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Stimuli and receptors
Stimulus: detectable change in the environment.
Receptors: cells that detect specific stimuli and generate a generator potential.
Organism survival increases when appropriate responses occur.
Plant tropisms
Tropism: plant growth response to a stimulus via growth.
Positive tropism: growth toward stimulus.
Negative tropism: growth away from stimulus.
Main stimulus types: light (phototropism) and gravity (gravitropism).
Growth factor: indoleacetic acid (IAA, an auxin).
Produced in tips of shoots and roots; diffuses to other cells.
In shoots: IAA increases cell wall plasticity→ results in cell elongation → shaded side elongates → shoot bends toward light (positive phototropism).
In roots: high IAA inhibits elongation → lower side inhibited → root bends downward (positive gravitropism), roots show negative phototropism.
Gravitropism:
In shoots IAA causes cells on lower side to elongate → shoot grows upward (negative gravitropism relative to gravity when necessary).
In roots IAA inhibits lower-side elongation → root bends down (positive gravitropism).
Simple animal response
Taxis: directional whole-body movement toward/away from a stimulus.
Positive taxis: toward stimulus.
Negative taxis: away from stimulus.
Kinesis: non-directional change in activity (speed/turning rate) to stay in favorable conditions.
Increase turning in poor conditions to find better area; if surrounded by poor conditions, decrease turning to move straight.
Receptors and nervous system
Reflex: rapid, automatic, involuntary response protecting tissues.
Nervous system:
Central Nervous System (CNS): brain and spinal cord (coordination center).
Peripheral Nervous System (PNS): sensory and motor neurons (receptors and effectors).
Reflex arc: receptor → sensory neuron → relay neuron (in spinal cord) → motor neuron → effector.
Typically three neurons, two synapses, fast response bypassing conscious brain.
Key human receptors
Pacinian (Pacinian) corpuscle: pressure receptor in skin; sensory neuron wrapped in lamellae.
Stretch-mediated Na+ channels open when deformed → Na+ influx → generator potential.
Rod cells (retina): detect low light, black-and-white, high sensitivity, retinal convergence (many rods → one bipolar cell) → low visual acuity.
Cone cells (retina): three types with iodopsin (red, green, blue), require high light intensity for color vision, one cone → one bipolar cell → high visual acuity.
Distribution: fovea dense with cones (high acuity); rods concentrated away from fovea.
Control of the heart
Cardiac muscle is myogenic (contracts spontaneously); rate controlled by electrical conduction and nervous input.
Conduction system:
Sinoatrial node (SAN): natural pacemaker in right atrium; emits depolarization wave.
Atrioventricular node (AVN): at atrial-ventricular border, delays signal.
Bundle of His → Purkinje fibers: conduct to ventricles; ventricles contract from apex upwards.
Medulla controls heart rate via autonomic nervous system:
Sympathetic → increases SAN firing → increases heart rate.
Parasympathetic → decreases SAN firing → decreases heart rate.
Receptors affecting heart rate:
Chemoreceptors detect blood pH (CO2/H+); low pH → sympathetic stimulation → increase heart rate.
Baroreceptors (pressure receptors) detect blood pressure; high pressure → parasympathetic stimulation → decrease heart rate; low pressure → sympathetic stimulation → increase heart rate.
Neuron structure and action potential
Motor neuron structure:
Cell body: organelles, neurotransmitter synthesis.
Dendrites: receive inputs.
Axon: long conductive fiber; Schwann cells form myelin sheath; gaps = nodes of Ranvier.
Resting potential: around −70 mV (inside negative). Maintained by Na+/K+ pump (3 Na+ out, 2 K+ in) and membrane permeability (more K+ channels open).
Action potential:
Stimulus opens voltage-gated Na+ channels → depolarization.
Threshold at ~−55 mV → rapid Na+ influx → peak ~+40 mV.
Na+ channels close; K+ channels open → repolarization and hyperpolarization (≈−80 mV).
Restored by Na+/K+ pump to −70 mV.
All-or-nothing principle: stimulus must reach threshold to trigger full action potential; larger stimulus increases frequency, not amplitude.
Refractory period: Na+ channels recover; ensures discrete impulses, forward propagation, and limits impulse frequency.
Factors affecting conduction speed
Myelination and saltatory conduction: action potentials jump node-to-node → faster conduction.
Axon diameter: larger diameter → less internal resistance → faster conduction.
Temperature: higher temperature → faster ion diffusion and enzyme activity → increased speed (within physiological limits).
Synapses and neuromuscular junctions
Synapse process:
Action potential arrives at presynaptic knob → Ca2+ channels open → Ca2+ influx.
Vesicles fuse with membrane → neurotransmitter released into synaptic cleft.
Neurotransmitter binds postsynaptic receptors → opens ion channels (e.g., Na+) → postsynaptic potential.
Neurotransmitter is broken down by enzymes and recycled.
Cholinergic synapse: uses acetylcholine (ACh); ACh broken down by acetylcholinesterase into acetate and choline.
Summation:
Spatial: many presynaptic neurons converge on one postsynaptic neuron.
Temporal: one presynaptic neuron fires repeatedly over short time.
Inhibitory synapses: open Cl− channels (or cause hyperpolarization) making AP less likely.
Neuromuscular junction: motor neuron to muscle fiber; ACh always the transmitter; triggers muscle action potential → T-tubules → Ca2+ release from sarcoplasmic reticulum → contraction.
Skeletal muscle structure and sliding filament theory
Key structures:
Myofibrils: cylindrical structures in muscle fibers composed of repeating sarcomeres.
Sarcomere: functional unit between Z-lines; contains actin (thin) and myosin (thick).
Sarcolemma: muscle cell membrane conducting action potentials.
Sarcoplasmic reticulum: stores/releases Ca2+ for contraction.
Sarcoplasm: cytoplasm with organelles, myoglobin, glycogen.
Sarcomere bands:
Z-lines mark sarcomere ends.
A-band: length of myosin (does not change length during contraction).
I-band: region of actin not overlapping myosin (shortens during contraction).
H-zone: myosin-only region (decreases during contraction).
M-line: center of myosin.
Sliding filament mechanics:
AP → Ca2+ release → tropomyosin shifts exposing myosin-binding sites on actin.
Myosin heads with ADP + Pi bind actin → crossbridge formation.
Power stroke: myosin pivots, pulling actin inward, ADP+Pi released.
ATP binds myosin head → detaches from actin.
ATP hydrolysis by myosin ATPase (activated by Ca2+) resets myosin head.
Cycle repeats while Ca2+ remains high.
Stop stimulation → Ca2+ pumped back into SR → tropomyosin blocks sites → muscle relaxes.
ATP & phosphocreatine:
ATP hydrolysis powers detachment and Ca2+ transport.
Phosphocreatine regenerates ATP rapidly during short intense activity.
Glycogen: stored glucose source for ATP production during respiration.
Muscle fibre types
Slow-twitch (Type I):
High myoglobin, rich blood supply, many mitochondria.
Slow contraction, sustain aerobic respiration, endurance activities.
Lower glycogen stores, produce ATP slowly but more overall via aerobic pathways.
Fast-twitch (Type II):
Thicker, more myosin filaments, large glycogen and phosphocreatine stores.
Fast, powerful contractions, suited to short bursts (sprinting, weightlifting).
Rely more on anaerobic respiration; rapid ATP production, smaller yield.
Homeostasis and negative feedback
Homeostasis: physiological control systems maintain internal variables within narrow limits (temperature, pH, blood glucose, water potential).
Negative feedback: mechanisms restore variables to set points; often separate mechanisms to raise or lower a level.
Blood glucose regulation
Key organs and hormones:
Pancreatic islets (islets of Langerhans): beta cells release insulin; alpha cells release glucagon.
Insulin: released when blood glucose high; promotes glucose uptake and glycogen synthesis in liver and muscle; increases insertion of GLUT4 channels (facilitated diffusion).
Glucagon: released when blood glucose low; activates second messenger cascade in liver to promote glycogenolysis and gluconeogenesis.
Adrenaline: also stimulates glycogenolysis via same second messenger pathway.
Important processes:
Glycogenesis: formation of glycogen from glucose.
Glycogenolysis: hydrolysis of glycogen to glucose.
Gluconeogenesis: synthesis of new glucose from non-carbohydrate sources (amino acids, glycerol).
Second messenger model (glucagon/adrenaline):
Hormone binds receptor → activates adenylate cyclase → converts ATP to cyclic AMP (cAMP) → cAMP activates protein kinase → phosphorylates enzymes to hydrolyze glycogen.
Diabetes types and management
Type 1: insufficient insulin production (often autoimmune destruction of beta cells); treated by insulin injections.
Type 2: insulin resistance (target cells less responsive); linked to obesity and poor diet; managed by diet, exercise, and sometimes insulin.
Osmoregulation and the kidney
Water potential regulation: keep blood water potential within safe limits to avoid cell swelling or shrinkage.
Nephron functions:
Ultrafiltration (glomerulus → Bowman’s capsule): high hydrostatic pressure forces water and small solutes into capsule; large molecules (proteins, RBCs) remain in blood.
Proximal convoluted tubule (PCT): selective reabsorption of all glucose (via Na+-glucose co-transport), most water by osmosis; epithelial cells have microvilli and many mitochondria.
Loop of Henle: creates medullary Na+ gradient for water reabsorption.
Descending limb: permeable to water, impermeable to ions → water leaves by osmosis, filtrate concentrated.
Ascending limb: impermeable to water, actively transports Na+ out → medulla becomes hypertonic; lower limb thickness and presence/absence of aquaporins differ.
Distal convoluted tubule and collecting duct: fine-tune water reabsorption; collecting duct carries urine to ureter.
Ultrafiltration filtration barriers:
Fenestrated capillary endothelium (blocks blood cells).
Basement membrane (protein-rich gel preventing large proteins).
Podocyte filtration slits (further restrict large molecules).
ADH and water balance mechanisms
Osmoreceptors in hypothalamus detect blood water potential changes:
Low blood water potential → osmoreceptors shrink → hypothalamus stimulates increased ADH production.
High water potential → osmoreceptors swell → decreased ADH production.
ADH pathway:
ADH produced in hypothalamus, stored/released from posterior pituitary into blood, travels to kidneys.
ADH binds receptors on distal convoluted tubule and collecting duct cells → activates intracellular enzyme cascade (phosphorylation) → vesicles fuse with membrane inserting aquaporins → increases membrane permeability to water.
Result: more water reabsorbed by osmosis → smaller volume, concentrated urine.
Responses summary:
Excess water (high water potential): less ADH → collecting duct less permeable → large volumes dilute urine.
Water deficit (low water potential): more ADH → collecting duct more permeable → small volumes concentrated urine.
Key information
Key resting potential value: −70 mV.
Threshold potential for action potential: about −55 mV.
Peak action potential: about +40 mV.