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23 Cards in this Set
- Front
- Back
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Capacitive vs. Ionic current |
Capacitive - rapid redistribution of charge along the membrane due to local changes in voltage (injection of current -> accumulated charges dissipate without ions flowing across the membrane) Ionic - delayed flow of carriers of charge (ions) |
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Time constant |
= time required to rise to ~63% of the total change in potential (speed of dissipation; usually 1-10 ms) - determines how closely spaced sequential stimuli must be for their temporal summation |
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Length constant |
= distance (in cm) at which ~37% of the original change in membrane potential still occurs (usually 0.1-1 mm) λ = sqrt[r(m)/r(i)] |
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Speed of propagation |
(speed) ~ 1/sqrt[r(m)*r(i)*C(m)] r(m) ~ 1/d r(i) ~1/d^2 C ~ d -> as the axon diameter increases, the speed of propagation increases |
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Action potential |
= rapid depolarization & subsequent repolarization of the membrane in response to membrane depolarization of sufficient magnitude (= threshold, C(Na) > C(K)) - depolarizing/rising phase (-> Eq(Na)) -> + = overshoot - repolarizing -> hyperpolarizing phase - back to RMP |
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Channel activation during an AP |
- Depolarization ~> Na equilibrium potential -> Na channels open & close w/ delay -> delayed rectifier K channels open w/ delay - Repolarization ~> K equilibrium potential -> drK channels close -> Na channels ready to open again => Afterhyperpolarization |
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Refractory period |
= period of time in which another AP cannot be generated, or only w/ some difficulty; due to: - Na channel inactivation - high K channel activity Absolute RP - <1ms after peak; cannot fire AP Relative RP - afterwards; more current required => unidirectionality of AP |
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Voltage-gated ion channels |
- 4-fold symmetry - (ion) selectivity filter (by size & hydration E) - S4 voltage sensors (depolarization -> activation) - intracellular loops/AA clusters (inactivation) - flow: up to 100M ions/sec - inactivation: ball and chain model |
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VGCC (voltage-gated calcium channel) |
T-type -> transient, Ca -> NT release L-type -> long-lasting, in cell body - contribute to "Ca shoulder" or "Ca plateau" - often modulated by GPCR pwy's -> ↓ NT release |
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K channels |
Delayer rectifier - closed @ RMP, open during depolarization
I(A)-producing channels - also respond to depolarization, but inactivate rapidly - prolong the interspike interval |
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HCN channel |
- hyperpolarization-activated -> pacemaking - cyclic nucleotide-gated (cAMP) - cation-selective -> I(H) |
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Toxins |
TTX (tetrodotoxin) - puffer fish (Fugu) STX (saxitoxin) - shellfish - bind w/ high affinity to external site of Na channel & block the pore Conus toxins --| VGCC TEA (tetraethylammonium) --| K channel |
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Drugs |
Procaine, Lidocaine --| Na channel - use-dependent effect: more active w/ neural activity |
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Neuroma |
Transected nerve endings -> tangle of axons & swollen nerve endings -> accumulation of VGNC -> ↑ excitability -> phantom pain |
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Mutations |
Seizures & epilepsy: VGNC, VGKC, VGCC, HCNC |
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AP initiation |
Axon hillock/axon initial segment (AIS): - accumulation of membrane proteins, lipids, cytoskeletal elements --| diffusion b/w axon & soma - high density of VGNC & VGKC |
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AP proagation |
1-120 m/s (speed) ~ 1/sqrt[r(m)*r(i)*C(m)] - myelin (CNS: oligodendroc., PNS: Schwann c.) -> ↓ C(m) => ↑ velocity -> ↑r(m) => ↑ λ - less space required |
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Myelination in PNS |
Schwann cells around axons: - unmyelinated - multiple axons, 1 layer of SC - myelinated - one axon, multiple SC wraps (150) - uncovered regions in between (/1mm) = nodes of Ranvier: ↑[VGNC]&[VGKC] => AP regeneration ~ saltatory conduction (speed, E conservation) |
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Myelin development |
CNS: little plasticity ~ parallels oligodendrocytes PNS: depends upon axonal contact - Axon d : myelin thickness (layer #) ~ constant - Myelin control signal comes from axon: Neuregulins = TM factors expressed in axons Receptor (ErbB R trk) expressed on glial cells-> increases myelin thickness |
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Myelin composition |
PM consistency, ↑ [cholesterol] & [PL]; proteins: - MAG (myelin-associated glycoprotein) - early expression (1st wrap), Ig-like: initial axonal-glial recognition, adhesion & myelination initiation - P(o) - PNS myelin structure -> compaction - PLP (proteolipid protein) - P(o) CNS equivalent - MBP (myelin basic protein) - cytosolic |
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Guillain-Barre syndrome |
- Inflammatory damage to myelin - PNS demyelination in motor neurons |
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Multiple Sclerosis (MS) |
- Autoimmune - Gaps/lesions in myelin in the CNS w/ oligodendrocytes absent, axons preserved - plaques: accumulation of activated astrocytes, microglia, macrophages -> local gliosis - blurring of vision, numbness, tingling, weakness, paralysis, gait disorders, incontinence |
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Charcot-Marie-Tooth (CMT) disease |
- neurogenetic: mutation in Cx32, gap jxns between different myelin layers - peripheral motor & sensory neuropathy - leg weakness, difficulty running, hand weakness, sensory loss |
