, reducing FSH and LH secretion and delaying ovulation. Menopause 1. Definition: Permanent cessation of menstrual cycles due to ovarian follicle depletion. 2. Hormonal Changes:  Decline in estrogen and progesterone as ovarian activity ceases. Increase in FSH and LH due to lack of negative feedback from ovarian hormones. 3. Symptoms: Hot flashes, mood changes, and loss of bone density (osteoporosis) due to estrogen deficiency. 4. Evolutionary Implications: Post-reproductive lifespan allows for increased investment in offspring and grandchildren. Reproductive Cycles 1. Estrous Cycle (Non-Primate Mammals): Phases: Proestrus: Follicle development, rising estrogen levels. Estrus: Ovulation and peak sexual receptivity (“heat”). Metestrus: Corpus luteum forms, producing progesterone. Diestrus: High progesterone maintains uterine lining. 2. Menstrual Cycle (Primates): Uterine lining is shed during the menstrual phase. Involves follicular and luteal phases regulated by estrogen and progesterone. 3. Seasonal Breeders: Animals like sheep and deer have cycles controlled by day length (photoperiod). Melatonin levels influence GnRH secretion. General Reproductive Features Nonmammalian reproduction shows immense diversity, including external fertilization (e.g., in fish and amphibians) and internal fertilization (e.g., reptiles and birds). Strategies vary between: Oviparous species: Lay eggs (e.g., most fish, reptiles, and birds). Ovoviviparous species: Retain eggs internally until hatching (e.g., some sharks and reptiles). Viviparous species: Give live birth (e.g., some bony fishes and reptiles). Testicular Features Nonmammalian testes structure and function: Amphibians and Fish: Simple tubular testes with seasonal spermatogenesis. Reptiles and Birds: More complex testes with continuous or seasonal activity. Key Hormones:  FSH: Stimulates spermatogenesis. LH: Regulates testosterone production in Leydig cells. Ovarian Features Ovaries in nonmammalian species contain follicles at various stages of development. Follicle development: Vitellogenesis: Yolk production, stimulated by estrogen. Ovulation: Triggered by LH. Clutch Size: Ovaries are adapted for species-specific strategies, ranging from a few eggs (e.g., birds) to hundreds (e.g., bony fishes). Sexual Determination Genetic Determination: Birds: ZZ (male) and ZW (female) sex chromosomes. Reptiles: Varied mechanisms, including XY and ZW systems. Environmental Determination: Reptiles and some fish: Sex determined by temperature or social hierarchy. Agnathan Fishes (Jawless Fish, e.g., Lampreys and Hagfish) 1. Reproduction: Mostly external fertilization. Seasonal breeders with simple gonads and no ducts. 2. Key Hormones: GnRH-like peptides regulate reproductive cycles, with seasonal peaks in gonadotropin activity. Chondrichthyan Fishes (Cartilaginous Fish, e.g., Sharks and Rays) 1. Reproductive Modes: Exhibit internal fertilization using claspers in males. Viviparity and oviparity are both common. 2. Testicular and Ovarian Features: Testes have sperm-storage structures. Ovaries produce large, yolky eggs. 3. Hormonal Regulation: Prolactin and estrogen play roles in ovary function and egg development. Bony Fishes (Teleosts) 1. Spawning: External fertilization is common; eggs are released into water. Spawning may be triggered by environmental cues like temperature and photoperiod. 2. Spermatogenesis: Occurs in lobular testes.  Regulated by FSH (sperm production) and LH (testosterone production). 3. Follicle Hormones: Estrogen: Stimulates vitellogenin synthesis in the liver. Progesterone: Involved in final oocyte maturation and ovulation. 4. Key Hormones: GnRH regulates FSH and LH, controlling gametogenesis. Prolactin and growth hormone influence osmoregulation and reproduction. Amphibians 1. Reproductive Modes: Mostly external fertilization, with eggs laid in water. Some species show internal fertilization (e.g., salamanders). 2. Hormonal Regulation: FSH: Promotes gamete production. LH: Triggers ovulation and androgen production. Prolactin: Regulates parental behaviors and metamorphosis. 3. Seasonality: Breeding is synchronized with environmental cues like temperature and rainfall. Reptiles 1. Reproductive Strategies: Exhibit internal fertilization. Can be oviparous, ovoviviparous, or viviparous. 2. Sexual Determination: Temperature-dependent sex determination (TSD) is common: Higher temperatures often produce one sex (e.g., males in some turtles). 3. Hormonal Regulation: Estrogen promotes oviduct development and vitellogenesis. Progesterone supports egg retention in viviparous species. Birds 1. Reproductive Features: Strictly oviparous, laying shelled eggs. Females have a single functional ovary (usually the left). 2. Testes and Spermatogenesis: Testes are internal and shrink outside the breeding season. Sperm production occurs at lower temperatures in specialized sacs. 3. Ovarian Function: Estrogen stimulates yolk deposition. LH triggers ovulation. 4. Hormonal Regulation:  Prolactin regulates incubation behavior and brood patch development. Photoperiod is a key regulator of reproductive timing. Role of the Hypothalamus: Appetite Regulation 1. Key Centers in the Hypothalamus: Arcuate Nucleus: Contains two critical groups of neurons: Orexigenic (appetite-stimulating) neurons: Secrete neuropeptide Y (NPY) and AgRP (agouti-related peptide). Anorexigenic (appetite-suppressing) neurons: Secrete POMC (pro-opiomelanocortin) and CART (cocaine- and amphetamine-regulated transcript). Ventromedial Hypothalamus (VMH): Acts as a satiety center. Lateral Hypothalamus (LH): Stimulates hunger. 2. Signals Influencing Appetite: Hunger Signals (Orexigenic): Ghrelin: Produced by the stomach when empty, activates orexigenic neurons. Satiety Signals (Anorexigenic): Leptin: Secreted by adipose tissue in proportion to fat stores; suppresses appetite. Insulin: Signals nutrient abundance, reducing food intake. CCK (Cholecystokinin): Released from the small intestine during meals to suppress hunger. Bioregulators: Orexigenic vs. Anorexigenic Agents 1. Orexigenic Agents (Increase Appetite): Ghrelin: Produced by the stomach before meals. Stimulates NPY/AgRP neurons in the hypothalamus. Neuropeptide Y (NPY): Stimulates food intake and reduces energy expenditure. AgRP: Inhibits the anorexigenic melanocortin pathway. 2. Anorexigenic Agents (Suppress Appetite): Leptin: Released by adipocytes. Activates POMC/CART neurons, suppressing hunger. Insulin: Signals energy abundance, reducing hunger. CCK: Released during digestion to signal satiety. PYY:  Secreted by the ileum and colon; inhibits NPY secretion. Leptin Signal and Integration 1. Role of Leptin: A hormone secreted by adipose tissue. Acts on the hypothalamus to: Inhibit NPY/AgRP neurons. Stimulate POMC/CART neurons. Suppresses appetite and increases energy expenditure. 2. Leptin Resistance: Common in obesity, where high leptin levels fail to suppress hunger. Likely due to impaired leptin signaling in the hypothalamus. 3. Integration with Other Signals: Leptin works alongside insulin, ghrelin, and CCK to balance energy intake and expenditure. Feeding 1. Neural Regulation: Feeding behavior is influenced by hypothalamic centers and peripheral signals (e.g., ghrelin and leptin). 2. Behavioral Triggers: Hunger and satiety cues are influenced by visual, olfactory, and social factors in addition to physiological signals. Digestion: Acid Secretion Control 1. Stomach Acid Secretion: Parietal Cells in the stomach secrete HCl, regulated by: Gastrin: Produced by G-cells in response to food. Stimulates parietal cells to secrete HCl. Histamine: Released by enterochromaffin-like (ECL) cells. Activates H2 receptors on parietal cells, increasing acid production. Acetylcholine: Released by vagus nerve, directly stimulates parietal cells. 2. Inhibition of Acid Secretion: Somatostatin: Released by D-cells in response to low pH. Inhibits gastrin and acid secretion. Prostaglandins: Reduce acid production and protect the stomach lining. Pancreas: Digestion and Glucose Regulation  1. Exocrine Function: Secretes digestive enzymes (e.g., amylase, lipase, proteases) into the duodenum. Bicarbonate secretion neutralizes stomach acid. 2. Endocrine Function: Produces hormones to regulate blood glucose: Insulin (from β-cells): Lowers blood glucose by promoting cellular uptake. Glucagon (from α-cells): Raises blood glucose by stimulating glycogenolysis and gluconeogenesis. Insulin vs. Glucagon 1. Insulin: Released in response to high blood glucose (e.g., after meals). Promotes: Glucose uptake in cells (via GLUT4 transporters). Glycogenesis (storage of glucose as glycogen). Lipogenesis (fat storage). 2. Glucagon: Released in response to low blood glucose (e.g., fasting). Promotes: Glycogenolysis (breakdown of glycogen into glucose). ol Gluconeogenesis (synthesis of glucose from non-carbohydrate sources). Lipolysis (breakdown of fats for energy). 3. Opposing Actions: Insulin and glucagon work antagonistically to maintain blood glucose homeostasis. Stress Response 1. Acute Stress: Hypothalamus triggers the release of: Catecholamines (epinephrine and norepinephrine) from the adrenal medulla. Effects: Increased heart rate, blood pressure, and energy availability. Glycogen breakdown and lipolysis. 2. Chronic Stress: Hypothalamic-Pituitary-Adrenal (HPA) Axis: Hypothalamus releases CRH, stimulating ACTH secretion from the pituitary. ACTH stimulates cortisol release from the adrenal cortex.  Effects of Cortisol: Mobilizes glucose through gluconeogenesis. Suppresses immune function and promotes protein breakdown. Nonmammalian Feeding, Digestion, and Metabolism 1. Overview: Nonmammalian vertebrates, particularly teleost fishes, exhibit a wide variety of feeding strategies, digestive mechanisms, and metabolic pathways due to their diverse ecological niches. Teleost Feeding and Digestion: Key Features and Exceptions 1. Feeding Strategies: Teleosts include herbivores, carnivores, omnivores, and filter feeders. Feeding behavior depends on adaptations like teeth structure, mouth position, and jaw mechanics. 2. Digestive System: Teleost digestion typically involves: A stomach (in carnivorous and omnivorous species). Intestines varying in length based on diet (longer in herbivores, shorter in carnivores). 3. Exceptions: Stomach-Less Teleosts: Some teleosts (e.g., cyprinids like carp) lack a stomach. Instead, they rely on an alkaline digestive environment and enzymes like amylases and proteases. Pyloric Caeca: Present in many teleosts, these finger-like projections near the stomach increase surface area for digestion and absorption. No Gallbladder: Some species lack a gallbladder but have alternative bile secretion mechanisms. 4. Metabolism: Adapted to environmental factors (e.g., water temperature, oxygen availability). Rely more on protein catabolism for energy compared to mammals, which rely on carbohydrates and fats. Pancreas: Teleosts vs. Mammals 1. Structure: In mammals: The pancreas has distinct exocrine and endocrine regions. In teleosts:  The pancreas is often diffuse, with endocrine and exocrine cells scattered in the mesentery, liver, or intestines. This integration varies by species. 2. Exocrine Function: Similar to mammals: Secretes digestive enzymes like amylases, lipases, and proteases into the intestine. 3. Endocrine Function: Both teleosts and mammals have pancreatic islets that secrete hormones like insulin and glucagon Teleost islets are termed Brockmann bodies and may be more numerous and scattered. 4. Differences in Islet Distribution: Mammals: Islets of Langerhans are confined within the pancreas. Teleosts: Islets are separate structures (Brockmann bodies) near blood vessels for efficient hormone distribution. A-Cells and B-Cells Ratios 1. Mammals: Pancreatic islets typically contain: 70–80% B-cells (produce insulin). 15–20% A-cells (produce glucagon). 5–10% other cells (e.g., somatostatin-producing D-cells). 2. Teleosts: Higher Proportion of A-Cells: A-cells (glucagon producers) may be more prominent than in mammals. This reflects a greater reliance on protein metabolism for gluconeogenesis, where glucagon plays a critical role. B-cell numbers vary but tend to be lower relative to mammals. 3. Physiological Implications: In teleosts: Glucagon dominance aligns with their high-protein diets. Insulin plays a less significant role in carbohydrate metabolism compared to mammals. Calcium and Phosphate Endocrine Relationship 1. Overview: Calcium and phosphate levels in the body are tightly regulated to maintain: Bone health. Neuromuscular function.  Energy metabolism (e.g., ATP synthesis). These ions are interrelated: High phosphate levels can bind calcium, reducing its availability. Hormonal regulation ensures a balance between the two. 2. Key Hormones Involved: Parathyroid Hormone (PTH): Increases blood calcium by stimulating bone resorption, enhancing calcium reabsorption in the kidneys, and activating vitamin D. Vitamin D (Calcitriol): Promotes calcium and phosphate absorption in the gut. Calcitonin: Lowers blood calcium by inhibiting bone resorption. Calcium Extraction 1. Sources of Calcium: Dietary sources (e.g., dairy products, leafy greens). Absorbed in the small intestine under the influence of vitamin D. 2. Bone as a Reservoir: 99% of the body’s calcium is stored in bones as hydroxyapatite. Bones release calcium during resorption when blood calcium levels drop. 3. Renal Handling of Calcium: Kidneys filter calcium, reabsorbing 98% in the proximal tubules and loops of Henle. PTH increases calcium reabsorption in the distal tubules. Key Cells in Calcium and Phosphate Homeostasis 1. Osteoblasts: Bone-forming cells. Deposit calcium and phosphate into the bone matrix. Stimulated by calcitonin. 2. Osteoclasts: Bone-resorbing cells. Break down bone, releasing calcium and phosphate into the bloodstream. Stimulated by PTH and inhibited by calcitonin. 3. Osteocytes: Mature bone cells derived from osteoblasts. Regulate bone remodeling by sensing mechanical stress and signaling osteoblasts and osteoclasts. 4. Kidney Tubular Cells: Regulate calcium and phosphate reabsorption under the influence of PTH and vitamin D. 5. Enterocytes:  Absorb dietary calcium and phosphate in the small intestine, facilitated by vitamin D. Role of Parathyroid Hormone (PTH) 1. Secretion: Produced by the parathyroid glands in response to low blood calcium levels. Regulated by calcium-sensing receptors (CaSR) on parathyroid cells. 2. Actions of PTH: Bone: Stimulates osteoclast activity to release calcium and phosphate. Kidneys: Enhances calcium reabsorption in the distal tubules. Reduces phosphate reabsorption to prevent calcium-phosphate precipitation. Intestines: Indirectly increases calcium and phosphate absorption by activating vitamin D. 3. Feedback Regulation: Rising blood calcium levels inhibit PTH secretion via negative feedback. Hormone Synthesis 1. Parathyroid Hormone (PTH): Synthesized as a preprohormone in the parathyroid glands. Cleaved into active PTH before secretion. 2. Vitamin D: Synthesized from cholesterol: UV light converts 7-dehydrocholesterol in the skin to vitamin D3. Liver converts D3 to 25-hydroxyvitamin D. Kidneys convert 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D (calcitriol), under PTH stimulation. 3. Calcitonin: Produced by the parafollicular cells (C-cells) of the thyroid gland. Synthesis increases in response to high blood calcium. Summary Calcium and phosphate homeostasis is a dynamic process regulated by PTH, vitamin D, and calcitonin. Key organs involved include: Bones (storage and release). Kidneys (reabsorption and excretion). Intestines (absorption). Imbalances can lead to:  Hypocalcemia: Muscle spasms, cardiac issues. Hypercalcemia: Kidney stones, weakened bones. Clock Lecture Circadian rhythms regulate biological processes in a ~24-hour cycle, allowing organisms to synchronize with their environment. This system is driven by specialized neuronal structures, molecular clock genes, and external cues like light. Neuronal Structures Involved 1. Suprachiasmatic Nucleus (SCN): The master clock located in the hypothalamus. Receives direct input from light-sensing pathways. Synchronizes peripheral clocks in tissues and organs. 2. Retinohypothalamic Tract (RHT): Carries light signals from the retina to the SCN. Specialized photoreceptors (e.g., melanopsin-containing ganglion cells) detect light. 3. Peripheral Clocks: Found in almost all tissues (e.g., liver, muscle). Regulated by the SCN but can respond to local cues (e.g., feeding schedules). 4. Pineal Gland: Produces melatonin, a hormone that signals darkness and regulates sleep-wake cycles. Role of Light 1. Zeitgeber (“Time Giver”): Light is the primary environmental cue that entrains circadian rhythms to the external day-night cycle. 2. Mechanism: Melanopsin-containing retinal ganglion cells sense light. Signals travel via the RHT to the SCN. SCN adjusts its timing by regulating gene expression and neural outputs. 3. Blue Light Sensitivity: Melanopsin is particularly sensitive to blue light (~480 nm), which is effective in resetting the circadian clock. 4. Effects of Light Disruption: Shift work, jet lag, and artificial light exposure can desynchronize the SCN, leading to metabolic and behavioral issues. The Master Clock: SCN 1. Location: Bilateral structure located above the optic chiasm in the hypothalamus.  2. Function: Orchestrates circadian rhythms by regulating hormone release, body temperature, and sleep-wake cycles. 3. Mechanisms: Synchronizes peripheral clocks via: Neural pathways. Hormonal signals (e.g., cortisol, melatonin). 4. Redundancy and Robustness: SCN neurons communicate with each other to maintain precise rhythmicity, even under fluctuating environmental conditions. Clock Genes 1. Core Clock Genes: CLOCK and BMAL1: Form a transcriptional activator complex. Promote the expression of other clock genes like PER and CRY. PER (Period) and CRY (Cryptochrome): Form a repressor complex that inhibits CLOCK/BMAL1 activity, completing the feedback loop. 2. Mechanism: The molecular clock operates via transcription-translation feedback loops (TTFLs) with ~24-hour cycles. Positive Loop: CLOCK/BMAL1 activates PER and CRY. Negative Loop: PER/CRY inhibit CLOCK/BMAL1. 3. Output Genes: Regulate downstream processes, such as metabolism, cell division, and hormone secretion. Monarch Butterfly 1. Circadian Regulation in Migration: Monarch butterflies rely on their circadian clock to navigate during migration. Use both the sun compass and an internal clock to determine direction. 2. Neurobiology: Circadian control is located in the brain and synchronized by light. 3. Clock Genes: Similar to mammals, PER, CRY, and TIM (Timeless) are key genes in monarch butterflies. These genes regulate time-compensated sun compass navigation. 4. Role of Light: Light resets the monarch’s clock daily, ensuring precise navigation over long distances. Impact on Birds 1. Climate Change and Migration: Migration timing in birds has shifted due to climate change. For example: Migrating birds now spend 9 more days in northern parts than before. Changes in environmental conditions have advanced male gonadal activation by several days annually. 2. Physiological Effects: Birds rely on cues like temperature and photoperiod to regulate reproductive cycles. Disruptions in these cues lead to mistimed breeding, affecting population dynamics. Opioids and Cannabinoids 1. Endocannabinoid System (ECS): ECS consists of endogenous ligands similar to THC and CBD. Plays a crucial role in: Modulating the hypothalamic-pituitary-adrenal (HPA) axis during stress. Inhibiting glutamate release via retrograde signaling, reducing excitatory input to stress centers like the hypothalamus. 2. Cannabinoid Signaling and Seasonality: Melatonin modulates the ECS to regulate seasonal hormonal rhythms like prolactin release. Interactions between melatonin and ECS ensure adaptation to seasonal changes. 3. Opioid System: Endogenous opioids modulate pain, stress, and endocrine functions. Opioids influence hormone release from the pituitary by acting on hypothalamic neurons. Diabetes 1. Overview: Diabetes results from dysregulated blood glucose levels due to: Type 1 Diabetes: Insufficient insulin production by pancreatic β-cells. Type 2 Diabetes: Insulin resistance in target tissues. 2. Impact on Metabolism: Elevated blood glucose leads to glucosuria (glucose in urine) when renal glucose reabsorption capacity is exceeded. Chronic glucosuria can cause kidney damage and failure. 3. Endocrine Complications: Diabetic conditions alter normal hormone feedback, further worsening insulin secretion and glucose uptake. Obesity significantly increases the risk of developing Type 2 Diabetes due to adipose tissue-induced inflammation and insulin resistance.