BIOL353 flashcards TOP70

Mechanism = how a function works now (firefly: luciferase makes light). Origin = how/why it evolved (sexual selection for mate attraction).

Acclimation = reversible change in an individual (days-months; lab = acclimation, field = acclimatization). Adaptation = genetic change over generations.

Evolutionary (acute < chronic < developmental < evolutionary).

More UNsaturated fatty acids (keeps membranes fluid) AND change enzyme amount/isoforms.

Warm = more SATURATED. Cold = more UNsaturated (kinked tails keep fluidity).

Higher LDH activity: makes more lactic acid per time (faster anaerobic ATP).

Permits diffusion of solutes (ion channels) or osmosis of water (aquaporins) through the membrane.

3 Na+ out, 2 K+ in (active transport).

K+ leak channels (K+ leaks out, leaving net negative interior).

Kinase phosphorylates kinase phosphorylates kinase: one signal triggers many downstream molecules.

Body fluids saltier than water, so water enters by osmosis and fish make lots of dilute urine.

Open, closed, closed.

Higher FREQUENCY of spikes (spike train). Amplitude stays the same.

Voltage-gated Na+ channels open, Na+ rushes in.

Depolarization opens Na+ channels, Na+ enters, more depolarization opens more Na+ channels.

Current through a SINGLE channel.

ALL ionic currents across the membrane.

Gray = cell bodies, synapses, unmyelinated processes. White = tracts of myelinated axons.

Schwann cells (PNS) and oligodendrocytes (CNS).

Electrical (gap junctions). Then ionotropic, then metabotropic.

Ionotropic: receptor IS a channel, fast. Metabotropic: G-protein/second messengers, slow, can excite, inhibit or other.

EPSP depolarizes toward threshold. IPSP hyperpolarizes away from threshold.

Acetylcholinesterase.

Ionotropic ligand-gated channel: Na+ in (K+ out), excitatory (NMJ).

Metabotropic: G-protein itself opens a K+ channel (no second messenger). Slows the heart.

G-protein, adenylyl cyclase, ATP to cAMP, protein kinase, phosphorylation cascade. Raises heart rate.

Preganglionic ACh (nicotinic), postganglionic norepinephrine (adrenergic). Short pre, long post.

ACh at BOTH synapses (nicotinic then muscarinic). Long pre, short post.

Less stretch, weaker afferent signal. Medulla raises sympathetic, lowers parasympathetic: HR, contractility, vasoconstriction up.

Medulla. Sense PaCO2/pH in CSF. CO2 up lowers pH, signaling up, ventilation up.

Carotid and aortic bodies. Sense LOW PO2, plus pH and PaCO2 in plasma.

Conversion of stimulus energy into an electrical signal.

Photoreceptors, sweetittermami taste, vertebrate smell. (Mechano, thermo, vestibular, auditory, salt/sour are ionotropic.)

Toward = depolarize (excited). Away = hyperpolarize.

Hair cell bending (stereocilia against the tectorial membrane).

High frequency = base (oval window end). LOW frequency = APEX.

cGMP high, binds Na+ channels, channels open, cell depolarized (dark current).

Rhodopsin activated, transducin, phosphodiesterase breaks down cGMP, channels close, cell HYPERpolarizes.

A rhodopsin-based photoreceptor cell (prototype eye).

Vasopressin (= ADH) and oxytocin, MADE in the hypothalamus. Vasopressin and ADH are the SAME hormone.

Neuron that releases hormone into blood. Transduces neural signal into endocrine signal.

Paracrine = neighboring cells, autocrine = same cell (no blood). Hormone = blood, distant targets.

Synthesized at ribosomes (ER), proinsulin, C-peptide cleaved in Golgi, stored in vesicles, released by exocytosis on demand.

Glucose and insulin rise, glucagon falls.

Amino acids rise; insulin AND glucagon both rise; glucose about flat.

Vasopressin up (water reabsorption), aldosterone up (Na+ reabsorption), renin-angiotensin up. Raises volume and pressure.

Binds receptor, cAMP/PKA, AQP-2 vesicles fuse to apical membrane, water reabsorbed. Less ADH = fewer AQP-2 = more dilute urine.

Released by stretched atria. Inhibits Na+ reabsorption, vasopressin and renin: lowers volume and pressure.

Thick = myosin. Thin = actin + troponin + tropomyosin.

Myosin heads pull thin filaments, Z discs move together. Filaments don't shorten; I and H bands shrink.

Ca2+ binds troponin, tropomyosin moves, myosin-binding sites on ACTIN exposed; cross-bridges cycle until Ca2+ drops.

ATP binding detaches myosin from actin; hydrolysis re-cocks the head. One cycle = one ATP, about 10 nm.

Peak active tension at optimal sarcomere length (~2.0-2.25 um). Stretched too far = fewer cross-bridges = less tension.

Maximum shortening velocity at NO load. Max force at zero velocity (isometric).

Slow, red, many mitochondria and myoglobin, fatigue resistant, low force.

Fast, white, few mitochondria, high force, fatigue quickly (use ATP rapidly).

Same function, different kinetics (e.g., ATPase speed).

Single-unit: gap junctions, acts as unit (gut, small vessels). Multi-unit: few gap junctions, independent, direct neural control (iris, hair erectors, large arteries).

Burst of spindle afferents causes the muscle to contract MORE forcefully.

CPGs initiate AND maintain locomotion; reflexes correct and fine-tune.

An isolated system changes toward greater disorder (entropy). Heat flows hot to cold.

Direct = heat production. Indirect = O2 consumption and/or CO2 production.

RQ = CO2 produced / O2 consumed. Carbohydrates 1.0, proteins 0.83, lipids 0.71.

Rise in metabolic rate after eating; proportional to meal size.

Environmental temperature (plus physical activity). Smaller: meals, size, age, hormones, time of day.

CO2 and H2O (Krebs makes CO2; ETC consumes O2, makes H2O).

Oxygen (becomes water).

H+ back through ATP synthase = ATP. H+ back through UCP1 = HEAT (less ATP). UCP1: hibernators warming up.

Creatine phosphate first, then anaerobic glycolysis, then aerobic.

Repetitive movements, low force, aerobic metabolism.