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PSY209 Exam 3
| Question | Answer |
|---|---|
| Sensory receptor organs detect.... | .....energy or substances |
| Sensory processing begins in.... | .....receptor cells |
| sensory information processing is.... | .....selective and analytical |
| What does the dorsal column system carry? | somatosensory information from the skin to the brain |
| sensory systems | specialized to detect a certain stimulus |
| receptor cells within each system | convert the stimulus into an electrical signal |
| Each system... | .....can be very diverse and has restricted range of responsiveness |
| Why does the brain recognize distinct senses? | Because each sensory system generates action potentials that travel along separate nerve tracts |
| What are the different sensory receptor systems? | stretch, vibration, pain, touch |
| What are the different skin sensations? | pain, temperature, touch, vibration, pressure, and stretch |
| What do free nerve endings sense? | pain and temperature |
| What does Merkel's disc sense? | fine touch |
| What does Meissner's corpuscle sense? | light touch |
| What do hair follicle receptors sense? | touch |
| What does Pacinian (or lamellate) corpuscle sense? | vibration and pressure |
| What does Ruffini's ending sense? | stretch |
| Pacinian corpuscle | skin receptor detecting vibration (fast-adapting) |
| What happens after vibration to corpuscle? | It stretches the membrane which leads to enlarging Na+ ion channels which leads to the entry of Na+ |
| What happens when vibration (stimulus) is strong enough? | receptor reaches threshold which leads to the generation of action potential |
| What do all sensory pathways except for smell pass through? | regions of the thalamus |
| Where do sensory pathways terminate? | the cerebral cortex |
| primary somatosensory cortex (S1) | receives touch information from the opposite side of the body |
| synesthesia | condition in which a stimulus in one modality creates a sensation in another |
| What may neural basis of synesthesia include? | cross-reactivity of sensory systems |
| Meissner's corpuscles | touch, fast-adapting |
| Merkel's disc | touch, slow-adapting |
| Ruffini's endings | stretch, slow-adapting |
| What do Meissner's corpuscles and Merkel's discs make? | a specialized ion channel called Piezo2, allowing them to respond to edges |
| What are Merkel's discs required for? | Braille encoding |
| dermatome | strip of skin innervated by a particular spinal nerve |
| What does the cortical map represent? | the innervation of a body region |
| If nerve is severed or body region is removed.... | .....cortical area devoted to that body region shrinks and cortical area or adjacent body regions expands |
| Stimulation of specific body regions will... | ....expand their cortical representation |
| sensory pain | unpleasant experience associated with tissue damage, helps us to withdraw from its source, engage in restoring actions, and to signal others |
| free nerve endings | specialized receptor proteins in the skin, respond to temperature changes, chemicals, and pain, damaged cells release substances that activate free nerve endings |
| transient receptor potential vanillin type 1 (TRPV1) | detects painful heat, binds capsaicin (chemical making chili peppers "hot"), found on C fibers (thin unmyelinated axons that conduct slowly, producing lasting pain) |
| transient receptor potential type M3 (TRPM3) | detects even higher temperatures, does not bind capsaicin, found on Sigma fibers (large myelinated axons that register pain quickly) |
| cool-menthol receptor 1 (CMR1) | responds to menthol and cool temperatures, found on C fibers |
| C fibers | unmyelinated thin axons that conduct slowly, producing lasting pain |
| Asigma fibers | large myelinated axons that register pain quickly |
| Order of the sensation of pain from C/Asigma fibers | crosses the midline in the spinal cord to > the spinothalamic system (through the medulla, pons, and midbrain) to > the thalamus in the forebrain to > the somatosensory cortex in the forebrain |
| neuropathic pain (phantom limb pain) | due to inappropriate signaling of pain by neurons, neurons can become hyper excitable and cause chronic pain |
| cingulate cortex | activated when experiencing pain |
| social rejection | activates the anterior cingulate cortex, extent to which a person is upset by rejection correlates with activation of the cingulate cortex, shows overlap with brain circuitry activated in response to physical pain |
| periaqueductal gray (PAG) | area in the midbrain, involved in pain perception, produces opioids=potent analgesia |
| PAG projects to.... | ....medulla to release opioids |
| medulla projects to.... | .....spinal cord to release serotonin |
| local spinal cord neurons release..... | .....opioids to block pain signal coming from the skin |
| opiates like morphine mimic.... | .....effects of opioids |
| What does the behavioral view consider? | reflexes vs plans |
| What does the control systems view consider? | accuracy vs speed |
| What does the neuroscience view reveal? | hierarchical systems |
| What does the behavioral view consider? | reflexes vs plans |
| What does the control systems view consider? | accuracy vs speed |
| What does the neuroscience view reveal? | hierarchical systems |
| What is the spinal cord a crucial link to? | controlling body movement |
| What do pathways from the brain control? | different aspects of movements |
| What do extrapyramidal systems mediate? | motor commands |
| What can brain disorders disrupt? | movement |
| Spinal connections between what two roots are basis for simple movements? | dorsal (sensory) and ventral (motor) |
| reflex | simple and unlearned responses to sensory stimuli (such as touch, pressure, pain) |
| motor plan | set of muscle commands established before the action occurs |
| closed-loop control mechanisms | maximize accuracy, movement is regulated and adapted, decisions are made in the brain, information can be sent in separate messages, information is received by the muscles to initiate the movement, feedback to brain allows corrections of movement patterns |
| open-loop control mechanism | maximizes speed, movement is pre-programmed without feedback control, decisions are made in the brain before performing the skill, information for one movement is sent in a single message, information is received by the muscles to perform the movement |
| skeletal system and muscles | allow for movement |
| spinal cord | controls skeletal muscles |
| brainstem | integrates motor commands and relays sensory information, passes commands to spinal cord (body movements) and head (face, head, neck movements) |
| primary motor cortex | initiates commands for action |
| nonprimary motor cortex | provides additional source of motor commands |
| cerebellum and basal ganglia | modulate activities of cortical control systems, sometimes via the thalamus in a loop back to the cortex |
| motor cortex | sends commands to basal ganglia, cerebellum, brainstem and spinal cord |
| basal ganglia and cerebellum | adjust commands by sending info to thalamus and brainstem |
| thalamus | provides feedback to motor cortex |
| skeletal muscle | composed of muscle fiber |
| muscle fiber | a single, large cell containing thick (made of myosin) and thin (made of actin) filaments |
| myosin heads | bind to actin, then bend to slide filaments toward one another, shortening the muscle and causing muscle contraction |
| spinal motor neurons | send axons to muscles where each axon splits into several branches |
| What does each branch innervate? | a separate muscle fiber at the neuromuscular junction |
| presynaptic motor neuron | terminal releases acetylcholine to stimulate postsynaptic muscle tissue, which triggers muscle contraction |
| muscular dystrophy | a group of more than 30 genetic disorders that cause progressive weakness and loss of muscle mass, more common in males, no cure |
| dystrophin | a protein found in muscle fibers, it is needed for muscle strength, it regulates calcium levels and supports actin filaments |
| What is dystrophin produced by? | a gene on the X-chromosome |
| amyotrophic lateral sclerosis (ALS) (Lou Gehrig's disease) | degeneration of motor neurons in brain and spinal cord and subsequent loss of their target muscles, characterized by stiff muscles, muscle twitching, difficulty speaking, swallowing, and eventually breathing |
| mutation in SOD1 gene | accounts for about 20% of the heritable cases of ALS, these mutations lead to misfiling of proteins in motor neurons |
| What are other factors involved in ALS? | mitochondria, axon transport, proteins, glutamate, neuroinflammation |
| cranial motor nuclei | muscles controlled directly by the brain, in the brainstem, innervate muscles of the head and neck |
| pyramidal system (corticospinal system) | muscles controlled by the spinal cord, following commands from the brain, consists of cerebral cortex neurons with axons that form the pyramidal tract to the spinal cord |
| where do pyramidal system fibers cross? | to the opposite site at the level of the medulla |
| motor neurons in the brain change firing rate according to.... | ....the direction of the movement |
| each neuron has.... | .....one direction that elicits highest activity |
| an average of the activity can predict the.... | ....direction of the movement |
| what do motor cortex neurons have preference for? | leftward, rightward, upward, downward, or diagonal movement |
| primary motor cortex changes as a result of.... | .....learning |
| new skills show changes in.... | .....electrical activity |
| early musical training results in.... | .....an expansion of M1 in humans |
| while learning a skill, metabolic activity in M1 during the task.... | ....declines (M1 becomes more efficient) |
| cortical remodeling may occur.... | .....at the expense of other regions (survival of the fittest; use it or lose it) |
| mirror neurons in the premotor cortex are active when... | ....an individual makes a particular movement, when an individual sees anotherr individual make a particular movement |
| mirror neurons are important in the.... | .....imitation of specific movements made by another individual and facilities social learning and cooperation |
| inhibition of these mirror neurons (using trans cranial magnetic stimulation).... | .....in humans impairs their perception of other's actions |
| reticulospinal tract | neurons in the reticular formation in the brainstem project to the spinal cord; main function is to maintain tone, balance, and posture during body movements |
| rubrospinal tract | red nucleus in the midbrain projects to the spinal cord; mediates voluntary movements |
| basal ganglia | striatum (caudate, nucleus, putamen), globus pallidum, subthalamus nucleus, and substantia nigra; mediate voluntary movements |
| cerebellum | does not initiate movements, but contributes to coordination, precision, accurate timing, and motor learning |
| Humans without a cerebellum or with cerebellar dysfunction or damage.... | .....are still able to generate motor activity, but they lose precision, coordination, and timing producing erratic, uncoordinated, or incorrectly timed movements |
| Parkinson's disease | neurodegenerative disorder mainly affecting the motor system, characterized by tremors, loss of muscle tone, and difficulty movements |
| Patients with Parkinson's disease show... | ....degeneration of dopamine-containing cells in the substantial nigra, which is part of the basal ganglia and is essential for motor control |
| defects in the protein alpha-synuclein (a specific basal ganglia protein) or parkin can lead to.... | ....the formation of misfolded proteins in dopamine neurons |
| misfolded proteins | Lewy bodies |
| L-dopa | precursor to dopamine is effective in reduces some symptoms but no longer works when too many dopamine neurons are lost |
| deep-brain stimulation | consists of electrode and pacemaker that are chronically implanted; stimulation of electrode may mimic function of basal ganglia neurons |
| neurotrophic factors and stem cells | experimental treatments to restore or replace dopamine neurons in substantial nigra |
| globus pallidus and subthalamic nucleus | effective brain targets which are downstream brain regions of the substantial nigra |
| tremors and slow movement | Parkinson's symptoms that are relieved by mild electrical stimulation |
| physiological systems | regulated and maintained (e.g. acidity, saltiness, water level, oxygenation, temperature, energy availability) |
| homeostasis | active process of maintaining a relatively stable, balanced internal environment |
| motivation | psychological process that induces or sustains a particular behavior often in an attempt to restore homeostasis |
| thermoregulation | active process of closely regulating body temperature around a set value |
| ectotherms | get most of their heat from the environment (e.g. reptiles) |
| endotherms | generate most of their own heat through internal processes (e,.g. mammals, birds) |
| disadvantage endotherms | use a lot of food energy to produce their heat |
| advantages of endotherms | independence from environmental conditions, longer endurancee of muscular activity (due to greater capacity of oxygen utilization) |
| homeostatic mechanisms that regulate temperature, body fluids, and metabolism.... | ....are primarily negative feedback systems |
| negative feedback | property by which some of the output of a system feeds back to reduce the effect of input signals |
| deviation from the set value | results in compensatory action |
| set zone | range of tolerance in a system |
| responses to cold | increased thyroid activity, metabolism of brown fat, constriction of cutaneous blood vessels, and shivering of muscles |
| responses to heat | accelerated respiration, perspiration, and dilation of cutaneous vessels |
| thermoregulatory circuits | hypothalamus, brainstem (midbrain, pons, medulla), spinal cord |
| thermoregulation by the hypothalamus | pre optic are (POA) and lateral hypothalamus (LH) |
| Preoptic area (POA) | physiological regulation to hot/cold (e.g. shivering, blood vessel constriction when too cold) |
| lateral hypothalamus (LH) | behavioral regulation to hot/cold (moving to a warmer location when too cold) |
| cortex | senses "hot" but does not induce the appropriate physiological and behavioral responses to cope with the hot environment |
| pathway from the spinal cord to the lateral parabrachial nucleus to POA | induces autonomic heat loss (e.g. sweating) |
| pathway from the spinal cord to the lateral parabrachial nucleus to LH | mediates cold-seeking behaviors |
| From skin to... | ....spinothalamic pathway to thalamus |
| thalamus to.... | ....somatosensory cortex |
| Receptors in the skin, body core, and hypothalamus detect temperature which leads to.... | ....transmit information to spinal cord, brainstem and hypothalamus |
| transmitting information to spinal cord, brainstem, and hypothalamus which leads to.... | .....induce physiological and behavioral responses to return organism to set value |
| afferents | skin surface, body core, hypothalamus/POA |
| neural regions | spinal cord, brainstem, hypothalamus/POA |
| effectors (behavioral responses) | shivering, heat-seeking/avoiding behaviors |
| effectors (autonomic responses) | vasoconstriction/dilation, sweating, respiration, brown-fat stimulation, thyroid hormone secretion |
| How do newborn mammals generate heat? | they huddle together and use brown-fat deposits |
| oxytocin knock out mice | thermoregulation is impaired |
| warmest pup | always a normal wild type (WT) pup |
| coolest pup | always an oxytocin knock out (OTKO) pup |
| precise balance of fluids and salts | required for optimal functioning of cells in our body and brain |
| intracellular compartment | fluid within cells |
| extracellular compartment | fluid outside cells |
| interstitial fluid | the fluid between cells |
| blood plasma | protein-rich fluid that carries red and white blood cells |
| aquaporins | water channels that water moves in and out of cells through |
| what can impaired functioning of aquaporins lead to? | brain disorders (brain oedema, epilepsy) and other disorders (glaucoma, hypertension, diabetis insipidus) |
| diffusion | passive spread of molecules of the same kind to obtain equal concentration of molecules |
| semipermeable membrane | permeable to some molecules but not to others |
| osmosis | passive movement of water molecules, through a semipermeable membrane, from one place to another |
| what happens when you add water to one side? | water molecules will pass through the semipermeable membrane to achieve equal concentration of molecules on both sides |
| what happens when you add salt to one side? | water molecules will pass through the semipermeable membrane to achieve equal concentration of molecules on both sides |
| osmolality | number of solute particles per unit volume of solvent |
| isotonic solution | mammalian fluids (.9% salt), physiological saline |
| hypertonic solution | more salt than isotonic solution |
| hypotonic solution | less salt than isotonic solution |
| how have marine birds adapted? | by excreting salt (out of blood plasma) from the nostrils |
| osmotic thirst | induced by high extracellular (blood plasma/interstitial fluid) solute concentration, water is pulled out of the intracellular compartment |
| osmosensory neurons in hypothalamus respond to osmotic pressure which leads to... | ....cell membranes stretch |
| cell membranes stretch leads to.... | .....opens mechanically gated ion channels |
| opens mechanically gated ion channels leads to.... | .....generates action potentials |
| generates action potentials leads to.... | .....neurons signal to other brain regions that regulate thirst |
| hypovolemic thirst | (e.g. through hemorrhage, intense sweating, or diarrhea)induced by reduced extracellular volume, due to loss of fluids containing both water and solutes |
| baroreceptors | in blood vessels, heart, detect fluid loss which leads to less secretion of atrial natriuretic peptide which leads to blood pressure increases, water excretion decreases |
| vasopressin | antidiuretic hormone, released from posterior pituitary induces blood vessel constriction and reduces water flow to the bladder |
| to conserve water.... | ....kidneys release the enzyme renin which triggers the release of the hormone angiotensin 2 |
| angiotensin 2 | constricts blood vessels and increases blood pressure, releases vasopressin from the brain, constricts blood vessels, reduces water flow from bladder, releases the hormone aldosterone from the adrenal glands, acts on kidneys to conserve Na+ |
| what does angiotensin 2 act on? | circumventricular organs (mostly subfornical organ), activates the pre optic area (POA) which elicits drinking behavior |
| circumventricular organs | consist of 3 areas that lie in the wall of the brain ventricular system and monitor the composition of body fluids |
| central and peripheral mechanisms | cause behavioral and physiological responses, induce and maintain optimal hydration |
| thirst | a homeostatic signal associated with strong activation of brain regions such as the hypothalamus, cingulate cortex, and cerebellum |
| wetting the mouth | reduces thirst |
| drinking water | strongly reduces thirst |
| how long does it take before your blood is rehydrated? | 10-15 minutes |
| thirst-driving neurons | of the subfornical organ (SFO) activate a set of neurons in the pre optic area (POA) that induce drinking behavior |
| POA neurons are activated by.... | ....the ingestion of fluids but not solids (due to different motion of throat) |
| POA neurons facilitate thirst satiety by.... | ....monitoring real-time fluid ingestion |
| acute inhibition of POA neurons causes.... | .....overdrinking when thirsty |
| nervous system monitors | nutrient and energy levels, controls digestion (breaking down food), and anticipates future requirements |
| basal metabolism | energy used for heat production, maintenance of membrane potentials, and life-sustaining processes |
| Kleiber's equation | kcal/day = 70 x weight^{.75} |
| to prevent losing weight, the basal metabolic will.... | ....fall |
| glucose | primary energy source |
| glycogen | complex carbohydrate used for short-term energy storage in the liver and muscles |
| insulin | pancreatic hormone that regulates the conversion of glucose > glycogen (glycogenolysis), hormone levels rise in the anticipation or presence of glucose (food) (short-term satiety signal) |
| lipids | fats; deposited in adipose tissue for longer-term energy storage |
| gluconeogenesis | conversion of fat and proteins to glucose and ketones, another form of fuel |
| insulin's second role is to | enable the body to use glucose |
| glucose transporters | span the cell membrane and interact with insulin to bring glucose into the cell |
| what does not require insulin to use glucose? | brain cells |
| what mechanisms trigger insulin release? | cephalic phase, digestive phase, and absorptive phase |
| cephalic phase | the sensory stimulus of food evokes insulin release, in anticipation of glucose |
| digestive phase | food causes gut hormone release, which stimulates insulin release |
| absorptive phase | glucodetectors in the liver detect glucose and signal insulin release |
| diabetes mellitus | caused by lack of insulin signaling |
| type 1 diabetes | juvenile-onset; the pancreas stops producing insulin |
| type 2 diabetes | adult-onset; reduced sensitivity to insulin |
| satiety | the feeling of fulfillment or satisfaction |
| hunger | the internal state of an animal seeking food |
| the brainstem can coordinate | some aspects of food intake on its own |
| decerebrate rats do | show normal promotor responses, show normal taste reactivity, regulate meal size based on post ingestive GI signals |
| decerebrate rats do not | spontaneously approach food, increase food intake after acute food deprivation, acquire conditioned taste aversions |
| the hypothalamus is important for the full regulation of | metabolic rate, food intake, body weight |
| efferent vagus nerve regulation of | gastrointestinal motor and secretory functions, hepatic glucose production, glycogen synthesis, pancreatic endocrine (insulin) and exocrine secretion |
| afferent vagus nerve | gastrointestinal tract and hepatic portal system |
| dual-center hypothesis | proposed two appetite centers in the hypothalamus (ventromedial hypothalamus and lateral hypothalamus) |
| ventromedial hypothalamus (VMH) | lesions caused hyperplasia (overeating) (a satiety center) |
| lateral hypothalamus (LH) | lesions cause aphagia/hypophagia (absence of/reduced eating) (a hunger center) |
| arcuate nucleus of the hypothalamus | also an appetite center, and its activity is governed by feeding-related hormones |
| leptin | hormone produced by fat cells and secreted into the bloodstream, hormone levels are high when energy stores (fat) are high (long-term satiety signal) |
| ghrelin | hormone produced by the stomach and secreted into the bloodstream, levels rise during fasting and fall after a meal, short-term hunger signal |
| peptide YY (PYY) | hormone produced by the intestines and secreted into the bloodstream, levels are low before eating, but rise rapidly after a meal, short-term satiety signal |
| neurons that produce the peptides pro-opiomelanocortin (POMC) and cocaine-and-amphetamine-related transcript (CART) | inhibit appetite and raise metabolism (satiety neurons) |
| neurons that produce neuropeptide Y (NPY) and agouti-related peptide (AgRP) | inhibit POMC/CART neurons, stimulate appetite and lower metabolism (hunger neurons) |
| anorexigenic effect | leptin activates POMC/CART neurons but inhibits NPY/AgRP neurons, which suppresses hunger, PYY inhibits NPY/AgRP, recessing appetite |
| ghrelin and PYY have... | ....opposing effects on NPY/AgRP neurons |
| orexigenic effect | ghrelin stimulates these cells, increasing appetite |
| POMC/CART neurons | activate anorexigenic PVN neurons and inhibit orexigenic LH neurons (decrease food intake) |
| NPY/AgRP neurons | inhibit anorexigenic PVN neurons and block the inhibitory effect of POMC/CART neurons on orexigenic LH neurons (increase food intake) |
| cannabinoid antagonists | effectively suppress appetite, but cause depression symptoms |
| intranasal PYY | reduces appetite |
| potential obesity treatments include drugs that.... | ....affect the brain's reward circuitry, increase the body's metabolic rate, inhibit of fat formation, reduce absorption of fat during digestion |
| surgical options for obesity | liposuction, bariatric procedures (e.g. gastric bypass/Roux-en-Y, gastric sleeve, Lap-Band, EndoBarrier) |
| surgical options tend to have... | ...good short-term but poor long-term outcomes |
| anorexia nervosa | a syndrome in which individuals severely restrict energy intake, have an intense fear of gaining weight, and distorted body image |
| bulimia nervosa | a syndrome marked by recurrent episodes of bingeing associated with a sense of lack of control, and compensatory purging behaviors |
| binge eating disorder | a syndrome marked by recurrent binge eating episodes, and by a sense of lack of control |
| anorexia and bulimia | can be fatal in part due to a lack of proper nutriction, which damages organ systems |
| biological causes of anorexia nervosa | elevated levels of ghrelin and low levels of leptin during illness, but leptin levels increase prior to full recovery; suggests peripheral hunger and satire signs are present, but the premature rise in leptin could hinder recovery |
| biological causes of bulimia nervosa | blunted post-meal ghrelin decline and decreased leptin levels; sigesstes dysregulation in short and long-term peripheral satiety signals |
| eating disorders are difficult to treat because.... | ....they involve a combination of genetic, endocrine, personality, cognitive, and environmental variables |
| twin studies suggest eating disorders are.... | ....heritable |
| in ~60% of cases, eating disorders are pre-dated by.... | ....anxiety disorders |
| gut microbiota | the microbiome; humans have 2.5-5 lbs of it; mood, anxiety, cognitive functions, obesity |
| fecal transplantation | an effective treatment for restoring a healthy gut microbiome |
| circadian rhythms | functions with a rhythm of about 24 hours; generated by endogenous clock |
| rhythms can be... | ....behavioral, physiological, and biochemical |
| diurnal | active during the light |
| nocturnal | active during the dark |
| zeitgeber (timer) | cue that an animal uses to synchronize with the environment |
| phase shift | shift in activity in response to a synchronizing stimulus (light, food) |
| entrainment | process of shifting the rhythm |
| free-running | animal maintaining cycle without external cues |
| individual is mostly active in.... | ....the dark phase with anticipation activity before lights go off |
| endogenous clock | biological clock; enables animals to anticipate events and help with survival |
| suprachiasmatic nucleus (SCN) | biological clock located above the optic chasm (OX) in the hypothalamus |
| what are circadian rhythms disrupted by? | SCN lesions |
| isolated SCN neurons.... | ....maintain electrical activity synchronized to the previous light cycle |
| hamsters with SCN lesions that received a SCN transplant from donor hamsters.... | .....had restored circadian rhythm in SCN-lesioned hamsters |
| neuronal pathway that entrains circadian rhythms to light-dark cycles is.... | ....species-specific |
| neuronal pathway of amphibians and birds | pineal gland is sensitive to light because the skull over the gland is thin |
| neuronal pathway of mammals | SCN receives info of light through the eyes |
| How does SCN receive input? | via retinohypothalamic pathway |
| retinal ganglion cells | in the eyes; do not rely on rods and cones, project directly to the SCN |
| melanopsin | special photopigment; makes retinal ganglion cells sensitive to light |
| retinohypothalamic pathway | carries information about the light-dark cycle in the environment via retinal ganglion cells through the optic chasm to the SCN |
| how many proteins in the SCN determine 24 hour cycle? | four |
| circadian clock first step | clock and cycle proteins form dimer |
| circadian clock second step | clock/cycle dimer binds to DNA and promotes transcription of Period (per) gene and Cryptochrome (cry) gene |
| circadian clock third step | Per and Cry proteins form dimer |
| circadian clock fourth step | Per/Cry dimer inhibits activity of Clock/Cycle dimer |
| circadian clock fifth step | Per/Cry protein production is slowed down until the Per/Cry proteins degrade (takes approximately 24 hours) |
| circadian clock sixth step | retinal ganglion cells release glutamate that binds to receptors that stimulate Per gene transcription |
| light entrains the molecular clock in flies | light reaches the brain directly, degrades the Cry protein, thereby synchronizing the molecular clock to light |
| light entrains the molecular clock in mammals | retinal ganglion cells detect light and release glutamate in the SCN; glutamate binds to membrane receptors triggering events that promote Per protein production, thereby synchronizing the molecular clock to light |
| sleep is synchronized to.... | ....external events, including light and dark |
| in the absence of cues, human have.... | ....a free-running period of approximately 25 hours |
| what are the two distinct classes of sleep? | non-REM sleep (NREM) and Rapid-eye-movement sleep (REM) |
| Non-REM sleep (NREM) | stages 1-3, no rapid eye movements |
| Rapid-eye-movement sleep (REM) | small-amplitude, fast EEG waves, no postural tension and rapid eye movements |
| how long do sleep cycles last? | approximately 120 minutes |
| How much time is in stage 2 sleep? | 50% |
| How much time is in REM sleep? | 20% |
| is REM more present in early cycles or later cycles? | later cycles |
| stage 1 | light sleep; heart rate slows, muscle tension decreases, eyes roll about, lasts several minutes; alpha rhythms and vertex spikes |
| stage 2 | stable sleep; defined by sleep spindles and K-complexes |
| sleep spindles | bursts of 12 and 14 Hz waves |
| K-complexes | sharp negative EEG potentials |
| stage 3 | deep sleep or slow-wave sleep; defined by delta waves |
| delta waves | large-amplitude, very slow waves occurring once per second |
| REM sleep | high brain activity and lack of muscle activity |
| high brain activity | active EEG with small-amplitude, high-frequency waves |
| lack of muscle activity | muscles are flaccid, unresponsive |
| at puberty.... | ....shift in circadian rhythm of sleep with most individuals getting up later in the day |
| vivid dreams during REM sleep | visual imagery, story; sense that the dreamer is "there" |
| nightmares | long frightening dreams that awaken the sleeper from REM sleep |
| night terrors | sudden arousals from NREM sleep, marked by fear and autonomic activity |
| nearly all mammals.... | ....display both REM and NREM |
| birds display both.... | ....REM and stage 3 sleep (slow wave/deep sleep) |
| why do dolphins not show REM sleep? | relaxed muscles are incompatible with the need to come to the surfaceto breathe |
| What allows dolphins and birds to continue functioning while resting? | that they show stage 3 sleep, but only one hemisphere at a time |
| Mammals sleep more during.... | .....infancy than in adulthood |
| infant sleep is characterized by | shorter sleep cycles, 50% more REM sleep, providing essential stimulation to the developing nervous system |
| when does sleep pattern become stable for humans? | 16 weeks of age |
| as people age, total time asleep.... | ....declines, and the number of awakenings increases |
| effects of sleep deprivation | increased irritability, difficulty in concentrating, episodes of disorientation |
| total sleep deprivation | compromises the immune system and leads to death |
| fatal familia insomnia | defect in gene for prion protein, patients stop sleeping in midlife, die within 2 years after onset insomnia, autopsy shows degeneration in the brain |
| how does sleep restore the body and brain? | rebuilding of materials used during waking, promoting growth (growth hormones released during SWS), removal of waste products (build up toxins removed by glia), resisting illness |
| how does sleep aids memory consolidation? | improves declarative (facts and events) memory, decreases likelihood of creating false memories, consolidates non declarative memory(during REM sleep), increases dendritic spines (with fewer after sleep deprivation) |
| basal forebrain | generates SWS by releasing GABA that suppresses activity of the tuberomamillary nucleus in the hypothalamus; stimulation induces sleep, lesioning induces insomnia |
| reticular formation | located in the brainstem, activates the forebrain into wakefulness; stimulation promotes wakefulness and alertness, lesions induce constant sleep |
| subcoeruleus | located in the pons, triggers REM sleep, and inhibits motor neurons (to prevent muscle tone); promotes REM sleep and muscle atonia |
| hypocretin | hormone secreted by the hypothalamus and affecting A-C and tuberomamillary nucleus to regulate normal transitions between wakefulness, NREM, and REM; neurons in hypothalamus, enforces sleep patterns, lack of hypocretin causes narcolepsy |
| narcolepsy | caused by lack of hypocretin neurons (humans) or by mutant gene for the hypocretin receptor (dogs), have frequent sleepattacks and daytime sleepiness, enter REM immediately after falling sleep, may show cataplexy - a sudden loss of muscle tone |
| "off" periods of neurons lead to.... | ....behavioral impairments |
| muscle contraction | spinal motor neurons are activated; acetylcholineis released at the neuromuscular junction; myosin heads bind to actin filaments; actin filaments are pulled closer together |
| in the pyramidal system, fibers cross to.... | ....the opposite side of the body at the level of the medulla. |
| humans without a cerebellum or cerebellar dysfunction | show incorrectly timed movements |
| Parkinson's disease is characterized by.... | .....degeneration of the substantia nigra. |
| What might your body do if you are cold? | constrict blood vessels, metabolize brown fat, increase thyroid activity |
| Afferents | a general feature of homeostatic mechanism is redundancy |
| moving from a cool to a warm spot as a way to regulate body temperature is.... | .....particularly impaired by lesions of the lateral hypothalamus. |
| container A and B have each 50mL of water and separated by semipermeable barrier. 5g salt in A, 10g salt in B. | Water will travel from A to B, concentration of solutions will become the same |
| What happens if you put a saltwater fish in freshwater? | the hypertonic cells in the fish will become hypotonic and the fish will die. |
| the receptors that detect hypovolemia are named ----- and are located in the ---- | baroreceptors; vascular system |
| lesioning the POA may result in | over drinking when thirsty, impaired physiological temperature regulation, not drinking when thirsty |
| comparing the basal metabolic rates of 2 animals each with body weight of 100g, you discover species A has a higher rate than species B. Which animal is most likely a mammal? | species A |
| select the roles of insulin in energy utilization | regulate the conversion of glucose to glycogen, allows cells in the body to take in glucose for use as energy |
| lesions of the lateral hypothalamus cause ---- suggesting that this region is a ---- center | aphagia; hunger |
| light is absorbed by ---- in the ----- which project via the ---- to the ---- | melanopsin; retinal ganglion cells; opticchiasm; SCN |
| the length of the circadian cycle.... | ....is a product of the time it takes for per/cry dimers to degrade |
| the pattern of sleep in elderly humans is characterized by.... | ....increases in awakenings |
| define basal forebrain | produces SWS and induces sleep |
| define hypocretin | enforces transitions between sleep patterns |
| define reticular formation | promotes wakefulness |
| define subcoreruleus | promotes REM and stops muscle movement |
| lesions of the ---- produce persistent sleep in animals | reticular formation |
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Cramdela
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