뒤로exam 3
04:26
이 집합의 용어 (37)
CNS: brain and spinal cord; integrates and coordinates. PNS: nerves and ganglia outside CNS; connects CNS to receptors, muscles, glands. PNS has sensory (afferent) and motor (efferent) divisions.
Sensory (afferent): carries info toward CNS from somatic, visceral, and special senses. Motor (efferent): carries commands from CNS to effectors; includes somatic (skeletal muscle) and autonomic (cardiac, smooth muscle, glands).
Dendrites: receive signals; cell body: integrates inputs; axon hillock: trigger zone; axon: conducts action potentials; axon terminals: release neurotransmitters; myelin sheath: insulates axons.
Sensory neurons: carry signals to CNS; often pseudounipolar. Interneurons: within CNS, process info. Motor neurons: carry commands from CNS to effectors.
Astrocytes: regulate K+, neurotransmitters, BBB. Oligodendrocytes: myelinate CNS axons. Microglia: immune defense. Ependymal cells: line ventricles, move CSF. Schwann cells: myelinate PNS axons. Satellite cells: support PNS neuron bodies.
White matter: myelinated axons, appears pale, transmits signals. Gray matter: neuron bodies, dendrites, synapses; site of processing and integration.
Degeneration of axon and myelin distal to injury. Macrophages and Schwann cells clear debris. Proximal stump may sprout to regenerate if pathway intact. CNS regeneration limited by inhibitory factors.
Electrical potential difference across membrane; inside relative to outside. Typical resting potential ~ -70 mV (inside negative).
Na+ higher outside, tends to enter cell; K+ higher inside, tends to leave. Electrical forces attract both inward. Net K+ movement outward; net Na+ movement inward.
Uses ATP to move 3 Na+ out and 2 K+ in, maintaining concentration gradients and resting potential. Also contributes small negative charge inside.
High K+ permeability allows K+ to leave cell, making inside negative. Negative proteins inside attract K+ back. Small Na+ leak reduces negativity. Result is stable resting voltage dominated by K+.
Leak channels: always open, provide background permeability. Gated channels: open in response to stimuli (ligand, mechanical, voltage).
Local changes in membrane voltage due to ion channel opening. Can be depolarizing or hyperpolarizing, vary in size, and decrease with distance.
Current leaks across membrane and cytoplasmic resistance limits spread, causing decremental decrease in voltage.
Resting state; threshold reached; rapid Na+ channel opening and depolarization; Na+ channel inactivation; K+ channel opening and repolarization; after-hyperpolarization; return to rest.
Membrane voltage where enough Na+ channels open to trigger self-sustaining action potential; typically around -55 mV.
Na+ influx depolarizes adjacent membrane, triggering new action potentials sequentially along axon; signal amplitude remains constant.
Recently activated membrane is refractory due to Na+ channel inactivation, preventing 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 allowing direct ionic current flow; very fast and often bidirectional transmission.
Action potential arrives; voltage-gated Ca2+ channels open; Ca2+ influx triggers vesicle fusion; neurotransmitter released; binds postsynaptic receptors; action terminated by reuptake, enzymatic breakdown, or diffusion.
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, fast and brief effects. Metabotropic: G-protein coupled, slower onset, longer-lasting, and varied effects via second messengers.
EPSP: depolarizes membrane, increases action potential likelihood, often via Na+ channels. IPSP: hyperpolarizes or shunts membrane, decreases likelihood, often via K+ or Cl- channels.
Temporal: repeated inputs from one synapse sum over time. Spatial: inputs from multiple synapses sum at once. Both integrate to influence action potential generation.
From superficial to deep: dura mater (tough), arachnoid mater (web-like), pia mater (delicate, vascular, adheres to CNS).
Lateral ventricles → interventricular foramina → third ventricle → cerebral aqueduct → fourth ventricle → subarachnoid space → arachnoid villi → dural venous sinuses → venous blood.
Tight junctions between CNS capillary endothelial cells, supported by basement membrane, pericytes, and astrocyte end-feet; selectively restricts substance passage.
Sympathetic: thoracolumbar origin, short preganglionic, long postganglionic, NE postganglionic transmitter. Parasympathetic: craniosacral origin, long preganglionic, short postganglionic, ACh postganglionic transmitter.
CNS preganglionic neuron → autonomic ganglion (nicotinic receptor) → postganglionic neuron → effector (adrenergic or muscarinic receptor).
Alpha-1: excitatory, contracts vascular smooth muscle. Alpha-2: inhibitory, reduces NE release. Beta-1: excitatory, increases heart rate. Beta-2: inhibitory, relaxes smooth muscle. Beta-3: metabolic activation and smooth muscle relaxation.
Modified ganglion; preganglionic ACh activates nicotinic receptors on chromaffin cells, which release epinephrine and norepinephrine into blood for widespread effects.
Receptor → sensory neuron → integration center (CNS) → motor neuron → effector; enables rapid automatic responses.
Muscle spindle senses stretch → sensory neuron excites alpha motor neuron → same muscle contracts; reciprocal inhibition inhibits antagonist muscle.
Pain activates nociceptors → sensory neuron excites ipsilateral flexor motor neurons and inhibits extensors → limb withdraws from stimulus.
During withdrawal reflex, contralateral side excites extensors and inhibits flexors to support body weight; involves interneurons crossing spinal cord.