Summary
Highlights
A stimulus is a detectable change in the environment, detected by receptors. Organisms respond to stimuli to increase their chances of survival. Plants exhibit tropisms, which are growth responses to stimuli. Positive tropism means growing towards the stimulus, while negative tropism means growing away. Examples include phototropism (response to light) and gravitropism (response to gravity). Auxins, specifically indoleacetic acid (IAA), control these growth factors. IAA promotes cell elongation in shoots and inhibits it in roots. Shoots are positively phototropic and negatively gravitropic, while roots are negatively phototropic and positively gravitropic.
Animals exhibit simple responses like taxis and kinesis to remain in favorable environmental conditions. Taxis is a directional movement towards (positive) or away from (negative) a stimulus. Kinesis is non-directional, involving changes in movement speed and turning rate. Organisms increase turning rate in unfavorable conditions to find favorable ones and decrease it in highly unfavorable conditions to travel in a straighter line to a new location. These responses often relate to seeking dark, moist areas to avoid predators or desiccation, and moving towards certain chemicals indicating food.
Simple reflexes are rapid, automatic, involuntary responses in complex organisms with a nervous system. They involve a receptor, coordinator (spinal cord), and effector. A reflex arc typically has three neurons: sensory, relay, and motor. The speed of a reflex is due to bypassing the conscious brain and having only two synapses. Specific receptors include Pacinian corpuscles (pressure changes), rod cells (black and white vision, low light), and cone cells (color vision, high light). Rod cells demonstrate retinal convergence and low visual acuity, while cone cells offer high visual acuity.
Cardiac muscle is myogenic, meaning it contracts on its own. The sinoatrial node (SAN) in the right atrium acts as the natural pacemaker. The atrioventricular node (AVN) delays the electrical impulse, which then travels through the bundle of His and Purkinje fibers, causing the ventricles to contract from the apex upwards. This ensures efficient blood pumping. Heart rate is controlled by the medulla in the brain via the autonomic nervous system. Chemoreceptors detect pH changes, and baroreceptors detect blood pressure changes. Increased CO2 (lower pH) or low blood pressure increases heart rate, while high blood pressure decreases it.
A motor neuron consists of a cell body, dendrites, and an axon. Schwann cells wrap around the axon to form the myelin sheath, interrupted by nodes of Ranvier. The resting potential (-70 mV) is maintained by the sodium-potassium pump (active transport) and differential permeability of the membrane to ions, leading to more positive ions outside the neuron. The pump actively transports 3 sodium ions out and 2 potassium ions in. The membrane is more permeable to potassium ions, which diffuse out, making the inside more negative.
An action potential is a rapid depolarization and repolarization of the neuron membrane in response to a sufficiently strong stimulus. When the threshold potential (-55 mV) is reached, voltage-gated sodium ion channels open, causing an influx of sodium ions (depolarization to +40 mV). Subsequently, sodium channels close, and potassium channels open further, leading to potassium efflux (repolarization and hyperpolarization). The 'all or nothing' principle states that if the threshold is met, an action potential of constant magnitude will occur; otherwise, it won't. This prevents over-stimulation.
The refractory period is a brief time after an action potential during which the neuron cannot be stimulated again. This ensures discrete impulses, unidirectional transmission, and limits the frequency of impulses. Myelination dramatically increases conduction speed via saltatory conduction, where the action potential jumps between nodes of Ranvier. A wider axon diameter reduces resistance and increases speed. Higher temperature increases ion diffusion and ATP production for active transport, thus increasing speed.
Synapses are gaps between neurons where neurotransmitters transmit impulses. An action potential arriving at the presynaptic knob causes calcium influx, leading to neurotransmitter release into the synaptic cleft. The neurotransmitter binds to receptors on the postsynaptic membrane, opening sodium channels and potentially generating an action potential if the threshold is reached. Enzymes then break down neurotransmitters for recycling. Cholinergic synapses use acetylcholine. Summation (spatial or temporal) ensures sufficient neurotransmitter release. Synaptic transmission is unidirectional. Inhibitory synapses hyperpolarize the postsynaptic membrane, making action potentials less likely. Neuromuscular junctions are similar to synapses but transmit impulses from a motor neuron to a muscle fiber, using acetylcholine to initiate muscle contraction.
Skeletal muscles contract in response to nerve impulses. Myofibrils, found inside muscle fibers, are made of repeating sarcomeres, the functional units. A sarcomere is defined by two Z-lines and contains actin (thin) and myosin (thick) filaments. Key structures include the A-band (myosin length), I-band (actin only), M-line (center of myosin), and H-zone (myosin only). During contraction, actin filaments slide over myosin, shortening the H-zone and I-band, and bringing Z-lines closer; the A-band remains unchanged.
Muscle contraction begins with calcium ion release from the sarcoplasmic reticulum, which removes tropomyosin from actin binding sites. Myosin heads, with ADP and Pi attached, bind to actin, forming cross-bridges. The 'power stroke' occurs as myosin heads pivot, pulling actin inwards and releasing ADP/Pi. ATP then binds to myosin, causing detachment. ATP hydrolysis (catalyzed by ATPase, activated by calcium) resets the myosin head for another cycle. This process continues as long as calcium levels are high. When nerve stimulation stops, calcium is actively pumped back, and the muscle relaxes.
ATP is crucial for breaking actin-myosin cross-bridges, repositioning myosin heads, and active transport of calcium ions. Phosphocreatine rapidly regenerates ATP during short bursts of intense activity by donating a phosphate to ADP. Glycogen granules provide glucose for respiration to produce ATP. Calcium ions initiate contraction by binding to troponin, causing tropomyosin to expose actin binding sites, and activating ATPase.
Muscle fibers are categorized into slow twitch and fast twitch. Slow twitch fibers are best for endurance (e.g., calf muscles), have high myoglobin, rich blood supply, many mitochondria, and primarily use aerobic respiration to produce ATP slowly but abundantly. Fast twitch fibers are for short, powerful bursts (e.g., biceps), are thicker with more myosin, store more glycogen and phosphocreatine, and primarily use anaerobic respiration to produce ATP quickly but less efficiently.
Homeostasis maintains internal conditions within restricted limits, vital for enzyme function (temperature, pH) and cell survival (blood glucose, water potential). Negative feedback restores systems to their original levels. Blood glucose concentration is critical as too low levels cause cell death, and too high levels lower blood water potential, affecting osmosis and cell function. The pancreas (specifically, islet of Langerhans cells) regulates blood glucose. Alpha cells release glucagon (increases glucose), and beta cells release insulin (decreases glucose). Adrenaline also increases blood glucose, mimicking glucagon.
Key terms for blood glucose metabolism: Glycogenesis (converting excess glucose to glycogen, mainly in the liver and muscle cells), Glycogenolysis (hydrolysis of glycogen back to glucose), and Gluconeogenesis (making new glucose from non-carbohydrate sources like amino acids or glycerol).
When blood glucose is high (e.g., after eating), pancreatic beta cells release insulin. Insulin increases liver cell permeability to glucose, stimulating its uptake and conversion to glycogen (glycogenesis). This removes glucose from the blood, returning levels to normal. When blood glucose is low (e.g., during exercise or fasting), pancreatic alpha cells release glucagon. Glucagon triggers a second messenger model, activating enzymes to hydrolyze liver glycogen into glucose (glycogenolysis) and release it into the blood. If glycogen stores are depleted, gluconeogenesis can occur.
Glucagon (or adrenaline) acts as a first messenger, binding to receptors on liver cell membranes. This activates adenylate cyclase, which converts ATP to cyclic AMP (cAMP), the second messenger. cAMP then activates protein kinase, an enzyme that phosphorylates and activates other enzymes (e.g., phosphorylase kinase), ultimately leading to the breakdown of glycogen into glucose. This glucose is then released into the blood, increasing blood glucose levels.
Type 1 diabetes is an autoimmune condition where the body cannot produce insulin due to beta cell destruction, usually starting in childhood. Treatment involves insulin injections. Type 2 diabetes occurs when target cells become unresponsive to insulin, often developing in adults due to diet and obesity. It's managed by diet, exercise, and sometimes insulin or other medications.
Osmoregulation is the control of blood water potential. Too low water potential (hypotonic) occurs from dehydration; too high (hypertonic) occurs from over-hydration. The kidneys, specifically nephrons, are central to this. Nephrons filter blood (ultrafiltration), selectively reabsorb useful substances (proximal convoluted tubule, loop of Henle, distal convoluted tubule), and excrete waste as urine.
Ultrafiltration occurs in the renal (Bowman's) capsule. High hydrostatic pressure in the glomerulus (due to a wider afferent arteriole) forces water, glucose, ions, and urea from the blood into the capsule. Large molecules like proteins and red blood cells are retained. Filtration barriers include the fenestrated capillary endothelium, the basement membrane (blocking large proteins), and podocytes (foot-like extensions creating filtration slits).
All glucose and most water are reabsorbed in the proximal convoluted tubule (PCT). PCT cells have microvilli and abundant mitochondria. Sodium ions are actively transported out of PCT cells into the blood by sodium-potassium pumps, creating a concentration gradient. Sodium then diffuses into PCT cells from the lumen via co-transporter proteins, bringing glucose with it. Glucose then moves into the blood via facilitated diffusion. Water follows by osmosis due to the created water potential gradient.
The Loop of Henle is crucial for establishing and maintaining a sodium ion gradient, which enables water reabsorption. In the descending limb, water leaves by osmosis, but ions cannot. In the ascending limb, sodium ions are actively transported out, but water cannot leave. This creates a low water potential in the medulla surrounding the loop, allowing further water reabsorption in the distal convoluted tubule and collecting duct, regulated by ADH.
The hypothalamus detects changes in blood water potential via osmoreceptor cells. If water potential is low, osmoreceptor cells shrivel, stimulating the hypothalamus to produce more ADH (antidiuretic hormone). If water potential is high, osmoreceptor cells swell, leading to less ADH production. ADH is produced in the hypothalamus but released from the posterior pituitary gland. ADH increases the permeability of the collecting duct and distal convoluted tubule walls to water by inserting aquaporins, leading to more water reabsorption into the blood and more concentrated urine.