뒤로Anatomy & Physiology Exam 3 Study Guide
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CNS: brain and spinal cord; integrates and coordinates responses.
PNS: nerves and ganglia outside CNS; connects CNS to receptors, muscles, glands.
Functional PNS divisions: sensory (afferent) and motor (efferent).
Dendrites: receive signals.
Cell body (soma): integrates inputs.
Axon hillock: trigger zone.
Axon: conducts action potentials.
Axon terminals: release neurotransmitters.
Myelin sheath: insulates axons.
Sensory neurons: carry signals to CNS.
Interneurons: process and relay within CNS.
Motor neurons: carry commands from CNS to effectors.
Astrocytes: regulate K+, neurotransmitters, BBB.
Oligodendrocytes: myelinate CNS axons.
Microglia: immune surveillance.
Ependymal cells: line ventricles, move CSF.
Schwann cells: myelinate PNS axons.
Satellite cells: support PNS neuron bodies.
White matter: myelinated axons, communication pathways.
Gray matter: neuron bodies, dendrites, synapses; site of processing.
Degeneration of axon and myelin distal to injury; debris cleared by macrophages and Schwann cells; proximal stump may sprout for regeneration in PNS.
Electrical potential difference across membrane; inside negative relative to outside; typical resting potential ~ -70 mV.
Na+: higher outside, moves inward.
K+: higher inside, moves outward but electrical force pulls inward; net movement outward at rest.
Uses ATP to move 3 Na+ out and 2 K+ in, maintaining concentration gradients and contributing slightly to negative resting potential.
High K+ permeability allows K+ to leave cell, making inside negative; Na+ leaks in slightly; pump maintains gradients; resting potential reflects ion permeabilities.
Leak channels: always open, background permeability.
Gated channels: open in response to stimuli (ligand, mechanical, voltage).
Local changes in membrane voltage caused by ion channel opening; vary in size; can be depolarizing or hyperpolarizing; decremental spread.
Resting state → threshold → rapid Na+ influx (depolarization) → Na+ channel inactivation → K+ efflux (repolarization) → after-hyperpolarization → return to rest.
Membrane voltage where enough Na+ channels open to trigger self-sustaining action potential; typically around -55 mV.
Local Na+ influx depolarizes adjacent membrane to threshold, regenerating AP along axon; refractory period prevents backward propagation.
Larger axon diameter reduces internal resistance; myelination increases membrane resistance and enables saltatory conduction at nodes of Ranvier.
Cells connected by gap junctions; ionic current flows directly; very fast; often bidirectional; synchronize activity.
- AP arrives at terminal
- Voltage-gated Ca2+ channels open
- Ca2+ influx triggers vesicle fusion
- Neurotransmitter released
- Neurotransmitter binds postsynaptic receptors
- Signal ends by removal mechanisms
Reuptake into presynaptic terminal or glia; enzymatic breakdown (e.g., acetylcholinesterase for ACh); diffusion away from synapse.
At nicotinic receptors, ACh opens cation channels allowing Na+ influx, causing depolarization; muscarinic receptors have variable effects depending on subtype.
Ionotropic: ligand-gated ion channels, rapid effects.
Metabotropic: G-protein coupled, slower, longer-lasting, varied effects via second messengers.
EPSP: depolarizes membrane, increases AP probability, usually via Na+ channels.
IPSP: hyperpolarizes or shunts membrane, decreases AP probability, usually via K+ or Cl- channels.
Temporal: repeated inputs from one synapse sum over time.
Spatial: inputs from multiple synapses sum at once.
Stronger stimuli increase action potential firing frequency; individual AP amplitude remains constant.
From superficial to deep: dura mater (tough), arachnoid mater (web-like), pia mater (vascular, adheres to CNS).
Produced by choroid plexuses in ventricles; flows lateral ventricles → third ventricle → cerebral aqueduct → fourth ventricle → subarachnoid space → arachnoid villi → venous sinuses.
Tight junctions between capillary endothelial cells; supported by astrocytes; allows lipid-soluble gases and selective transport of glucose and amino acids; restricts many substances.
Sympathetic: fight or flight; increases heart rate, dilates pupils, bronchodilation.
Parasympathetic: rest and digest; slows heart, constricts pupils, increases digestion.
CNS preganglionic neuron releases ACh → nicotinic receptor on postganglionic neuron → postganglionic neuron releases NE (sympathetic) or ACh (parasympathetic) → effector receptors.
Cholinergic: nicotinic (ionotropic, excitatory), muscarinic (metabotropic, variable effects).
Adrenergic: alpha and beta receptors (metabotropic), effects depend on subtype and tissue.
Modified sympathetic ganglion; preganglionic ACh activates nicotinic receptors on chromaffin cells, which release epinephrine and norepinephrine into blood.
Dual innervation: organs receive both sympathetic and parasympathetic input.
Autonomic tone: baseline activity allowing graded control of effectors.
Gray matter central (H-shaped), white matter surrounds; dorsal horns receive sensory input; ventral horns contain motor neurons; lateral horns contain sympathetic neurons (T1-L2); spinal nerves formed by dorsal and ventral roots.
Receptor → sensory neuron → integration center (spinal cord) → motor neuron → effector.
Muscle spindle senses stretch → sensory neuron excites alpha motor neuron → same muscle contracts; inhibitory interneuron inhibits antagonist muscle.
Pain receptor activates sensory neuron → interneurons excite ipsilateral flexors and inhibit extensors → limb withdraws from stimulus.
During withdrawal reflex, contralateral interneurons excite extensors and inhibit flexors to support body weight on opposite side.