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Psych230 Exam 3
| Question | Answer |
|---|---|
| what are hormones | chemicals, secreted by a group of cells (i.e. gland) that travel through the bloodstream to act on targets |
| what are endocrine galnds | glands that release hormones within the body |
| what are exocrine glands | glands that use ducts to secrete fluids such as tears and sweat outside the body |
| endocrinology | study of endocrine glands and their associated hormones |
| what is castration | removal of gonads |
| who conducted the first formal study of endocrinology | Arnold Berthold |
| what happened in Arnold's study when he removed the testes of a rooster | during development, the roosters displayed neither the appearance nor the behavior of a normal rooster as adults |
| how do normal roosters left undisturbed behave and grow to be? | They grew up to have large red wattles and combs, to mount and mate with hens readily, and to fight one another and crow loudly |
| what happens if one of the tests was reimplanted into the abdominal cavity of a rooster immediately after removal in Arnold's study? | rooster developed normal wattles and normal behavior |
| what were Arnold's findings | demonstrated that a product released from the testes into the blood was necessary for an immature chicken to develop into a normal male rooster both behaviorally and physically |
| what is synaptic communication? | involves chemical release into the synaptic cleft for action on the postsynaptic membrane |
| what are characteristics of synaptic communication | - travels only across a synaptic cleft to act on a receptor - signal travels along a laid path - very fast |
| what is endocrine commuication? | hormone is released into the bloodstream to act on target tissues |
| what are characteristics of endocrine communication? | - spreads anywhere throughout the body if there is a blood supply - can act on cells with appropriate receptors - relative slower (has to travel thru blood to find target receptors) |
| what are neuroendocrine/neurosecretory cells? | neurons that release hormones into the blood |
| what is autocrine function? | a released chemical acts on the releasing cell |
| what is pheromone function? | hormones can be used to communicate between individuals of the same species |
| where are pheromones released | into the environment |
| what is allomone function | chemicals that released by one species that affect the behavior of another species (ex: skunks, flowers and bees) |
| what are the general principles of hormone action? | - act in a gradual fashion - behavior and hormones relationship is reciprocal - may have multiple effects - often act in a pulsatile secretion pattern (i.e. bursts) - able to interact with other hormones and change their effects |
| can hormones affect more than one target? | yes, also some targets are affected by more than one hormone |
| what does it mean by hormones act in a gradual fashion? | they act by changing the probability or intensity of a behavior |
| what does it mean when the relationship between behavior and hormone is bidirectional/reciprocal | hormones can affect behavior and behavior can affect hormones |
| can one behavior be affected by several hormones | yes |
| what is peptide/protein hormones | made up of strings of amino acids |
| is it a peptide or protein hormone if it's only a few amino acids in length | peptide hormone |
| is it a peptide or protein hormone if it's >50 amino acids in length | protein hormone |
| what is the most common type of hormone found in mammals | peptide/protein hormones |
| where are peptide/protein hormones found in | can be stored within the cell (in vesicles) |
| can peptide/protein hormones pass through cell membranes | no (too big) |
| what are examples of peptide/protein hormones | insulin, oxytocin, leptin |
| what are amine hormones | - modified amino acids called monoamine hormones - they're derived from single amino acids |
| what are the two classes of amine hormones that affect behavior | indoleamines and catecholamines |
| what kind of hormone that are monoamines but don't affect behavior | thyroid hormones |
| how do protein and amino hormones act | - bind to specific receptors embedded within the cell membrane and cause release of a second messenger which brings about changes in cellular function - action is relatively fast (effect on order of ms to min) |
| what are steroid hormones? | small, lipophilic hormones made up of four rings of carbon atoms (derivatives of cholesterol) that come from the adrenal glands |
| can steroid hormones pass through cell membranes | yes, but some may require carrier proteins or cofactors |
| examples of steroid hormones | estrogens, androgens |
| how do steroid hormones act | - pass thru cell membrane and bind to receptors inside the cell - steroid receptor complex binds to DNA in the nucleus and acts as a transcription factor, controlling gene expression and protein production (effects long lasting) |
| what does it mean when a steroid hormone as genomic action | affects the cell by binding to DNA and controls for gene expression and protein production |
| what does it mean when a steroid hormone has nongenomic action | it has a faster brief effect involving neuronal membrane receptors |
| what are neurosteroids | steroids made in the brain including testosterone and estrogens |
| how are many steroid hormones made | by combining an enzyme with a different hormone (ex: aromatase) |
| what does aromatase do | it's an enzyme that can convert testosterone into estrogens inside a cell |
| how can some chemicals act as both neurotransmitters and hormone | depending on the cell that releases them and where they are released and act |
| what is negative feedback | output feeds back and inhibits further secretion |
| what is positive feedback | output feeds back and increases furhter secretion |
| what does an autocrine negative feedback loop involve | involves endocrine cells releasing a hormone whose presence feeds back on the endocrine cells |
| what is target cell feedback | - hormone acts on its target cells and has a biological effect - the biological effect is detected by the endocrine gland and further release is inhibited (ex: insulin released in response to glucose after eating) |
| what are the two parts that make up the pituitary gland | posterior and anterior pituitary |
| what are the two principal hormones secreted by the posterior pituitary | oxytocin and vasopressin |
| what neurons synthesize oxytocin and vasopressin | neurons in the supraoptic nucleus and paraventricular nuclei of the hypothalamus |
| once secreted where does oxytocin and vasopressin travel | along the pituitary stalk and into the blood supply in the posterior pituitary where they are released |
| where do axons of hypothalamic neuroendocrine cells that synthesize releasing hormones converge | on the median eminence above the pituitary stalk |
| where are releasing hormones secreted by and where are they carried to | into blood vessels called the hypophyseal portal system and are carried to the anterior pituitary |
| what do the releasing hormones stimulate the release of in the anterior pituitary | tropic hormones into general circulation where they'll travel thru the body to their targets |
| what influences the hypothalamic neuroendocrine cells that synthesize releasing hormones | - circulating messages (other hormones, blood sugar, immune system products) - synaptic inputs from other brain areas |
| what does the release of CRH (corticotropin releasing hormone) from the hypothalamus affect the release of | ACTH, CRH has a positive input on the tropic hormone ACTH (adrenocorticotropic hormone) in the anterior pituitary |
| what's the main target of ACTH after it's released | adrenal cortex where it then secretes corticosteroids |
| what tropic hormone is affected by the release of GnRH (gonadotropin releasing hormone) or GnIH (gonadotropin inhibiting hormone) | LH (luteinizing hormone) or FSH (follicle stimulating hormone) in the anterior pituitary |
| what is the main target of LH and FSH | testes and ovaries |
| what hormone is released by testes | androgens such as testosterone |
| what hormone is secreted by the ovaries | estrogens, progestins |
| hormones can affect both physiology and ____ | behavior |
| how does oxytocin affect physiology | it stimulates uterine contraction and is involved in milk letdown |
| how does oxytocin affect behavior | it's released during nursing interactions and during orgasm to facilitate bonding |
| what is sex | - biological sex, the physical body - the biological and physiological characteristics that distinguish females from males |
| what is gender | - social concept, self-identification - includes socially constructed roles, relationships, behaviors, relative power, and other traits societies ascribe to women and men |
| what is sex determination | - process by which the decision is made for a fetus to develop as a male or female - chromosome driven - if sperm that enters the egg has a Y chromosome, then offspring is male, if X chromosome, offspring is female |
| what is sexual differentiation | - process by which individuals develop either male or female bodies and behaviors - whether gonads are testes or ovaries - hormone driven |
| the gonads are what when they are first made | bipotential |
| what does it mean when gonads are bipotential | the same gonad can become either testes or ovaries |
| what is the SRY gene | - sex determining region of the Y chromosome that codes for the development of testes from the bipotential gonad |
| what happens if the SRY gene isn't present | ovaries form |
| what are the two purposes of gonads | - production of gametes (sperm & eggs) - production of steroid hormones |
| what are steroid hormones required for | gamete production, development of secondary sex characteristics, behaviors that bring gametes together |
| what are the male gonads | testes |
| what is the primary steroid hormone produced by the testes and when does production begin | - Testosterone, which is an androgen - Testosterone production begins as soon as the testes are formed in utero |
| what does the production of testosterone help guide | masculine development |
| what are the female gonads | ovaries |
| what is the primary steroid produced by the ovaries | estrogens and progestins |
| when are the steroids produced by the ovaries | during puberty |
| what do the hormones secreted early on by the gonads (mainly from testes) direct | sexual differentiation of internal and external sex organs |
| what are the wolffian ducts | precursors to the male system and develop into the epididymis, vas deferens, and seminal vesicles, and the Mullerian system shrinks |
| what are the mullerian ducts | precursor to the female system and develop into the oviducts, uterus, and vagina |
| what happens if testes are present | it secretes anti-mullerian hormone (AMH) and testosterone |
| what happens when AMH is secreted | it causes the regression of the Mullerian system (defeminizing) |
| what happens when testosterone is released | masculinizes the internal organs by promoting the developing of the wolffian system |
| what does DHT do and how is it made | 5 alpha reductase converts testosterone to dihydrotestosterone (DHT) which masculinizes external structures (induces skin to form scrotum; tubercle forms penis) |
| what happens if there is a lack of DHT | the external genitalia is feminized (skin forms labia and outer vagina, tubercle forms clitoris |
| what happens if there is an absence of AMH | mullerian ducts form oviducts, uterus, and inner vagina |
| what happens in absence of testosterone | wolffian ducts regress, and no prostate gland forms |
| what hormone masculinizes the brain during early development and how is it made | estradiol which is formed when testosterone is aromatized via aromatase |
| what is Turner's syndrome | person only have one sex chromosome, a single X chromosome |
| what happens when someone has Turner's syndrome | the individual develops as a female, due to a lack of the SRY gene with abnormal ovaries (no steroid hormone production or eggs) |
| what type of treatment is given to someone with Turner's syndrome and what does it cause | estrogen treatment which induces breast growth and a female typical puberty |
| what is Klinefelter's syndrome | person has an extra chromosome --> XXY |
| what happens to someone that has Klinefelter's syndrome | - masculine body develops (due to Y chromosome) - testes and penis are abnormally small - low testosterone production (little to no sperm produced) |
| what therapy is given for someone with Klinefelter's syndrome so they can develop secondary sex characteristics | hormone replacement therapy is required for development of secondary sex characteristics |
| what is congenital adrenal hyperplasia (CAH) | where someone lacks 21-hydroxylase that normally produces cortisol |
| what is the result of CAH | there's an increased amount of androgen (testosterone) output from the adrenal gland |
| why is there an increased amount of testosterone when someone has CAH | the cortisol normally negatively feeds back on the hypothalamus, without it there's a constant production of ACTH and the adrenal gland relieves that stress by producing testosterone |
| what happens to females with CAH | their external genitalis is partially masculinized bc of exposure to increased DHT during development |
| who does androgen insensitivity syndrome (AIS) normally occur in and what does it cause | occurs in XY people and they have defective androgen receptors so androgens can't have action |
| what is the phenotype of individuals with AIS | female |
| what hormones will be produced in an individual with AIS | testosterone and thus DHT and AMH |
| will someone with AIS develop testes or ovaries | testes |
| when do ovaries start producing hormones | during puberty |
| what is sexual dimorphism | condition in which males and females exhibit marked sex differences in appearance |
| what area is important for reproductive behavior in males | sexually dimorphic nucleus of the pre-optic nerve (SDN-POA) |
| what happens when a female rat is injected with testosterone at the time of male perinatal surge | she develops a large SDN-POA |
| what happens if testosterone is injected later in female rats | it'll have no effect on the female |
| does a female rate have a larger SDN-POA or do male rats | male rats --> have testosterone peak perinatally and a second rise at puberty |
| how does the organizational effect of estradiol permanently alter the brain and when does it occur | - does things like altering apoptosis, changing synaptic connectivity, and affecting densities - occurs early in development during the critical period when brain is still developing |
| can the same hormone be organizational AND activational? if so, what is the deciding factor? | yes, deciding factor is timing of its action |
| when does a steroid hormone have an organizational effect | only when present during the critical period of development |
| when is the critical period of development | depending on the species and the behavior, it may be before birth or just afterwards, in the neonatal period |
| why do females not become masculinized during fetal development? | - ovaries are quiescent until puberty - maternal estrogen in developing females doesn't enter the brain |
| what prevents estrogen from crossing into the brain thus preventing masculinization | alpha-fetoprotein |
| what are characteristics of organizational effect of gonadal steroid hormones | - structural changes in brain - permanent - occurs before brain matures - critical period |
| what are characteristics of activational effects of gonadal steroid hormones | - biochemical changes - transitory - occurs in adulthood - no sensitive period |
| are there exclusively "male" and "female" hormones | no, the two sexes differ in the proportion of these steroids |
| what is the process of gastrulation | where the human embryo develops three cell layers |
| what are the three cell layers developed by the human embryo | ectoderm, mesoderm. endoderm |
| what happens when the ectoderm thickens | it grows into a flat neural plate |
| what becomes the midline | the neural groove which is formed by uneven rates of cell division |
| what eventually becomes the CNS | the neural tube which transforms from the neural groove after cells continue to push upwards |
| what are the three subdivisions of the anterior part of the neural tube | forebrain, midbrain, and hindbrain |
| what does the interior part of the neural tube become | cerebral ventricles |
| how does the peripheral nervous system develop | the neural crest cells pinch off at the top and migrate extensively to contribute to the PNS |
| when is the embryo called a fetus | after 10 weeks |
| what is a genotype | sum of all the genetic information that we inherit |
| what is the genotype determined upon and does it change | fertilization and it doesn't change |
| what is a phenotype | sum of the physical characteristics that make up an individual |
| does our phenotype change and why | - Yes because it's affected by experiences - reason why genetically identical twins look different |
| what controls whether and when cells use genes during neural development | environmental influences including experiences |
| what is gene expression | cell expresses a gene when it transcribes the gene and starts making the protein it encodes |
| what does gene expression help guide | helps guide cellular differentiation |
| what is cellular differentiation | when cells become a particular type depending on what genes are expressed |
| what can gene expression also result in | long term behavioral changes in the organism due to early experiences |
| what is epigenetics | study of factors that affects gene expression without changing the sequence of the genes |
| what are different ways to alter gene expression | histone modification and methylation |
| what does methylation do | modifies the DNA and reduces expression of the genes following the site of methylation |
| what effects can maternal care have on epigenetic effects | low licking and grooming results in increased methylation of the stress hormone receptor gene --> less receptors made (more stress hormones needed to be produced to turn stress axis off and animals exhibit a heightened stress axis and higher anxiety) |
| what effects does high licking and grooming result in | - reduced methylation of stress hormone receptor gene --> more receptors made resulting stress axis being able to shut off sooner as hormone can find receptor more rapidly) - animals exhibit reduced stress response and lower anxiety |
| what are intrinsic factors | instructions from within the cell |
| what is lineage | each cell can be mapped and is born with specific instructions as to its fate |
| what are extrinsic factors | factors that include other cells (cell to cell interactions) or chemicals in their environment that can turn on/off certain genes |
| what do extrinsic factors allow for | more flexibility |
| what are examples of extrinsic factors that negatively impact development | teratogens or alcohol |
| what is teratology | study of pathological effects of early exposure to toxic substances |
| what is intellectual disability | variety of conditions that impede mental grown |
| what examples of conditions that impede mental grown | - transient lack of oxygen at birth (hypoxia) can affect the brain - undernourished mothers may have underweight children who may suffer from brain abnormalities - maternal viral infections and drug exposure can cause developmental disorders |
| what is phenylketonuria (PKU) | recessive genetic disorder where the individual doesn't produce an enzyme that metabolizes phenylalanine which is an amino acid present in a variety of foods |
| what can be a result of phenylketouria | brain can be damaged due to phenylalanine buildup which becomes toxic |
| what happens when PKU is detected after birth | child gets placed on a low phenylalanine diet to reduce brain impairment (esp important before age of 2) |
| what are the 6 stages of nervous system development | neurogenesis, cell migration, differentiation, synaptogenesis, neuronal cell death, synapse rearrangement/synaptic remodeling |
| what is neurogenesis | mitotic production of neurons from nonneuronal cells |
| how is the ventricular zone formed | cells dividing through mitosis |
| where are cells born and where do they migrate to | cells are born in the ventricular zone and ten migrate outward where they can differentiate into neurons or glial cells |
| what is the principle of cell migration | movement of cells away from ventricular zone to establish distinct population |
| how are cells arranged in the cerebral cortex | in cortical columns |
| what type of cells populates cortical columns and what do they do | radial glial cells; act as guides for cells to migrate along |
| in what kind of fashion do cells establish themselves in and what does it mean | - inside out fashion - as new cells are born, they move over the existing cells and settle in layer sabove them |
| what are cell adhesion molecules (CAMs) | proteins on cell surfaces that guide cell migration when cells migrate further distances |
| what do migrating cells have that responds to chemicals in the environment and those released by target cells | growth cones |
| what are chemoattractants | chemical signals that attract certain growth cones |
| what are chemorepellants | chemical signals that repel growth cones |
| what are filopodia | outgrowths of growth cones |
| what is filopodia important for | - detecting and processing environmental signal - movement of the migrating axon as they adhere to CAMs in the environment and pull the growth cone in a particular direction |
| what is the stage of differentiation | transformation of precursor cells into distinctive neurons or glial cells |
| what can limit the specific fate of cells and how | - extracellular factors the precursor cell comes in contact with including other cells and environmental signals - the chemical signals can turn on/off certain genes guiding the cell towards a specific fate |
| what happens when a cell reaches their destination | they express specific genes to make the proteins they need for their cell type. This allows a cell to acquire its specific appearance and function for its final destination |
| what is an example of flexibility from using extrinsic factors | when notochord releases a protein (called Sonic hedgehog) that diffuses to the spinal cord and induces the cells in the ventral regions to be motor neurons → called induction |
| what is regulation and how might it be used | - when the developing animal compensates for missing or injured cells - might be used in response to early injury where some cells might get injured or lost |
| what is the stage of synaptogenesis | - establishment of synaptic connections - extensive growth of axons and dendrites and the generation of synapse |
| what is the biggest factor for increasing brain size | synaptogenesis |
| what happens to the nerve cell body in order for it to support the dendritic tree | the cell body increases in volume |
| what happens once axons reach their final destination | they induce nearby glia to ensheathe them in myelin |
| when does the most intense phase of myelination occur | shortly after birth, extending into young adulthood |
| what is the stage of neuronal cell death | selective death of many nerve cells |
| what are many more cells made then needed | - ensures you have enough good cells - easier to make them all at once than to have to turn neurogenesis back on |
| what do cells undergo when they aren't needed | apoptosis |
| what happens in the process of apoptosis | - cells turn on death genes during apoptosis - these genes code for caspases which kills off the cells |
| what are caspases | family of proteases that cut up proteins and DNA |
| what do neurons compete for, so they won't die | neurotrophic factors (chemicals that target cells make) |
| what are nerve growth factor (NGF) | produced by targets and taken up by the axons of innervating neurons keeping them alive |
| what do brain derived neurotrophic factor (BDNF) and other members of the neurotrophins family do | save cells from undergoing apoptosis |
| what can hormones act as to save cells from dying | act as trophic factors |
| what does the stage of synapse rearrangement/synaptic remodeling do | loss of development of synapses to refine synaptic connections |
| what is one influence that influences synaptic survival | neural activity --> "cells that fire together, wire together" |
| what can also contribute to synaptic survival | neurotrophic factors |
| how is synaptic remodeling evidence in humans? | - evident in the thinning of the gray matter in the cortex as pruning of dendrites and axon terminals progresses - the thinning process continues in a caudal-rostral direction during maturation so prefrontal cortex matures last |
| what occurs in people with fragile X syndrome | - there is multiple trinucleotide repeats in a particular gene that makes the DNA unstable and prone to breakage - individuals exhibit distinct physical features and wide ranges of cognitive effects |
| what is homeostasis | active process of maintaining a relatively stable balanced internal environment |
| what is thermoregulation | the active process of closely regulating body temperature around a set value |
| what does thermoregulation help prevent | - proteins from denaturing when too hot and prevents chemical reactions from slowing or ice crystals from forming and destroying cells when too cold |
| how do endotherms generate heat | generate their own heat through internal processes such as metabolism and muscular activity |
| what are some advantages and disadvantages of endotherms generating their own heat | - con: uses a lot of food energy - pro: independence from environmental conditions and improved oxygen use capacity sustains greater muscular activity |
| are homeostasis mechs that regulate temperature, body fluids, and metabolism primarily positive or negative feedback | negative |
| what happens when there is deviation from a set point | results in compensatory action |
| what is a set zone | range of tolerance in a system |
| what is the basic mammalian thermoregulatory system | Receptors in skin, body core, and hypothalamus detect temps and transmit info to spinal cord, brainstem, hypothalamus If body temp is outside set zone, these neural regions can initiate physiological and behavioral responses to return temp to set zone |
| how do ectotherms get their heat | get most of their heat from the environment |
| do ectotherms regulate body temperature behaviorally, physiologically, or both | ONLY by behavior |
| what area of the hypothalamus is important for thermoregulation | preoptic area (POA) |
| what are the two separate thermoregulatory systems | POA and lateral hypothalamus |
| what is the preoptic area responsible for | the physiological responses to cold, such as shivering and constriction of the blood vessels |
| what does lateral hypothalamus control | behavioral regulation of temperature, such as turning on heat lamps or cooling fans |
| what are the three strategies used in behavioral regulation | 1. change exposure of the body surface (ex: basking on a hot rock) 2. change external insulation (ex: adding another layer of insulation) 3. change surroundings (seek shade) |
| where does most of our water reside | in the intracellular compartment |
| what is the intracellular compartment | fluid contained within our cells |
| what is the extracellular compartment | fluid outside our cells |
| how does water move in and out of cells | through aquaporins via osmosis |
| what is osmosis | passive movement of a solvent to move through a membrane in order to equalize the concentration of solute |
| what is osmotic pressure | physical force that pushes or pulls water across the membrane |
| what is osmolality | number of solute particles per unit volume of a solvent |
| what is an isotonic salt solution | about 0.9% (physiological saline) and is the same as in mammalian fluids |
| what is the difference between a hypertonic vs a hypotonic solution | hypertonic solution has more salt compared to hypotonic solution which has less salt than an isotonic solution |
| what happens if a cell is surrounded by a saltier (hypertonic) solution | they will lose water |
| what happens when a cell is surrounded by a less salty (hypotonic) solution | water will push into the cell |
| what are the two kinds of thirst | osmotic and hypovolemic thirst |
| what is osmotic thirst stimulated by | stimulated by high extracellular solute concentration |
| how is osmotic thirst triggered | through obligatory water loss by normal physiological processes like respiration, perspiration, and urination along with eating salty foods |
| what do Osmosensory neurons in the hypothalamus respond to | changes in osmotic pressure as water is drawn out of cells by osmosis |
| how can fix osmotic thirst when its triggered | by drinking water to bring out extracellular compartment back to an isotonic state |
| how is physiological processes kicked off in response to osmotic thirst | aldosterone is released from the adrenal gland in response to thirst signals which stimulates the kidneys to conserve Na+ which aids water retention |
| what happens if physiological processes aren't enough to fight osmotic thirst | your body will stimulate behavioral processes via the circumventricular organs to get you to drink water to remedy thirst |
| where do the circumventricular organs lie in | the walls of the ventricles where the neurons can monitor salt and hormones in the blood |
| what is hypovolemic thirst stimulated by | - reduced extracellular volume (loss of water volume) like in the case of blood loss, vomiting, and diarrhea |
| what are the concentrations changed during hypovolemic thirst | no because solutes are also lost |
| what do baroreceptors in major blood vessels and heart do | detect the drop in blood pressure |
| what does a drop in blood pressure trigger | triggers the brain to activate responses such as thirst and salt hunger along with several hormone systems being activated |
| what does hypovolemia cause the release of | vasopressin (AVP) or antidiuretic hormone (ADH) from the posterior pituitary gland |
| what does vasopressin do | induces blood vessel constriction and reduces water flow to the bladder |
| what does the kidney do to further conserve water | releases renin which triggers a hormonal cascade resulting in circulation of angiotensin II |
| how does the release of angiotensin II conserve water | - constricts blood vessels - increasing blood pressure - releasing vasopressin and aldosterone - acts at the circumventricular organs to stimulate drinking |
| what hormone is reduced during hypovolemia | atrial natriuretic peptide (ANP) from the heart which causes increased blood pressure, stimulates drinking, and inhibits excretion of water |
| what is the process of digestion controlled by | the nervous system |
| what is glucose | principle sugar used for energy |
| what is glycogen | complex carbohydrate made by combining glucose molecules an d stored for a short time in the liver and muscles |
| what is glycogenesis | process of converting glucose to glycogen and is regulated by insulin |
| where is insulin released from | beta cells in the pancreas |
| what is glucagon and what does it do | a pancreatic hormone released by alpha cells in the pancreas which mediates glycogenolysis |
| what is glycogenolysis | conversion of glycogen back into glucose |
| what kind of storage is lipids for and where is it deposited in | used for long term storage and deposited in adipose tissues |
| what happens under prolonged food deprivation | gluconeogenesis kicks in to convert fat and proteins to glucose and ketones |
| where are glucose transporters found and what do they interact with and do | they span the cell membrane and interact with insulin to bring glucose into the cell |
| what organ doesn't need insulin to get glucose into the cells | the brain |
| what are the three sequential mechs/phases that trigger insulin release | cephalic, digestive, and absorptive phase |
| what happens during the cephalic phase | the sensory stimulus of food evokes insulin release in anticipation |
| what happens during the digestive phase | food causes gut hormone release which stimulates the pancreas to secrete insulin |
| what happens during the absorptive phase | glucodetectors in the blood and liver detect glucose and signal the pancreas to release insulin |
| what is diabetes mellitus caused by | failure of insulin to induce glucose absorption |
| what is type I diabetes mellitus | pancreas doesn't produce insulin |
| what is type II diabetes | primarily a consequence of reduced sensitivity to insulin |
| what is satiety | feeling of fulfilment or satisfaction |
| what is hunger | the internal state of an animal seeking food |
| how signals does the brain integrate to decide whether to initiate eating | integrates glucose and insulin signals along with other info such as hormone |
| what is the hypothalamus important for the regulation of | - metabolic rate - food intake - body weight |
| what is the satiety center in the hypothalamus | ventromedial hypothalamus (VMH) |
| what is the hunger center found in the hypothalamus | lateral hypothalamus (LH) |
| what is the arcuate nucleus of the hypothalamus critical for | integrating peptide hormone signals from the body |
| what are the two hormones important for appetite control | ghrelin and PYY |
| what does ghrelin do | works as an appetite stimulant |
| where is ghrelin synthesized and released | by endocrine cells of the stomach |
| what type of cell releases PYY | intestinal cells |
| when does ghrelin reach high levels | before eating and drops after eating |
| when does PYY reach high levels | after eating |
| what does PYY work as | appetite suppressant |
| what does the POMC neurons do | act as satiety neurons when activated and inhibit appetite and increase metabolism |
| what does NPY neurons do | act as hunger neurons and stimulate appetite and reduce metabolism when activated |
| how does ghrelin act on NPY hunger neurons | stimulates them and increases appetite |
| how does PYY act on NPY neurons | inhibits them and reduces appetite |
| where do appetite signals converge | on the nucleus of the solitary tract (NST) |
| what is cholecystokinin (CCK) | peptide released by the gut after feeding and acts on the vagus nerve to inhibit appetite |
| what hormone do fat cells release into the blood stream to provide info to the brain about long term energy reserves | leptin |
| what does leptin do | activates POMC neuron but inhibit NPY neurons so it works to suppress hunger |
| Mice with two copies of the obese gene have | defective leptin genes so it doesn't produce leptin making it become obese |
| what does a defect in leptin production or sensitivity give | a false reporting of body fat, causing animals to overeat |
| what does the evolutionary theory predict about | that there will be strong selection for individuals who are able to maximize their genes in the next generation |
| what is the female limiting factor to reproductive success | time and energy |
| what is the male limiting factor to reproductive success | the number of fertile females he can mate with |
| what is the male strategy to reproductive success | mate with as many fertile females during the short tenure (~2 yrs) as the alpha male |
| what do males do so females can become fertile | they kill unrelated dependent infants which accelerates mother's return to fertility. This feticidal and infanticidal males' sire next offspring earlier |
| what are female strategies for reproductive success | - select a mate with good healthy genes (alpha is a good bet) - invest in each offspring just enough to ensure survival on their own then wean first offspring and start investing in a new offspring - live a long life |
| what are female counterstrategies to infanticide | confuse reproduction, accelerate reproduction, or suppress reproduction |
| what is confuse reproduction | confuse males about paternity and/or confuse males about fertility |
| what does accelerate reproduction mean | give up on current reproduction and immediately move on to the next reproduction |
| what is suppress reproduction | wait to reproduce until a "better" time |
| what is the Bruce effect | induce abortion in pregnant females |
| what is the Vandenbergh effect | induce estrus in juvenile females |
| what is estrus | it makes females go into heat/be willing to mate and become capable of receive |
| what is the Whitten Effect | induce estrus in all adult females |
| most females find males extremely aversive during anestrus. What happens to reverse it | when she becomes estrus, there's a reverse in hormones making them want to mate |
| male HPG axis | hypothalamus releases GnRH --> (+) anterior pituitary which releases FSH and LH --> (+) testes (FSH on the Sertoli cells; LH on the lydig cells) --> testosterone releases which negatively feed backs on the anterior pituitary and hypothalamus |
| how is the female HPG axis like during the follicular phase | hypothalamus releases GnRH --> (+) anterior pituitary to releases FSH and LH onto the ovary and follicle --> causes release of estradiol from the ovaries which negatively feeds back onto the anterior pituitary |
| how is the female HPG axis like during ovulation | hypothalamus releases GnRH --> (+) anterior pituitary to releases FSH and LH onto the ovary and follicle --> causes release of estradiol from the ovaries which positively feeds back onto the anterior pituitary |
| what happens during the luteal phase with the female HPG axis | hypothalamus releases GnRH --> (+) anterior pituitary to releases LH onto the ovary --> causes release of progesterone from the ovaries which negatively feeds back onto the anterior pituitary |
| what hormone is released from the anterior pituitary during the luteal phase that's different from the follicular phase and ovulation | just releases LH because the corpus luteum is formed so you don't need FSH to stimulate the follicles |
| what's the difference between a rat's estrous cycle compared to a human menstrual cycle | rats don't have a spontaneous luteal phase until they mated thus their rise in progesterone is before ovulation while humans are after ovulation during the luteal phase |
| what are the 3 components of female sexual behavior | attractivity, proceptivity, and receptivity |
| what is attractivity | stimulus value for a male |
| what is proceptivity | extent to which female initiates copulation |
| what is receptivity | responsiveness to male's sexual advances |
| what does gonadotropin inhibitory hormone (GnIH) do | it's a hypothalamic hormone that suppresses reproductive function by inhibiting GnRH release which prevents gonadotropic hormone release (LH and FSH) |
| what does GnIH function as | a physiological brake on the reproductive axis and must be "lifted" for reproduction to occur since it's always produced |
| what happens to lactating females after male takeover | They produce fake swellings while continuing to lactate which fools males into not killing their kids |
| what mediates false fertility | estrogen appears to mediate both true and false sexual swellings with females showing a rise in estrogen regardless of how old their infant is each time there's a male takeover |
| what happens to pregnant females after male takeover | they produce true swellings and aborting their pregnancy to move on to the next kid (Bruce effect). Miscarriage indicated by estrogen |
| feticide vs. Bruce effect | - Feticide – when direct aggression from a male causes a female to terminate a pregnancy - Bruce effect – when the mere presence of a male causes a female to terminate a pregnancy (female becomes motivated to mate with him) |
| what mediates the Bruce effect | an increase in exogenous estrogens cause both the Bruce and Vandenbergh effect in mice in a pleiotropic effect |
| Is the Bruce effect in geladas pheromonal | probably not, thought that the Bruce effect must be a social trigger in geladas much like horses where they don't need to come into contact with each other. Geladas don't have functioning vomeronasal organs |
| is it adaptive to abort | By resetting female reproduction, the Bruce effect ensures that the new male will likely be around through weaning (Only abort only if they’re sure the new male will be around long enough for them to have a kid and is able to be weaned off) |
| when is reproductive suppression adaptive | adaptive if future prospects for reproduction are better than current prospects. if future conditions are likely to be better than current ones --> terminate reproduction; if unlikely to improve, continue with reproduction |
| what happened to immature females after male takeover | - some females appear sped up maturation while others suppressed maturation to avoid inbreeding if their father is the alpha male |
| what mediates maturation? | all immature females had a rise in estrogens after takeover |
| what is circadian rhythm | functions of a living organism that display a rhythm of about 24 hrs |
| why have a circadian rhythm | - Synchronizes an animal’s behavior and body states to daily rhythms in the environment - Endogenous clock enables animals to anticipate an event and help with survival |
| what does it mean when an animal is diurnal | active during the light/day |
| what does it mean when an animal is nocturnal | active during the dark/night |
| what is entrainment | process of synchronizing the rhythm with external cues |
| what is Zeitgeber | the cue that an animal uses to synchronize with the environment |
| what is a phase shift | shift in activity in response to a synchronizing stimulus such as light or food |
| what does a free running animal do | maintain its own cycle without external cues |
| where is the mammalian biological clock located | in the suprachiasmatic nucleus (SCN) which is located above the optic chiasm in the hypothalamus |
| what pathway does light info go from the eyes to the SCN | via the retinohypothalamic pathway |
| do the ganglion cells in the retinohypothalamic pathway rely on rods and cones | no |
| what do most of the retinal ganglion cells in the retinohypothalamic pathway contain | melanopsin which is a special photopigment that makes them sensitive to light esp blue light |
| what evidence is there that shows the SCN housing a circadian clock | - Circadian rhythms disrupted in animals with SCN lesions - Isolated SCN neurons can maintain electrical activity synchronized to the previous light cycle - rhythms in hamsters restored after SCN transplant which matched the shorter period of the donor |
| what mutations impacts circadian rhythmicity | - tau mutations --> period is shorter than normal - double clock mutants are severely arrhythmic |
| what alleles are different in people who are energetic in the morning compared to night owls | different alleles in the clock and per genes |
| what is infradian rhythms | biological rhythms longer than a day (ex: menstrual cycle) |
| what are examples of exogenous factors that drive annual rhythms | food availability and temperature |
| what is ultradian rhythm | biological rhythms shorter than a day (ex: bouts of activity, feeding, and hormone release), occur more than once per day and period length can be from mins to hrs |
| what is sleep synchronized to | external events including light and ark |
| what entrains us to be awake or asleep and what happens in the absence of cues | - stimuli like foods, lights, jobs, and alarm clocks entrain us - in the absence of cues, many humans have a free running period of approx. 25 hrs |
| what does electroencephalography (EEG) do | record electrical activity in the brain |
| what does an electrooculography (EOG) do | record eye movements |
| what does an electromyography (EMG) do | record muscle activity |
| what are the two distinct classes of sleep | Non-REM (NREM) and Rapid-eye movement sleep (REM) |
| what is NREM characterized by | - 3 stages (Stage 1, 2, and SWS) - lack of rapid eye movement |
| what is REM sleep characterized by | small amplitude, fast EEG waves, no postural tension, and rapid eye movement - have profoundly relaxed muscle tone (atonia) |
| what characterizes slow wave sleep (SWS) | - there's enough muscle tone to maintain posture - recognized by large slow delta waves |
| what is postural tension and which class of sleep does it occur in | - muscles completely inhibited so you don't get up and act out dreams - occurs in REM sleep |
| what is a typical night of sleep in a young adult like | - Sleep time ranges from 7-8 hrs or 4-5 cycles - 45-50% is stage 2 sleep, and 20% is REM sleep - Cycles last 90-110 mins (example of an ultradian rhythm) -- cycles early in the night have more stage 3 SWS and later cycles have more REM sleep |
| what happens to circadian rhythm at puberty | circadian rhythm of sleep shifts so that they get up later in the day |
| how does human sleep pattern change with age | - Mammals sleep more during infancy than in adulthood - Infant sleep is characterized by shorter sleep cycles and more REM sleep - As people age, total time sleep declines, number of awakenings increases, and less time is spent in stage 3 sleep |
| what are the biological functions of sleep | - conserve energy - enforces niche adaptation - restores body and brain - aids memory consolidation |
| what is the correlation between sleep and plant eaters | among plant eaters, small animals sleep more than larger ones in correlation with their normal, high metabolic rate |
| is there a correlation between predatory species and sleep | no such correlation, they tend to sleep much more than prey species |
| being nocturnal or diurnal is part of an animal's what | ecological niche (unique assortment of environmental opportunities and challenges to which each organism is adapted) |
| when do animals sleep | - sleep helps animals avoid predators so animals sleep during the part of the day when they are most vulnerable - animals that have a safe place to sleep tend to sleep more than those who don't |
| how does sleep restore the body and brain | - by replenishing metabolic requirements such as proteins - most growth hormones is released during SWS - the glymphatic system flushes waste products faster than when awake |
| what is one waste product that clears much faster during sleep | beta amyloids |
| what type of memory does sleep improve | - declarative memory - REM sleep may help consolidate nondeclarative memory |
| what does sleep deprivation increase the likelihood of creating | false memories |
| what happens to the number of new dendritic spines in mice with sleep or sleep deprivation | - stronger after sleep and decreased if sleep deprived |
| sleep is an active state mediated by what neural systems | - forebrain system - brainstem system - pons system - hypothalamic system |
| what does the forebrain system do to mediate sleep | - Basal forebrain promotes/generate SWS by releasing GABA into the tuberomammillary nucleus in the hypothalamus - Electrical stimulation of the basal forebrain makes animals sleepy while lesions of this region induce insomnia |
| how does the brainstem mediate sleep | activates the forebrain into wakefulness (especially the reticular formation) |
| what does the pons system do to mediate sleep | - The subcoeruleus (ventral to the locus coeruleus) sends widespread projections to promote REM sleep - Medullary axons projecting to spinal cord inhibit motor neurons so they can't fire causing muscle atonia |
| what does the hypothalamic system do to mediate sleep | - A region in the hypothalamus including neurons that use hypocretin as a neurotransmitter sends axons to the other three sleep centers and seems to coordinate them enforcing the patterns of sleep |
| what happens if there is a loss of hypocretin | can lead to disorganized sleep such as REM like muscle atonia while still awake (in narcolepsy) |
| what occurs if there is a lesion in the locus coeruleus | blocks atonia |
| what stage does sleepwalking typically occur in | stage 3 (SWS) |
| what does most sleeping pills bind to and act as | to GABA receptors throughout the brain and act as an agonist |
| what does continued use of sleeping pills cause | - makes them ineffective - produces marked changes in sleep patterns that persist during use and for days afterward - can lead to drowsiness and memory gaps |
| what are some good sleep hygiene practices | - keep the same sleep time routine - sleep in the dark and keep your room cool - avoid caffeine and computer screens at night - |
| what are some effects of sleep deprivation | - increased irritability - difficulty in concentration - episodes of disorientation |
| what is sleep deprivation | the partial or total prevention of sleep |
| what can total sleep deprivation do | compromise the immune system and lead to death |
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rach6774