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225 Cards in this Set
- Front
- Back
Van't Hoff Equation
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Q10=(MR2/MR1)^(10/(T2-T1))
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Q10
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-the change in a biological rate (HR, metabolism, etc.) for a 10C change in temperature.
-usually about 2-3 for physiological processes. |
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Net Change in Heat Content
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=metabolic heat production +/- conduction +/- radiation - evaportation
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Endothermy/Ectothermy
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defining animals based on where they get most of the heat in body.
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Ectothermy
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dominant source of heat comes from external environment
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Endothermy
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-dominant source of heat produced within the animal.
-3 to 8X great oxygen consumption (VO2) -can raise temp. above evironmental temperature. |
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Homeothermy
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body temperature remains at a constant temp throughout differing env. temps.
--maintain homeostasis across wide range of env. temps through physiological processes. |
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Poikilothermy
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thermoconformer
--usually ectotherms, not always. |
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Homeothermy/Poikilothermy
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defining animals based on the stability of their body temps
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Heterothermy
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-Regional : different strategies in different parts of the body
-Temporal : switching between endo/homeo and ecoto/poikilo based on time of day/temp of month |
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Characteristics of Ectotherms
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-dont produce much heat and quickly lose heat that is produced (poor insulation keeps heat in and out)
-do not totally conform to external environment. -low MR -Plasticity: some species have acclimatized so body functions optimally. -body functions adapt to the environment the organisms live in. -preferred body temp is not random, has biochemical/physiological correlations |
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Heliothermy
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-behavioral thermoregulation of basking in the sun
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Thigmothermy
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behavioral adaptation
-adjusting body temp by putting body against cool/warm substrate |
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How ectotherms gain heat
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-posture (larger surface area=more heat gained)
-microclimate -coloration |
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How ectotherms lose heat
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-posture
-microclimate -blood flow -evaporative water loss |
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Why do high temps kill?
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-denaturing of proteins: 3D structure of proteins can be altered so they cannot perform normal funtions; causes blood clotting; have heat-shock proteins as counteracting strategy.
-insufficient O2: MR can go faster than you are able to bring O2 to tissues; hemoglobin affinity goes down despite the need for more O2. -Reduced activity of enzymes -variable effects of temp on related reactions: imbalance. -membrane fluidity altered: more fluid/leaky. |
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Heat-shock Proteins
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-counteracting strategy to the denaturing of proteins due to high heat
-can be induced at high temps -helps proteins maintain structures and function correctly |
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Freezing Point of Cells
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-0.1 to -1.9C
--freezing point not zero because of the solutes in cells -formation of ice crystals inside cells can cause poking of hold in cell membrane and blood vessels |
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How body temps below zero are achieved
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-Supercooling
-Antifreeze |
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Supercooling
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-lowering a liquid below its freezing point without it becoming a solid.
-no nucleating agents -often combined with colligative antifreezing |
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Colligative Antifreeze
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Affect the freezing point by increasing the total concentration of solutes in the body fluids.
-Use glycerol, sorbitol, etc. -Don't use inorganic ions because the increase in concentration will mess up membrane potentials and change 3D structure of proteins |
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Noncolligative Antifreeze
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-Glycoproteins
--prevent big crystals -It takes a very low concentration to depress freezing. -As ice crystals grow, antifreeze will insert themselves in crystal and prevent further grotwth --end up with small, nonthreatening crystals |
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How animals actually survive freezing
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-Have nucleating agents (ice crystal promoters) in blood plasma and interstitial fluid, causing them to freeze first (before cells)
--Ice crystal formation in int. fluid and floods plasma: --Ice crystals first form in these locations --They grow by attracting water molecules so all the salt that was dissolved gets left behind. --Water moves out of the cells so the osmotic concentration within the cells increases, making their freezing point very low. -Cells do shrink while all the water moves into int. fluid and blood plasma so organic solutes must be substituted in --glycerol in insects, glucose in vertebrates |
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Countercurrent Heat Exchange
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-minimizes heat loss
-Arteries and veins run parallel and in close contact to one another. --blood moving twds periphery exchanges heat with artery/vein going back into body. |
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Rete mirabile
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-a complex of arteries and veins lying very close to each other
--enables countercurrent heat exchange |
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Why regulate at high body temps? (endothermy)
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-partially optimal conditions for enzymes (though adaptations can alter this)
-mostly because things work faster at higher temps --Q10 effect |
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Negative effects of increasing body temp
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Amount of protein needing replacement increases
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Temperature Neutral Zone (TNZ)
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Region of ambient temperatures in which an organism does not need to increase their MR
-as ambient temp increase or decreases away from TNZ, MR increases. |
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Upper-critical Temperature (UCT)
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Upper temperature threshold where animal need to expend more energy
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Lower-critical Temperature (LCT)
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Lower temperature threshold where animal needs to expend more energy
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Metabolically inexpensive ways for Endotherms to decrease heat loss
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Behavior, vasomotor responses, insulation
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Vasomotor Responses in Endotherms
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-In the cold, need to reduce blood flow to the skin
--larger distance from surface of skin when vasoconstriction occurs --blodd traveling more deep, conserving body heat. -Under normal conditions, lots of heat lost by conductance across skin, as lots of blood is able to go close to surface |
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Insulation in Endotherms
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-Use fur (piloerection) or feathers (tiloerection)
-feather/fur traps air by body --air has low k value, so its a good insulator (16X better than fat) --greatly increases distance between blood and external environment -Animals that live in water need a different mode of insulation --Blubber on the outer layer of an animal also acts as a way of keep heat in --since blubbler is 1/16 as effective as air at insulating, animals need very thick layer of it. |
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Mechanisms for increasing heat production in Endotherms
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-shivering thermogenesis
-nonshivering thermogenesis: --brown adipose tissue --liver/muscle (Na, K, Ca leaks) --mitochondrial mutations -Regional or temporal heterothermy |
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Shivering
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-alternating the contractions of antagonistic muscle pairs in order to burn through ATP and contract heat.
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Brown Adipose Tissue
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(mammals)
-contains much more mitochondria than regular yellow fat -located in regions between shoulder blades and near heart. -receive rich supply of blood vessels -Has electron transport chain without ATP synthesis (has thermogenin specialized for heat production) so heat is rapidly liberated |
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Na, K, Ca pumps in liver/muscle
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-Na, K, Ca pumps use ATP and by making cells more leaky, pumps need to work harder in order to maintain a gradient, thus releasing more heat.
--The increase in ATP use increases amount of heat loss |
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Mitochondrial Mutation
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-mutation decreases efficiency of mitochondrial membrane, making it have to work harder
--need to increase uptake of calories/have a high fat diet to help fuel this mutation. -Mutation found in ppl in cooler climates (0% africa, 75% arctic, 14% europe/temperate) |
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Regional Heterothermy in Endotherms
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-Maintaining warmer regions of the body relative to other parts
-Peripheral temps may approach ambient temp. --vasoconstriction (down side: less O2/nutrient/waste product removal in those areas causing pain -Countercurrent exchange saves energy without limiting transport of important nutrients etc --allows you to continue blood flow but heat barely arrives at periphery. -Maintain a constant core temperature (warmer) -Don't allow body temp to go below freezing point of cells (dont want ice crystal formation). |
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Temporal Heterothermy in Endotherms
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-Entire body alters its temperature
--happens at certain points during animals life -Programmed lowering of set point (daily, annually, etc) or reactive lowering (depends on environment temp, etc) -Reduction in the difference between ambient temp and body temp -Need to heat back up though, so cost of reheating must be less than energy saved to make this process worthwhile --Larger you are, the more energy it takes to warm back up |
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Continuum of controlled hypothermia
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-mild (nocturnal) hypothermia
-torpor -hibernation -winter sleep (carnivore lethargy) |
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Mild (nocturnal) Hypothermia
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-short period of time (12 hours or less)
-about a 7-10C drop in temp |
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Torpor
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-combined with behavior of hiding
-small mammals and birds -unresponsive while in this state -profound drop in body temp (body temp can reach ambient temp if not too low) -takes .5-1hr to warm back up -happens daily |
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Hibernation
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-medium (>100g) mammals; poorwill (bird)
-long-term torpor (days to months) associated with winter -periodic arousal |
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Winter Sleep (carnivore lethargy)
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-bears, badgers
-weeks to months -decrease body temp only by about 5C -around rapidly -like extended mild hypothermia |
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Seasonal control of body temp in Endotherms
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-animals may be able to withstand lower temps more efficiently depending on the season (i.e. winter)
--acclimatization -Insulation increases/decreases depending on season (more fur in winter) -migration (avoidance) |
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Adaptation in Endotherms to maintain body temp/MR
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-SA/V
--Bergmann's rule -Allen's rule -insulation -heat exchangers (heterothermy) |
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Bergmann's Rule
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animals at high latitudes have typically larger body size compared to ones in lower latitudes
-size of animal increase as latitude increases --larger animals have smaller SA/V so heat loss slower |
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Allen's Rule
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animals at higher latitudes have shorter appendages
--larger appendages lose more heat --smaller limb length with increased latitude |
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Metabolically Inexpensive ways to increase heat loss
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microclimates, posture, decrease insulation, vasodilation
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In response to heat, how to increase evaporative water loss
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-sweating/cutaneous water loss
-panting -gular flutter -breathe via mouth -saliva or urine |
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Defense of Brain Temp
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-Brain can only tolerate temp up to 40.5C though body temp may exceed that
-Use countercurrent exchange to maintain temp --carotid rete in mammals (keeps brain temp about 3-4C lower than core) --opthalmic rete in birds (warm blood heading to brain is cooled at nasal passage before getting to brain) --using evaporative cooling in nasal passage to indirectly cool brain. ---shunt when cold |
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What is a nervous system?
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Made up of glial cells and neurons
-Protists and sponges don't have true nervous systems |
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Glial Cell
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-Provide support and protection for neurons
-maintain extracellular environment -Wrap their membranes around axon --Oligodendrocytes --Schwann Cells |
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Typical parts of a neuron
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-dendrites
-soma -axon -axon terminal |
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Dendrites
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Attached to the soma and recieve information from other cells or the environment
-where stimuli enters |
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Soma
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The cell body
-has numerous projections: dendrites |
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Axon
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-Received signal to the neuron travels down it from soma
-serves to propagate action potential |
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Axon terminal
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Area where cell communicates with other neurons
-had presynaptic terminals where neuronal output occurs |
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Membrane Potential
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differences in electrical charge across a membrane
-cells are inside negative |
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Voltage at rest of a Neuron/proporties
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-20 to -100 mV (like all cells)
-many are excitable --can carry and action potential |
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Action Potential
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A momentary reversal of membrane potential followed by a restoration of original membrane potential
-rapid change in voltage of cell, propagated along it -The action potential is triggered by any depolarization of the membrane that reaches a critical value of depolarization, the voltage threshold |
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Ions inside/outside of typical cell
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-More K inside
-More Cl and Na outside -Maintained by action Na/K pumps and passive distribution of ions like Cl --Donnan Equilibrium -Equilibrium potential of cells at rest is closer to the ion equilibrium of K since cell is more permeable to K |
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Goldman Equation
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-The contribution of each ion is weighted by its ability to permeate the membrane, with the more-permeating ions having more of an effect. The value of the membrane potential (Vm) produced by the contributions of several permeating ion species is determined by this equation:
Vm=(RT/F)ln(ratio of ions in and out of cell) --positive ions: outside goes ontop, inside on bottom --negative ions: opposite |
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Depolarization
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a decrease in the absolute value of the membrane potential towards zero (becoming less negative inside the cell)
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Hyperpolarization
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an increase in the absolute value of the membrane potential away from zero (becoming more negative inside the cell)
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Graded Potential
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a change in potential that is proportional to the stimulus applied
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Anatomy of an Action Potential
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-has slow increase/depolarization, crossing voltage threshold
-followed by rapid depolarization in the "Rising Phase" -Can have an "Overshoot" if potential crosses over to + -"falling phase" characterized by rapid membrane repolarization -Some "undershoot", ducking below resting potential -return to resting potential |
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Sequence of Na and K channels during an action potential
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1. at rest, K is flowing in and out of cell; voltage gated Na and K channels are closed during resting membrane potential.
2. Rising phase: Some stimulus causes depolarization and the open of the voltage gated Na channel; since Na is very far from equilibrium potential, it flows rapidly into cell 3. Falling phase: inactivation gate for Na channel closes and voltage gated K channel opens, releasing K out of the cell --Absolute refractory period 4. Reaches equilibrium potential for K and then voltage gated K channel closes --Relative refractory period |
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Refractory Period
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Period in time, once an action potential has been initiated, where it is difficult to cause a second action potential.
-absolute refractory: due to Na channel inactivation --keeps action potential going one direction -Once some inactivation removed, relative refractory |
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Mechanisms for increase speed of action potential
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-increase diameter of neuron
--resistance to longitudinal spread decreases --trade off: spatial constraints -Myelination (vertebrates and some crustaceans) -increase temp |
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Myelination
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-Use glial cells to form myelin sheath around axon
-Oligodendrocytes in brain/spine -Schwann cells on rest of nerves -Increase transmembrane resistance and thickness and enhances current spread --resistance that occurs from having + less impressive since they are now farther away --also prevents + from leaking -Action potential can spread faster and for longer but still decrement over time-->nodes of Ranvier. |
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Nodes of Ranvier
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gaps between areas of myelination
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Saltatory conduction
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-Action potential jumping from node to node
-Areas wrapped with cells do not have voltage gated channels so the action potential can decrement -as long as the action potential is enough to start another one at each node, the action potential can carry through the axon |
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How action potential can cross to next cell
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-Electrical: used when you need rapid response and a whole bunch of cells acting in unison.
--use gap junctions called connexin -Chemical: --use neurotransmitters |
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Connexin
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-the gap junctions through which electrical signals travel between cells.
-arranged to form a pore directly between cell 1 and cell 2. -very quick communication -usually positive charges moving through junctions-->excitatory -signal is a graded potential, so it decrements over time |
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Why not only use electrical synapse?
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-Advantages of chemical synapse:
--can have both excitatory and inhibitory cells --more communication: more control, more functional plasticity |
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Synaptic Cleft
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the gap between the two cells where action potential is passes chemically
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How neurotransmitter is released/received chemically:
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-Presynaptic action potential opens voltage-gated Ca channels
-increase in Ca concentration initiates exocytosis of vesicles containing neurotransmitter -neurotransmitter diffuses across synaptic cleft -neurotransmitter activated ligand-gated ion channels (fast) or second messengers, changing voltage -neurotransmitter degraded and/or actively taken up |
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Spiking Neuron
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-has long axon
-information carried by an action potential -frequency of action potential related to amount of neurotransmitter released |
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Nonspiking neuron
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-Shorter axon relative to spiking neuron
-information carried using a graded potential -amount of neurotransmitter released is proportional to magnitude of depolarization |
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ionotropic receptors
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-located on the post-synaptic cell
-what receptors bind to neurotransmitter they open to allow ion flow in -fast response |
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metabotropic receptors
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-located on the post-synaptic cell
-produce a metabolic change in the postsynaptic cell --relatively slow, long-last modulatory effects |
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Excitatory Neurotransmitters
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Ach and glutamate
-excitatory because they open Ca/Na channels, causing depolarization (normally more inside than out) |
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Inhibitory Neurotransmitters
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GABA and glycine
-inhibitory because they open K/Cl channels, causing hyperpolarization (normally more in cell than out) |
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Magnitude of the effect of the AP depends on...
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-the ion being released
-the concentration gradient -how long the release occurs for (frequent AP can keep Ca channels open and create more release of neurotrans) --usually need more than one AP to make a large enough GP ---axon terminals all over receiving neuron |
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Integration
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-refers to processes (like summation) that produce coherency and result in harmonious function.
-refers to all the axon terminals found on the post-synaptic cell working together, each sending same/diff signals which result in different outcomes |
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Temporal Summation
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occurs when a nerve is stimulated rapidly and all those stimuli are added together to make an excitatory post-synaptic potential
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Spatial Summation
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Occurs when different nerves contribute and add together to create a stimulating/inhibitory potential
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Why have summation instead of a 1:1 relationship with stimulus and AP?
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-allows control
-allows plasticity |
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What other cells do neurons communicate with (besides other neurons)?
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-neuron-->effector cells (neuromuscular junction):causes some action
-sensor-->neuron |
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Labeled Line Principle
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-Action potentials look the same no matter the stimulus
-the brain knows that an AP comes from a certain location on the body (certain nerve) and understands what is being signaled --perceives stimulus based on where it comes from |
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Reflex Arc
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A neural pathway that controls an action reflex
-can be single-cell connection, monosynaptic reflex arc, or polysynaptic reflex arc |
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Afferent Neurons
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Carry signals from receptor/sense organ to the central nervous system
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Efferent Neurons
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Carry signals from the central nervous system to effectors
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Advantage of polysynaptic reflex arc
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have more control if more neurons are involved in relaying a message
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Cephalization
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the consolidation of the nervous system in the head
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General organization of the Vertebrate Nervous System
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-Central nervous system (brain/spinal cord): major sight of integration
-Peripheral nervous system (everything else): somatic and autonomic motor/sensory neurons |
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Somatic Nervous System
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part of the peripheral nervous system that control skeletal muscles (striated)
-effects most observable behavior |
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Autonomic Nervous System
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part of the peripheral nervous system that controls all neuron-controlled effectors other than skeletal muscle (cardiac muscle, smooth muscle, and glands)
-effects on visceral organs, mostly internal/unnoticable -divided into two nervous systems: --sympathetic --parasympathetic |
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Sympathetic Nervous System
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-division of the autonomic nervous system
-mostly inhibits functions related to autonomic system: --inhibits digestion, gastrointestinal secretion/motility --increases rate/force of heart --constricts vessels to kidney, gut --dilates vessels to skeletal muscle --dilates lung passages --increases blood pressure --stimulates epi (fight or flight) |
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Parasympathetic Nervous System
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-division of the autonomic nervous system
-mostly stimulates functions related to autonomic system: --stimulates digestion, gastrointestinal secretion/motility --slows heart --dilates blood vessels --decrease blood pressure -constricts lung passages |
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Endocrine System
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-Involves endocrine tissues, hormones, specific glands, neurohemal areas, and other organs of the body
-Secretions of the glands are released into the blood stream |
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Hormone
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chemical messenger produced and released by nonneural endocrine cells or neurons, carried in blood to communicate with target cells
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Neurosecretory Cells
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part of the endocrine system instead of the nervous system because they synapse with blood vessels
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Secretory cells
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-often filled with vesicles containing hormone molecules
-mixed into other organs as well as endocrine tissue |
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Target cells
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only respond to a hormone if they have the hormone receptor
-can have different ones on same cell |
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Exocrine Glands
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releasing secretion of glands into ducts that dump secretions outside of the body
-like in the digestive tract (tube within a tube design) |
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Paracrine secretion
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-different from endocrine secretion
-simple diffusion between cells close to each other --secretion taken up by adjacent cells |
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autocrine secretions
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-different from endocrine secretions
-signal messages to self --e.g. inhibiting own functions |
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Roles of Endocrine System
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Typically things occur over long period of time
-growth, development, reproduction --slow, many tissues involved Though things can happen over quicker time scale as well -homeostasis (digestion, osmoregulation, etc) |
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Vertebrate Endocrine Glands
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-each cell contacts a blood vessel
--has own blood supply --closed circulatory system |
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Invertebrate Endocrine Glands
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-bathed in hemolymph
-hormone diffuses to surface --open circulatory system |
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3 General Classifications of Hormones
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-Peptides (short chains of amino acids)
-Steroids (from cholesterol) -Amine Hormones (from tryptophan or something made from that) --composed of catecholamines, melatonin and thyroid hormones** |
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Where Peptide hormones are secreted from
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most sites of hormone secretion besides adrenal cortex and medulla, thyroid gland, and pineal gland
|
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Solubility of peptide hormone
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water soluble
|
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synthesis and storage of peptide hormone
|
-synthesized at rough ER, processed in golgi
-stored in vesicle |
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secretion of peptide hormone
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exocytosis
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transport of peptide hormone
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dissolved in plasma or some bound to carrier proteins
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half-life of peptide hormone
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minutes
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location of receptor for peptide hormone
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surface of target cell membrane
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action of peptide hormone at receptor cell
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activates second-messenger system (alters membrane channels)
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response of target cell to peptide hormone
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changes activity of preexisting proteins
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action duration of peptide hormone
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seconds to hours
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site of secretion of steroid hormone
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adrenal cortex, gonads, placenta
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solubility of steroid hormone
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lipid-soluble
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synthesis and storage of steroid hormone
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synthesized on demand in intracellular compartments and is not stored
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secretion of steroid hormone
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simple diffusion through cell membrane
|
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transport of steroid hormone
|
bound to carrier proteins
|
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half life of steroid hormone
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hours
|
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location of receptor at target cell for steroid hormone
|
cytoplasm or nucleus (occasionally surface)
|
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action of target cell in response to steroid hormone
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alter gene expression
-activated genes initiate transcription/translation |
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response of target cell to steroid hormone
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synthesize new proteins
--some may alter activity of preexisting proteins |
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action duration of steroid hormone
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hours to days
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site of secretion of amine hormones
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adrenal medulla or pineal gland
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solubility of amine hormones
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water soluble
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synthesis and storage of amine hormones
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synthesized in the cytoplasm and stored in vesicles
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secretion of amine hormones
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exocytosis
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transport of amine hormones
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dissolved in plasma
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half life of amine hormones
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seconds to minutes
|
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location of receptor molecule for amine hormones
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surface of target cell
|
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action at target cell that results from amine hormones
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activate second-messenger systems
|
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response of target cell to amine hormones
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change activity of preexisting proteins
|
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action duration of amine hormones
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seconds to hours
|
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site of secretion of thyroid hormones
|
thyroid gland
|
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solubility of thyroid hormone
|
lipid-soluble
|
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synthesis and storage of thyroid hormone
|
made prior to use and stored in a colloid island within gland
|
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secretion of thyroid hormone
|
simple diffusion across membrane
|
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transport of thyroid hormone
|
bound to carrier proteins
|
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half life of thyroid hormone
|
days
|
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location of receptor molecules for thyroid hormone
|
nucleus
|
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action of target cell that results from thyroid hormone
|
alter gene expression
-activated genes initiate transcription and translation |
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response of target cell to thyroid hormone
|
synthesize new proteins
|
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action duration of thyroid hormone
|
hours to days
|
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What stimulates a cell to release hormone
|
-synaptic trigger
-other hormones -environmental effect of membrane --ex. release of ADH For lipid soluble hormones: -no vesicle used, diffuse out as made For vesicle bound hormones: -released by exocytosis --AP, non-AP depolarization or intracellular signaling pathways raising Ca concentration ---ER or Ca channels |
|
effect of hormone on target cells
|
For receptor proteins in cytoplasm/nucleus:
-lipid-soluble hormones interact with -modulate gene expression (transcription/translation) -long-term effects For receptor proteins on plasma membrane: -mostly-lipid insoluble hormones interact with -effects membrane permeability, activity of existing proteins, etc. -short-term effects |
|
islets of Langerhans
|
the endocrine tissue regions of the pancreas
-made up of two cell types: --30-40% alpha-cells --the rest: beta-cells |
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Pancreas
|
endocrine and exocrine glands
-mostly exocrine -have islets of Langerhans -produces/synthesizes glucagon and insulin |
|
Glucagon
|
-produced/synthesized in pancreas
-secreted by alpha-cells -released in response to low blood sugar (hypoglycemia) |
|
Insulin
|
-produced/synthesized in pancreas
-secreted by beta-cells -released in response to high blood sugar (hyperglycemia) |
|
Type I Diabetes
|
-loss of beta-cells (cells producing insulin)
-autoimmune |
|
Type II Diabetes
|
-loss of insulin receptor/signaling
--producing insulin by its not effective (will see glucose in urine) -often associated with obesity because of observations about resistin --resistin is released by fat cells and antagonize insulin receptors |
|
Types of Animal Muscle
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-smooth
-striated --cardiac and skeletal |
|
Cardiac Muscle
|
-type of striated muscle
-each cell has 1 nucleus -interact with adjacent cardiac cells at gap junctions --electrical signaling ensures the muscles contract in unison |
|
Skeletal Muscle
|
-type of striated muscle
-made up of multiple nuclei --developed by the fusion of many cells -cells don't interact at gap junctions like cardiac cells -controlled voluntarily while cardiac/smooth muscles are not. |
|
What skeletal muscle is made up of
|
Sarcomeres make up a single muscle fiber(cell) and a bundle of fibers make a fascicle and muscle is made up of a bunch of fascicles wrapped together
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Fascicle
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a bunch of muscle fibers (cells)
|
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Tendon
|
connects bone to muscle
-convergence of connective tissue |
|
Sarcomere
|
-basic unit of a muscle
-overlapping filaments of actin and myosin |
|
Myofibrils
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-tubes that make up muscle fibers (cells)
-composed of repeating sections of sarcomeres |
|
Anatomy of Sarcomere
|
Made up of:
-Z disc -H zone -A band -M Line -I band |
|
M Line
|
-part of sarcomere
-helps anchor myosin -inside H zone |
|
I Band
|
-surrounds z disc
-distance from one myosin to next --only made up of action and z disc |
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A Band
|
-occupied by all the myosin
-also contains the actin not in the I band -MAde up of H zone and region where actin/myosin overlap |
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H Zone
|
-only myosin
-within the A band |
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Z Disc
|
-on both ends of sarcomere
|
|
Sliding-Filament Theory
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-Discovered by Huxley and Huxley independently
-The theory that the thin filaments (actin) slide alone the thick filaments (myosin). -Z discs move towards each other. -I band and H zone shorten while there is no change in the thickness of A band --shows that actin and myosin themselves dont shorten though the distance between them does |
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Thin Filament
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Made up of:
-Actin (primary component) --2 helical strings of beads (actin proteins) -Tropomyosin --filaments in the grooves of the helix that are involved in regulating muscle contractions -Troponin Complex --attached to tropomyosin and can move tropomyosin off of actin binding sites |
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Thick Filament
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Made up of:
-Myosin (primary component) --2 myosin chains with globular heads come in contact with tons of other chains, tails each anchored together my M line --aggregate into thick filament --have to biding sites (one for actin, one for ATP) |
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How do filaments slide?
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By forming cross-bridges
-formed by myosin head binding to actin |
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Concept behind how cross-bridges form/detach
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-at rest (in cocked position), ADP-P (ADP and inorganic phosphate--hydrolyzed ATP) is bound to myosin (though its binding to actin may not occur if tropomyosin is blocking the binding site)
-if tropomyosin is moved away, actin binding triggers release of the P causing a tighter bind between actin and myosin and then a power stroke -the myosin head swivels in the power stroke, causing it to pull the attached actin towards the middle of the myosin filament. -ADP is released at the end of the power stroke, though myosin is still tightly bound to actin -ATP binding to myosin causes it to detach from actin -Myosin hydrolyzes ATP to ADP-P, causing the angle of the head to change into cocked position and the whole process can begin again. |
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Role of ATP in formation/detachment of cross-bridges
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-physical binding of ATP to myosin changes its conformation, causing it to detach from actin binding site
-Provides energy to cock the myosin head |
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How Ca regulates muscle contractions
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-Discovered by Ringer & Buxton
-Troponin and tropomyosin block the myosin binding sites from actin while Ca is not present -Ca can bind to troponin complex, dragging tropomyosin away from binding sites. --Myosin rapidly binds since it is already cocked |
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Motor Neuron
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efferent neuron from spinal chord (CNS) to muscle
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Neuromuscular Junction
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-motor endplate
-where motor neuron synapses muscle. |
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Motor Unit
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(1) motor neuron and all the fibers it innervates
--only 1 in vertebrates |
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Sarcolemma
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The cell membrane of a muscle fiber (cell)
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Sarcoplasmic Reticulum
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endoplasmic reticulum of a muscle fiber (cell)
-specialized in Ca storage |
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The Excitation at the Neuromuscular Junction
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-AP travels downs the motor neuron and presynaptic AP triggers exocytosis of Ach.
-Ach opens ligand-gated cation channels on the muscle membrane, depolarizing sarcolemma --race with Acetylocholinesterase (breaks down Ach) in extracellular matrix of synaptic cleft. -Na rushes into the cell while much less K rushes out of cell -1:1 transmission in twitch fibers |
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Excitation of Muscle after motor neuron
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-Net inward movement of Na due to the binding of Ach to receptors on the muscle membrane initiates and action potential.
-AP propagates over the cell membrane and depolarizes t-tubules. -Depolarization of t-tubules reaches DHPR (dihydropyridine receptors), causing it to change formation and open RyR (ryanodine receptor) calcium channel on the sarcoplasmic reticulum. -Ca ions diffuse out of SR into cytoplasm and bind to troponin causing tropomyosin to move, exposing myosin-binding sites. -When the wave of depol. ceases, DHPR returns and RyR is closed. -ATP-dependent Ca pumps are continuously active, bringing Ca back into SR (2Ca per ATP). |
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DHPR
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Dihydropyridine receptors
-when depolarization comes down t-tubules, causes DHPR to change conformation and detach from RyR -On sarcolemma, connects to RyR on SR |
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RyR Calcium Channel
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Ryanodine receptor calcium Channel
-after depolarization, DHPR changes conformation and disconnects from RyR, allowing Ca to flow out freely from SR |
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T-Tubules
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Brings depolarization down to site of Ca pores
-depolarization alters configuration of DHPR, causing it to move away from RyR |
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What Requires ATP in Muscle Contractions
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-Myosin
-Ca pumps |
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Sources of ATP for Muscle Contractions
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-ATP "stores"
-Creatine phosphate -Anaerobic glycolysis -Aerobic catabolism |
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ATP stores as means of producing ATP for muscle contraction
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-Have small amount of reserved ATP in cytoplasm at rest
--can be used for a few seconds of muscle contraction |
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Creatine Phosphate as means of producing ATP for muscle contraction
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-Creatine is a phosphogen which stores high energy phosphate bonds.
-High energy phosphate of creatine can be donated to ADP to produce ATP -We typically have enough for a couple seconds of muscle contraction -Does not require O2 or create a waste product and donates P very rapidly |
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Anaerobic Glycolysis as means of producing ATP for muscle contraction
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-ATP made quicker than in aerobic metabolism
-produces lactic acid --negative effects of lactic acid: ---causing pain ---interfering with muscle contractions ---self-limiting: stops break down of glucose ---interferes with myosin/actin binding |
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Aerobic Metabolism as means of producing ATP for muscle contraction
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-Produces a lot of ATP but slower than anaerobic glycolysis
-requires O2 |
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Increase twitch size by...
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increasing the amplitude of the stimulus, thus incorporating more motor units involved in twitch.
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Why does it take time to reach peak tension?
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-Have series elastic components (tendons, Z-discs)
-Have parallel elastic components (parallel cells, connective tissue) --Need the force applied to muscle to deform elastic components before the force can be applied to a load. |
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Isometric Contraction
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A contraction where the load does not move when you apply a force
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Isotonic Contraction
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A contraction where you maintain a constant tension
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Length-Tension Relationship for muscles
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-maximal tension is achieved when muscles are at their normal lengths in organisms
-The set length of the muscle fibers affects the length of the sarcomeres within it and thus the degree of overlap of the thick and thin filaments within the sarcomeres. --the lengths that yield max tension were those in which the overlap of thick and thin filaments permits optimal cross-bridge binding with actin. (less overlap when muscles are fully stretched out, so less binding sites to myosin. At shorter lengths, thin filaments overlap H zone where there are no myosin cross-bridges or go to far overall. |
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How to physiologically control the strength of muscle contractions
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-size of active motor units
-recruitment (motor units, muscles) -length-tension relationship -temporal summation (tetanus) -Muscle size |
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Motor Unit
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a motor neuron and all the muscle fibers it innervates
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Recruitment for controlling muscle contraction strength
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Increasing the number of motor units being stimulated will increase the amount of muscle fibers twitching-->strengthens the twitch
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Temporal Summation for controlling muscle contraction strength
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-When a muscle is stimulated more than once within a brief period, the successive twitches produced add to each other, so the overall response is greater than the twitch response to a single stimulus.
-amplitude of the summed contractions depends on the interval of time between stimuli. -Low frequencies of stimuli with relatively long intervals between each produce contractions that sum but are not fused. |
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Tetanus
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-The smoothly fused muscle contraction produced as a result of a high frequency stimulation.
-Usually about 3-4X the amplitude of a twitch in mammals |
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How Ca enables summation/tetanus
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-each AP triggers the release of a sufficient number of Ca ions, ultimately allowing cross bridges to form
-The contractile apparatus requires time to pull on the elastic components of muscle -Ca is usually pumped back into the SR before the cross-bridges can fully stretch out the elastic elements -HOWEVER, successive AP open the RyR channels with sufficient freq. that the cytoplasmic concentration of Ca keeps the actin-binding sites exposed, allowing cross-bridges to cycle repeatedly until the elastic elements are stretched taut and the full contractile potential of the muscle fiber is realized. --length of twitch (time) is much longer than an AP so its relatively easy to catch a twitch before relaxation with a new AP |
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Trepe
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partial tetanus
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Effects of Muscle Size on muscle contractions
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-slower time domain than the other influences
-force of contraction is proportional to the cross sectional area of a muscle -resistance exercise changes size of muscles -hyperplasia |
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Hyperplasia
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-increasing the number of cells
-studies have shown that animals are able to increase the number of actual muscle cells that they have after extreme resistance training -no firm evidence that humans can do this. |
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Hypertrophy
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-increasing the actual size of a cell
Transient Hypertrophy -edema: initial increase in muscle size due to fluid leaking out of blood vessels immediately after working out. Chronic Hypertrophy -each muscle fiber increases in cross-sectional area due to an increase in actin and myosin |
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Traditional Classifications for Vertebrate Twitch Muscle Fibers
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-Slow oxidative (type I)
-Fast glycolytic (type IIB) -Fast oxidative (type IIA) |
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Slow Oxidative Muscle Fiber
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-Type I, MHCi (myosin heavy chain 1)
-slow contractions using aerobic metabolism -high concentrations of mitochondria, capillaries and myoglobin -will not fatigue rapidly because no lactic acid produced -used for postural muscles -red muscles -active for long periods of time without fatigue -small diameter since they have less room for actin/myosin with all the mitochondria -slow myosin ATPase -long twitches -slow Ca uptake by SR |
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Fast Glycolytic Muscle Fiber
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-Type IIB, MHCiib (non human) and MHCiix (mammals/humans)
-primarily anaerobic -produce lactic acid, so fatigue easily -less myoglobin -used in strenuous exercise -white muscle -fast myosin ATPase activity -short duration of twitch -high rate of Ca uptake by SR -few mitochondria -large diameter -many glycolysis enzymes |
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Fast Oxidative Muscle Fiber
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-type IIA, MHCiia
-primarily aerobic -fast myosin ATPase activity -short twitches -high rate of Ca update my SR -medium resistance to fatigue -many mitchondria -high myoglobin content -red -medium diameter -many capillaries |
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Composition of Fiber types in vertebrate skeletal muscle
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-given motor unit innervates same type of muscle fiber
-most muscles are about 50/50 fast glycolytic: fast oxidative/slow oxidative -Muscles involved in posture mostly composed of slow oxidative -There is some plasticity in terms of types of muscle fibers found in muscles: mostly is genetic, but training can convert fast oxidative and fast glycolytic to one or the other. |
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Twitch Fibers
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-generate action potentials that give rise to a twitch
-all or nothing-->full contraction |
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Tonic Fibers
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-found in postural muscles of amphibians, reptiles, and birds and found in eye muscles of mammals.
-Cannot produce an AP -contract very slowly -long-lasting contractions with low energetic costs --Ca pumps dont work as hard -graded release of Ca from SR=graded force -1 neuron still innervates the muscle fiber but can synapse multiple times --temporal summation |
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Striated muscles of arthropods (invertebrates)
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-same basic structure as in vertebrates (sarcomeres, t-tubules, SR, extracellular Ca, troponin, tropomyosin)
-Behaves like tonic muscle fibers -Have 1-10 motor neurons per muscle --no AP --integration at muscle cell (instead of at presynaptic neuron in vertebrates) -can have excitatory and inhibitory stimuli |
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Traditional Classifications for Vertebrate Twitch Muscle Fibers
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-Slow oxidative (type I)
-Fast glycolytic (type IIB) -Fast oxidative (type IIA) |
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Synchronous Flight Muscles
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-used in flight
-each muscle contraction is synchronized with the action potential that initiated it, like in vertebrate skeletal muscle. --1AP=1 muscle contraction -Muscles are arranged vertically to the long axis of the animal. -contraction up to 200Hz (200 contractions/s) compared to vertebrates that can do about 90 Hz |
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Asynchronous Flight Muscles
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-used in flight
-each muscle is capable of contracting at much faster frequencies than synchronous flight muscles. --1000Hz -Individual contractions not synchronized with individual nerve AP --many oscillating contractions per AP -Muscles not attached directly to wings -have opposing pairs of muscles --alternate stretching an relaxation to signal contraction and relaxation -Ca pumps in SR work very slowly relative to other animals (less ATP used and more Ca left in cytoplasm) --Tropomyosin is moved by both Ca binding to troponin and moved by muscle contractions themselves (both need to occur to move actin/myosin). --Just need AP at high enough frequencies to ensure enough Ca is present. |