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Hormone Regulation in Elasmobranch Physiology

Explore the intricate hormonal mechanisms governing digestion, energy metabolism, growth, stress response, osmoregulation, color change, and reproduction in elasmobranchs. Discover the key players and pathways in maintaining physiological balance.

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Hormone Regulation in Elasmobranch Physiology

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  1. Hormone Regulation of Elasmobranch Physiology Chris Bedore and Shannon Long

  2. What We’ll Be Covering • Digestion and Energy Metabolism • Growth • Stress • Osmoregulation • Physiological Color Change • Reproduction • Reproduction • Reproduction • Research methods

  3. Things to Remember

  4. DIGESTION AND ENERGY METABOLISM

  5. The Players • Secretin—stimulates secretion of bicarbonate-rich pancreatic juices • Cholescystokinin (CCK)—regulates supply of bile and pancreatic enzymes • Somatostatin (SS)—suppress production of gastric acid, inhibit rectal gland secretion, inhibitory regulation of GH from hypothalamus • Neuropeptide Y (NPY)—promote digestion by increasing blood flow, inhibits gastric acid secretion, pancreatic enzyme release, and gallbladder contraction, inhibit rectal gland secretion • Bombesin/Gastrin-releasing peptide (GRP)—promote digestion by increasing blood flow, effecting acid/enzyme secretion/gut motility, inhibit rectal gland secretion

  6. Vasoactive intestinal polypeptide (VIP)—suppress digestion by reducing blood flow, effecting acid/enzyme secretion/gut motility, stimulates salt excretion by vasodilating the rectal gland and increasing cellular cAMP enzyme, used to regulate water and ion balance • Tachykinins—promote digestion by increasing blood flow, effecting acid/enzyme secretion/gut motility • Insulin—storage/conversion/uptake of energy substrate, pancreas, regulated by nutrient levels, reduction in circulating amino acid levels, no effect on ketones • Glucagon—antagonistic to insulin • Thyroid—alter levels of enzymes in amino acid/lipid metabolism

  7. DIGESTION AND ENERGY METABOLISM

  8. GROWTH

  9. The Players • Growth hormone (GH)—pituitary gland, regulated by GHRH, promotes somatic and skeletal growth • Growth hormone-releasing hormone (GHRH)—regulates GH, stimulatory from hypothalmus • Insulin-like growth factors (IGF-I)—promotes growth of vertebral column

  10. STRESS

  11. The Players • Chromaffin tissue—masses of neurosecretary cells on kidney, cells secrete epinephrine and norepinephrine, response to acute stress • Catecholamines—epinephrine and norepinephrine, promote mobilization, of energy reserves, increase blood pressure, blood flow to gut reduced, increase oxygen uptake in gills • Hypthalamo-Pituitary-Interrenal axis (HPI axis)—mid-axis lengthwise down body, helps to regulate ions

  12. Corticosteroids—interrenal body, regulated by ACTH, promote nutrient movement through body, inhibit growth and energy storage, aid in retention of sodium • Adrenocorticotropic hormone (ACTH)—regulates corticosteroids, stimulated by CRF, induces hyperglycemia • Corticotrophin-releasing factor (CRF)—hypothalamic compound, stimulates ACTH, regulate interrenal production of 1α-OHB • 1α-Hydroxycorticosterone (1α-OHB)—corticosteroid produced only in elasmobranchs, stimulate retention of sodium and chloride

  13. OSMOREGULATION

  14. The Players • Renin-angiotensin system (RAS)—used to regulate water and ion balance, series of biochemical steps 1. convert hepatic glycoprotein angiotensinogen to ANG I 2. cleavage to ANG I by ACE makes ANG II • Angiotensin I (ANG I)—inactive form • Renin—enzyme used to convert to ANG I, secreted by juxtanglomerular cells of kidney • Angiotensin converting enzyme (ACE)—promotes cleavage in ANG I to make ANG II • Angiotensin II (ANG II)—biologically active, receptors in interrenal gland/gill/rectal gland/intestine, modulate HPI axis, stimulates 1α-OHB secretion, promotes sodium retention, influence electrolyte balance by reducing GFR and UFR, inhibits salt release from rectal gland, increase drinking rate

  15. C-type natriuretic peptide (CNP)—used to regulate water and ion balance, stimulates production of VIP and rise in salt secretion, expressed in heart and brain, responds to increased cardiac pressure, directly affects rectal gland epithelial cells, binds to NPR-B to increase cGMP and PKC, dilates rectal gland to cause increase in salt release • Natriuretic peptide type-B (NPR-B)—in rectal gland epithelium • Cyclic granosine monophosphate (cGMP) • Protein kinase C (PKC) • Arginine vasotocin (AVT)—regulates osmoregulation, reduces diuresis

  16. PHYSIOLOGICAL COLOR CHANGE

  17. The Players • Melanocyte—type of chromatophore, contains melanosome which has brown-black melanin • α-Melanocyte-stimulating hormone (α-MSH)—regulates physiological color change, produced in neurointermediate lobe of pituitary, when removed- sharks lighten in color, when expressed- sharks darken, controlled by neural signals to hypothalamus • Melatonin—induces skin pallor • Prolactin (PRL)—in par distalis of pituitary, in freshwater ray, regulates physiological color change

  18. What Goes On Inside

  19. Reproductive Endocrinology- Overview diverse breeding strategies in elasmos therefore, probably diverse regulatory mechanisms this area is largely unknown and mostly hypothetical information is from hormone concentration at a specific time in mating season and deduced from other vert spp. well studied in only a few species (ex: D. sabina, S. tiburo)

  20. Reproductive Endocrinology- Overview Brain-Pituitary-Gonad (BPG) axis: primary endocrine regulation, initiated by env. stimuli

  21. Reproductive Endocrinology- Overview gonadal steroids: regulate gametogenesis, modulate reproductive behavior, modulate development and function of 2⁰ sex characteristics influence production of GnRH and GTH (neg. feedback) steroid binding sites in hypothalamus potential to alter production of relaxin, calcitonin, thyroid most cycle throughout mating season

  22. Reproductive Endocrinology- Anatomy

  23. Reproductive Endocrinology- Anatomy

  24. GnRH Gonadotropin-releasing hormone: many forms (7?), therefore many functions dfGnRH, sGnRH, cIIGnRH, mGnRH GnRH and GnRH-BPs present in systemic circulation direct action on gonads? different forms present in different parts of the brain Hypothalamus/Forebrain: regulate GTH

  25. GnRH Pituitary/Forebrain: regulate pituitary/gonads, convey env. info to initiate BPG

  26. GnRH Terminal nerve: regulate repro. processes?!

  27. GnRH Midbrain/Hindbrain: regulate sensory sensitivity during reproduction (ie-e-reception)? clasper movement

  28. GTH gonadotropin hormone pituitary gland partially regulate steroidogenesis, gametogenesis (systemic GnRH) response to GTH may depend on env. stimuli (H2O temp, photoperiod) and reproductive stage 2 types found so far in elasmos similar structure to FSH, LH in tetrapods? *future research*

  29. Female Steroids-Gonadal 3 major gonadal steroids: 17β-estradiol (estrogen)- E2 Progesterone- P4 Testosterone- T

  30. Female Steroids-Gonadal

  31. Female Steroids-Gonadal E2 2 peaks 1. pre-ovuation/follicle development stimulate vitellogenesis regulate development of oviducal gland 2. late gestation (Squalus acanthias) regulate vitellogenesis regulate secretion of histotroph (Dasyatis sabina)

  32. Female Steroids-Gonadal P4 suppress vitellogenesis (opposes E2) viviparous: peaks close to ovulation ↓ late gestation-permits next follicles to develop (S. acanthias) oviparous: regulate timing of oviposition (↑=oviposit)

  33. Female Steroids-Gonadal T and DHT (androgens) ↑ during follicle development precursor to E2 synthesis modulate copulatory behavior sperm storage (T) regulate oviposition? *future research- distribution of receptors*

  34. Female Steroids-Other

  35. Female Steroids-Other Relaxin (Rlx) found in ovary of several species implant and removal experiments- ↑ cervical area- prep for parturition probably aids pupping and oviposition maintains uterus during gestation (↓ contractions) Sphyrna tiburo- participates in ova release?

  36. Female Steroids-Other Thyroid (T3 and T4) interacts with BPG axis, role unknown ↑ during ovulation and gestation (D. sabina) associated with > metabolic costs at this time? S. tiburo highest levels- placental formation

  37. Female Steroids-Other Thyroid (T3 and T4) embryo- passed to young through yolk (McComb et al. 2005) regulate rate of development > concentration found in yolk from populations with: larger birth size faster rate of development greater size at maturity higher maternal investment

  38. Female Steroids-Other Calcitonin (CT) produced in ultimobranchial gland muscles between pharynx and pericardial cavity ↑ in response to E2 binding on gland maternal gill: ir-cells regulate Ca2+ homeostasis during gestation? mechanism/role unclear

  39. Female Steroids-Other Calcitonin (CT) S. tiburo: peaks during yolk dependent stage asstd w/digestion of yolk? ir-cells in duodenum & pancreas of early embyros

  40. Female Steroids-Other Calcitonin (CT) D. sabina: peaks during histotroph production no ir-cells in embryo, therefore not involved in embryo nutrition

  41. Male Steroids-Gonadal mostly produced in Sertoli cells (in testes) Leydig cells: supplements gonad steroids for regulating stages of spermatogenesis (epididymis and ductus deferens) trends differ among spp, but all regulate aspects of repro.

  42. Male Steroids-Gonadal 4 major gonadal steroids: Testosterone (T) Dihydrotestosterone (DHT) Progesterone (P4) 17β-estradiol (E2)

  43. Male Steroids-Gonadal

  44. Male Steroids-Gonadal T and DHT (androgens) ↑ middle to late spermatogenesis = peak GSI (high # spermatocytes in testes) influence development of spermatogonia and repro. ducts routes of hormone transfer between testes and urogenital system: systemic circulation, binding sites in spermatozoa, enzymes in semen

  45. Male Steroids-Gonadal T and DHT (androgens) claspers/cartilage: calcification due to androgens? indirect evidence, but no direct evidence coincides with androgen peak enlarged S. tiburo cephalofoil during male pubertal development but- implant/removal experiments showed no relationship mediated through GH and IGF-1 (after E2 peak)? *future studies*

  46. Male Steroids-Gonadal T and DHT (androgens)

  47. Male Steroids-Gonadal E2 unsure of role in males- some spp show cycling patterns (D. sabina), irregular variations in others (S. tiburo) D. sabina: receptors in epididymis and seminal vesicles maintain repro. tract function? peak early-middle spermatogenesis regulate early spermatogenesis? *future studies*

  48. Male Steroids-Gonadal P4 cycle mirrors androgens (S. tiburo) substrate for androgen synthesis? but- pubertal S. tiburo & D. .sabina: peak precedes androgen peak regulate spermiogenesis and/or spermiation?

  49. Male Steroids-Other Relaxin (Rlx) produced by gonads other verts: regulate male fertility S. tiburo: ↑ during late spermatogenesis and copulatory period [relaxinsemen]=1000x [relaxinblood] facilitate insemination through contractability of repro tract of postmated female?

  50. Male Steroids-Other Thyroid (T3 and T4) seasonal cycling peak spring and fall aid in ↑ metabolic needs during migration? *future studies*

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