Biology 155 Notes - Winter Final PDF

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Biol 155 - Winter Final Review Notes Nursing: - Two hormones involved for lactation to occur, PRL (more evolved) and oxytocin - PRL controls mammary gland development (in utero, in puberty [second wave] and during pregnancy [third wave]) - As long as mother is breastfeeding after pregnancy, PRL levels will remain elevated - PRL stimulates milk production - oxytocin is required for the expression of milk from the breast - Mammary glands look like a bunch of grapes (each grape is a alveolus/synase) - Around each alveolus has contractile cells (modified smooth muscle cells) that respond to oxytocin - When mother starts to suckle offspring, mechanical tension of muscle will trigger release of oxytocin

What happens when calcium is released from the sarco-plasmic reticulum? How does it lead to cross-bridge cycling occuring? - Remember that on the thin filament we have 2 actin strand

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Tropomyosin attached to troponin Troponin only occurs periodically along thin filament Tropomyosin covers up myosin binding sites so that myosin heads cant come in and bind to the actin

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When action potential comes down, (activates dihydropyridine receptor which pulls open ryanodine receptor), this opens up calcium gates which allows calcium to come out of terminal cisternae Calcium then binds to Troponin C, which creates a conformational change in Troponin C which results in larger conformational change in entire troponin complex (whole thing kind of bends and pulls over) When that happens, the tropomyosin gets pulled out of the way so that the myosin binding sites gets exposed Myosin heads can then come in and spontaneously bind with actin (cross-bridge formation) Once that occurs, we get binding, release of phosphate, pulling, release of ADP, ATP comes in and replaces it, that breaks the head away, ATP gets hydrolyzed to ADP and phosphate, the head gets energized and binds to next binding site, and we get a repeat of that cycle (cross-bridge cycling)

Thick Filament Centering (00:10:10) ●

Thick Filament Centering ○ The role of titin, is that it is attached to the end of the thick filament and to the Zplate, it helps keeps the geometrical arrangement between the thin and thick filaments ○ When the sarcomere relaxes and gets stretched out (not an active process), there is nothing to guarantee that the thick filaments will be evenly placed between the Z lines, except for the Titin, the top filament (myosin filament 1) represents a thick filament that is not evenly spaced, as the two z lines pull apart we get tension being put on both titans, the top titin is not being stretched (not storing energy) on the other one has a lot of energy because it is being stretched out. ○ The Titin that is being stretched out more is going to start to release, and the titin that isn’t being stretched will start to stretch. Titin makes sures the thick filaments are evenly spaced between the z lines in all the sarcomeres in the muscle cell.

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The role of hormones in regulating calcium levels in the body (plasma) ○ Calcium is involved in synaptic transmission, blood clotting, heart contraction, etc. ○ The two hormones are parathyroid hormone and calcitonin ○ If calcium starts to drop below the min. Level, the parathyroid glands start to release parathyroid hormones which stimulate osteoclasts and inhibit osteoblasts. Osteoclasts break bone down and they break the calcium crystals in the bone which goes in the blood. The parathyroid also stimulates kidneys, which makes sures we don’t pee out calcium when calcium levels are dropping. ○ Parathyroid hormones also stimulate the calcitriol, it increases calcium ATP and speeds up calcium uptake from your meal. This will increase calcium by mobilizing calcium ions from the bones, increasing uptake in calcium ions from your meal, and decreasing the loss of calcium ions with ur kidneys.

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When you have an excess of calcium, you want to lower the calcium ion concentration, but you do not want to lose it to the environment. Calcitonin (released by C-cells in thyroid gland proper) will help reduce calcium levels in two ways. ○ Increases calcium recovery across the convoluted tubule, then it stimulates osteoblasts and inhibits osteoclasts, so you stop breaking down bones and you start laying down new bony tissue, this will decrease plasma calcium levels and restore homeostasis.

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6 steps synthesis of thyroid hormone 1. Synthesis of thyroglobulin 2. Uptake of iodide from the blood, this is a chloride iodide exchanger, we are bringing in iodide in exchange for chloride. Both of these are stimulated by thyroid stimulating hormone 3. Iodination: Thyroid peroxidase takes iodide from the cytoplasm and pumps it into

the secretory vesicle that contains the thyroglobulin that is about to be released, that thyroid peroxidase removes the electron from the iodide and turns it into atomic iodine. 4. Coupling, we get neighbouring iodinating tyrosines in the thyroglobulin, the benzene ring will get attached to another and so this is where we get form pro t4 and t3 5. Uptake, Endocytosis fusion with lysosome where the proteolytic enzymes will break down thyroglobulin (has pro T3 and T4), as the peptide bonds are broken down the amino acids are liberated, t3 and t4 are both basically amino acids 6. Diffusion of the liberated T3 and T4 out of the cell into the blood -> carried by carrier proteins

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Dynamic Range ○ In any sensory receptor we have a range where the receptors output will change in relation to the strength of the stimulus ○ Below that, any stimulus intensity below the threshold, we can increase stimulus intensity, but it won’t affect output on the receptor because it is below the sensitivity level ○ At threshold that is where we get enough stimulus intensity that we start to change the output of the sensory receptor, it could be as simple as the change of action potential frequency in the sensory neuron, it could be the receptor potential in a modified epithelial cell, we can detect the change ○ In the range between the threshold and the saturation, as we increase the stimulus intensity, we increase the magnitude of response, this range is called the dynamic range. Over the dynamic range we get a proportional increase in magnitude of response with an increase of stimulus intensity. However, we get to a point beyond the receptor proteins, they get saturated, then increasing the stimulus intensity will not give us an increase in magnitude of response because they are already working at full capacity

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Dynamic Range and Discrimination ○ Trade off between dynamic range and discrimination ○ Large dynamic range (to cover what you normally see) ■ Large change in stimulus causes a small change in AP frequency ● Large dynamic range ● Poor sensory discrimination ○ Narrow dynamic range (gives you more sensitivity)

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Small change in stimulus causes a large change in AP frequency ● Small dynamic range ● Good sensory discrimnation

Receptor A has a large dynamic range, the problem is this, is that if we increase 250 up to 300, if we look at the change in magnitude of response, it isn’t much change. We prefer to have a bigger change Receptor B has a smaller dynamic range, but 250-300 it has a much bigger magnitude of response. By having this narrow dynamic range, we get better discrimination, but we do not cover the entire range that we normally see. This is always the tradeoff.

Control of pituitary secretion ● Posterior pituitary gland axonal projections of neurosecretory cells that have their cell bodies in the hypothalamus, these are neurons so an AP travels down axons to the end, where the modified synapses, large are now a neurohemal organ terminates on blood vessels that release neural hormones into the bloodstream ● Secretion of each hormone by the adenohypophysis is controlled by neurohormones secreted by neuroendocrine cells in the hypothalamus. ● Two neurohormones control the secretion of pituitary hormones Oxytocin and Vasopressin. ● The hormones secreted by the anterior pituitary are also controlled by the hypothalamus ● The two purple cells are neurosecretory cells that release the neurohormones that will control anterior pituitary function. ● Each hormone from the pituitary will have two neurohormones regulating it. Stimulatory and Inhibitory neurohormones. ○ Example - Growth hormone (GHRH) and its inhibiting hormone Somatostatin (GHIH) ● As the action potential travels down the neurohormone organs, they terminate on to a capillary bed, As they go into the blood they flow down and are branched into portal veins. ● The portal veins carry the blood down to the anterior pituitary which is branched into another capillary bed. The endocrine cells will secrete or inhibit hormone production according to the neurohormone. ● The advantage in the neurohormones releasing cells is that they don't make a lot of neurohormone as there is a very little dilution factor so it does not take a lot to reach the dilution factor.

Adrenal Gland Anatomy 2 major regions: - Adrenal Medulla - made of chromaffin, an extension of the sympathetic nervous system, synthesizes catecholamines (adrenaline mostly, some noradrenaline) - Outer- cortex - 3 layers, each one synthesizes a different group of steroid hormones. a. Outer layer = zona glomerulosa cells produces mineralocorticoids (Mainly Aldosterone) helps you regulate ion and electrolyte balance (Na) in the plasma and extracellular fluid (blood) b. Middle = zona fasciculata cells produces glucocorticoids (cortisol) act as stress hormones, mobilize deep energy reserves and help conserve energy c. Inner = Zona reticularis cells produce gonadocorticoids (sex hormones) after puberty (the ones opposite your sex, ie men also produce a bit of estrogen which would come from here whereas the majority of their hormones, testosterone, comes from the testes) testosterone influences sex drive

Action Potential Propagation -

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Accomplished by the opening of voltage gated Na channels, influx of + ions, depolarization is caused inside the cell There is already K+ inside the cell, and the influx of Na+ ions displaces the K+ ions and moves them laterally underneath the membrane (towards the negatively charged proteins) if the threshold is reached the Na Gates to open in the next section and depolarize that section and continue… Takes a while for the voltage gated Na channels to return to sensitive state: they won’t respond to a second depolarization until after repolarization when the activation gate is closed and the inactivation gate has reopened) The refractory membrane has voltage gated K channels open, causing efflux of extra positive charges, along with the K leak channels, returning membrane to resting potential, putting the membrane back into the voltage sensitive state VG-Na Channels: responsible for inducing an action potential via the influx of sodium ions VG-K Channels: along w/ K+ leak channels, responsible for resetting the VG-Na Channels via the efflux of K+ ions

Ear - Semicircular Canals and Cupula ● Each side we got 3 semicircular canals oriented at 90 degrees to one another. ● Cupulas are in each of the three axis of rotation. These are located in enlarged areas of the end of the semicircular canal called Ampulla. ● Cupula extends across the Ampulla and is not attached to one side. One the other side there is a bride of epithelial cells which has hair cells. ● The hair cells are embedded into the jelly like material of cupula. It is a type of Colloid that has cross linked proteins. The spaces between the proteins are filled with endolymph. ● Endolymph has a high potassium concentration similar to the intracellular fluid. The apical membrane of the hair cells is exposed to the high potassium. ● The Cupula is attached at the cristae region, the cilia help anchor the cupula so only the other end can move = a flap across the ampulla ● System relies on ○ Density of cupula = density of the endolymph ■ The cupula will not float or sink important to if we were lying down which would bend the cells and send artificial stimulation ○ Endolymph(fluid of semicircular canals) has mass = inertia ■ Canals rotate when we move our head but the endolymph and its inertia will keep it still as cupula moves ■ As the cupula moves, it will hit the still fluid causing it to bend in the opposite, deflecting the hair cells changing the action potential frequency out the sensory neuron ● GROWTH HORMONES IN LONG BONES

● Growth hormones stimulate chondrocytes and osteocytes ○ After mitosis, cells stop responding to growth hormone ■ Start growing, get bigger and bigger ■ Modifies cartilage around it by secreting calcium ■ Makes it more spongy, easier for osteoclasts to break down ■ Osteocytes replace old cartilage ● Note: as old cartilage is being chewed up, new cartilage is being made at the top ○ ... Epiphyseal plate actually stays at the same thickness! ● Another note: ○ As growth hormone decreases (like when we get older)... ■ It decreases past the threshold of chondrocyte stimulation FIRST ■ Chondrocytes stop dividing ■ No more new cartilage ■ BUT, osteocytes are still growing upward! Chews into old cartilage ■ Keep going until they reach the top and fuse with

bone in the head ■ No more growth :(

FOVEA VS. OPTIC DISC FOVEA ● Thinner part of the retina ● At the back of the visual path to the eye ● The center of your field of view ● High density of photoreceptors ○ Mostly cones, not rods ● Less material here that can disrupt the resolution of the image ○ No blood vessels ● ... Best colour vision and resolution! ● Looks darker because it reflects back less light OPTIC DISC ● All of the axons exit through here ○ Lots of myelin, reflects light ● No photoreceptors ○ ... Blind spot ● Here is where all of the blood vessels are coming in ○ Would Block light anyways if it reached this spot

Rods, Cones, and Vision (extra info for background knowledge) - Rods have a high density of one particular photoreceptor, making it sensitive to

brightness Cones have a wide variety of different photoreceptors, making it able to perceive different wavelengths of visible light - Light Pathway - Retina > Ganglion Cell > Amacrine Cell > Bipolar Cell > Horizontal Cell > Rods and Cones - Melanin pigments wrap around the photoreceptive regions in the rods and cones to prevent the loss of light by bouncing it - Retinals are organic molecules - Cis-retinals activates binding sites for photons in opsin (a photoreceptive protein) - Combination of opsin and retinal form rhodopsin - Light is able to be absorbed by opsin - Light absorption transforms cis to trans-retinal - Trans-retinal closes photon binding site in rhodopsin - Trans-retinal and opsin separates, ATP converts trans to cis-retinal - Opsin is reset for further light absorption - Light absorption by opsin causes transducin activation - Transducin activates phosphodiesterase which causes Cyclic-GMP levels to fall - This causes the closing of Na+ channels, reducing the release of neurotransmitters Synaptic activity in the retina falls in the light and is more active in darkness -

Smooth Muscle Cells and Increase of Sarcoplasmic Reticulum - this leads to crossbridge formation and cycling Sarcoplasmic calcium increased by: - Hormone stimulating a GQ pathway (1. On diagram) - Mechanically gated Ca Channel - Ligand gated Calcium channel Calcium binds to Calmodulin (CaM), CaM binds to myosin light-chain kinase (MLCK), MLCK phosphorylates the myosin heads, myosin forms into thick filaments, myosin head can spontaneously bind to actin (must be phosphorylated, (in smooth muscle we don’t have tryptomyosin or troponin meaning the Actin sites are exposed)

Steroid Hormones and Thyroid hormones -

Neither strictly require a cell surface receptor (unless we need something quick acting), needed for gonadocorticoids (steroid) but NONE for thyroid Both have permeable membranes

Steroid Hormone - Diffuses through membrane lipids and binds to a cytoplasmic receptor (is as specific as

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a cell surface receptor) It floats free in the cytoplasm. This complex is pulled into the nucleus and binds to promoter regions genes that need to be transcribed. DNA, specific Genes are transcribed which results in mRNA which gets transported into the cytoplasm where translation and protein synthesis occur This gives us our target cell response, often change in structure

Thyroid hormone - Same process as above, the genes transcribed are involved in metabolic process which results in changes in cellular metabolism - Can bind to mitochondrial hormone receptor instead of nucleus, this increases rate of oxidative phosphorylation in the mitochondria which speeds up production of ATP and heat production (this is why the thyroid controls basal body temperature)

Spatial Summation In Neurons - Measure voltage near stimulatory synapse = depolarization - Voltage near inhibitory synapse = hyperpolarization (EPSP) Can cancel eachother out^ so there is no change in membrane potential at initial segment If the initial segment goes over threshold based on the sum total of the inputs there will be generation of action potential, if it doesn't go over threshold there will be no action potential.

Slow Twitch High Oxidative Fibres VS. fast Twitch low oxidative fibres -

We have mostly fast twitch low-oxidative fibres

STHO fibres - smaller diameter = higher surface area to volume ratio = more chance for oxygen to diffuse in (good bc these cells are aerobic) - High myoglobin (makes muscle red), stores oxygen (have their own supply incase the circulation falls short of oxygen delivery) - Rely on oxidative phosphorylation to provide ATP for contraction, mitochondria are plenty and very active during contraction - Many capillaries to deliver oxygen (also red) - Low anaerobic capacity due to their reliance on oxygen - High fatigue resistance - These are SLOW twitch because they require crossbridge cycling which takes longer - Small diameter = fewer myofibrils = not as strong, but better endurance FTLO Fibres - Lower SA to V ratio means harder for oxygen to get in - Plenty myofibrils = very powerful, but run out of energy quickly due to not using oxygen to generate ATP - Almost No myoglobin - Not as many mitochondria, not used to produce ATP for contraction, only to build up ATP

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at rest Lower capillaries due to not relying on oxygen Low aerobic capacity - high anaerobic capacity = not resistant to fatigue, run out of energy very quickly Go through crossbridge cycles rapidly, Break down atp very fast = more force Must have glucose supply available to break down atp Have LOTS of glycogen, very light in colour making these muscles light in general

Tyrosine Kinase Signal Transduction -

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Many membrane subunits, receptor subunits are unassembled Ligand binds to the receptor, exposing binding sites that allow dimerization to occur Dimerization =Two identical subunits with a molecule of hormone bound to them, stick together The dimer assembles the active catalytic site (tyrosine kinase) and we get autophosphorylation We then get phosphorylation and activation of intermediate kinases (very from cell to cell) these activate ras (monomeric g protein with single subunit) Ras has Guanine nucleotide binding site, in inactive form this has GDP stuck in the nucleotide fold Activated - GDP falls of and is replaced by GTP, GTP binds to nucleotide binding fold and ras becomes active and changes shape, activates Mitogen Activated Protein (MAP) Kinase Cascade GTP is hydrolyzed into GDP and phosphate - the energy from this goes to ras, and it goes back to its original configuration

MAP Kinase Cascade -turned on by activation of RAS - ras -> phosphorylation of MAPKKK -> phosphorylates MAPKK ->phosohprylates MAPK -> Map kinase ph...