Description
Action Potential Propagation 9/25/15 4:13 PM
• conduction of AP:
• action potential = CHANGE IN PERMEABILITY of membrane
• generated at axon hillock
• passive spread of cations through axon
• depolarization of membrane:
o opening of channels create more permeability
• crosses threshold – voltage gated sodium channels open
o in initial segment: influx of Na+ - positive charge spreads If you want to learn more check out When is consumer surplus used?
passively BOTH downstream and upstream (passive Don't forget about the age old question of What refers to pragmatic utility of an object?
If you want to learn more check out Where is westmnister hall located?
depolarization on both sides of initiation side)
• downstream flow charges next segment of axon: + charge
depolarizes this segment to threshold
o voltage-gated Na+ channels open, passive spread both
downstream and upstream
o AP REGENERATING – all-or-none
• when charge goes upstream: does not generate AP due to the absolute refractory period
o those voltage-gated sodium channels are INACTIVATED –
WILL NOT flux current
o cannot cause any more sodium to go in until membrane
repolarizes
• if you stick electrode into MIDDLE of axon (inject positive charge): o sodium will fan out and depolarize membrane BOTH upstream and downstream ???? backpropagation and forward We also discuss several other topics like What are yarns for?
▪ antidromic spikes
▪ this is experimental, unknown if can occur naturally
• no one is ever at equilibrium – steady state at resting potential • set up combination of active and passive properties Don't forget about the age old question of What is the term for the chemical activities of cell?
• active voltage-gated sodium channels
• passive fan out of charge
• refractory membrane upstream
• prevents back propagation
• propagation of the action potential
• orthodromic: action potential travels in one direction (down axon to the axon terminal)
• antidromic (experimental ONLY):
o only experimental in axon – antidromic spike
o backpropagation CAN happen in dendrites:
▪ so much positive charge coming in, some makes it to
dendrites
▪ this can result in dendritic nt release in certain cells
(with nt packaged in vesicles INSIDE dendrites)
???? influences nt release for synapse from presynaptic
membrane
▪ depends on number of voltage gated channels,
leakiness in dendrites
• typical conduction velocity:
o unmyelinated axon: 2m/s
o myelinated: 120 m/s
• duration of AP: around 2ms Don't forget about the age old question of What is computed in unit-elastic demand?
• factors influencing conduction velocity:
• axonal diameter (bigger=faster)
o ex: pain receptors in skin:
▪ C fibers – unmyelinated pain and temperatures
???? thin and unmyelinated – SLOWEST
▪ other pain fibers – thin but myelinated – faster
▪ touch sensors are faster – pain comes later (ex: when
touching hot pan)
• myelin: layers of myelin sheath facilitate current flow
o myelinating cells:
▪ Schwann (PNS) – take entire body and wrap it around
axon (one to one)
▪ oligodendrocytes (CNS) – has branches that can wrap
around segments of 3 or 4 separate axons
• saltatory conduction: myelinated axons
• nodes of Ranvier – unmyelinated segment in between myelin o high Na channel density
o increased Cm
o conduction slows
• internodes - myelin
o thin layers of cell membrane
▪ virtually no charge in the inner layers myelin
▪ very little interaction between charges inside and
outside
o charges on inside of cell very separated form charges on outside of myelin
o fewer Na channels
o decreased Cm
o charges “jump” to next node
o rapid conduction
• demyelinating diseases:
• multiple sclerosis: multiple CNS sites
o “many scars”
o one of the most common diseases in CNS
o inflammatory demyelinating condition
o disrupts conduction of electrical impulses to and from brain o effects speed and efficiency with which impulses are conducted
o effects smooth, rapid and coordinated movement
o sites where myelin is los ???? plaques or lesions
▪ scars in brain and spinal cord
• Guillain-Barre disease: PNS
o sensory and motor nerves
9/25/15 4:13 PM
9/25/15 4:13 PM
Action Potential Propagation 9/25/15 4:13 PM
• conduction of AP:
• action potential = CHANGE IN PERMEABILITY of membrane
• generated at axon hillock
• passive spread of cations through axon
• depolarization of membrane:
o opening of channels create more permeability
• crosses threshold – voltage gated sodium channels open
o in initial segment: influx of Na+ - positive charge spreads
passively BOTH downstream and upstream (passive
depolarization on both sides of initiation side)
• downstream flow charges next segment of axon: + charge
depolarizes this segment to threshold
o voltage-gated Na+ channels open, passive spread both
downstream and upstream
o AP REGENERATING – all-or-none
• when charge goes upstream: does not generate AP due to the absolute refractory period
o those voltage-gated sodium channels are INACTIVATED –
WILL NOT flux current
o cannot cause any more sodium to go in until membrane
repolarizes
• if you stick electrode into MIDDLE of axon (inject positive charge): o sodium will fan out and depolarize membrane BOTH upstream and downstream ???? backpropagation and forward
▪ antidromic spikes
▪ this is experimental, unknown if can occur naturally
• no one is ever at equilibrium – steady state at resting potential • set up combination of active and passive properties
• active voltage-gated sodium channels
• passive fan out of charge
• refractory membrane upstream
• prevents back propagation
• propagation of the action potential
• orthodromic: action potential travels in one direction (down axon to the axon terminal)
• antidromic (experimental ONLY):
o only experimental in axon – antidromic spike
o backpropagation CAN happen in dendrites:
▪ so much positive charge coming in, some makes it to
dendrites
▪ this can result in dendritic nt release in certain cells
(with nt packaged in vesicles INSIDE dendrites)
???? influences nt release for synapse from presynaptic
membrane
▪ depends on number of voltage gated channels,
leakiness in dendrites
• typical conduction velocity:
o unmyelinated axon: 2m/s
o myelinated: 120 m/s
• duration of AP: around 2ms
• factors influencing conduction velocity:
• axonal diameter (bigger=faster)
o ex: pain receptors in skin:
▪ C fibers – unmyelinated pain and temperatures
???? thin and unmyelinated – SLOWEST
▪ other pain fibers – thin but myelinated – faster
▪ touch sensors are faster – pain comes later (ex: when
touching hot pan)
• myelin: layers of myelin sheath facilitate current flow
o myelinating cells:
▪ Schwann (PNS) – take entire body and wrap it around
axon (one to one)
▪ oligodendrocytes (CNS) – has branches that can wrap
around segments of 3 or 4 separate axons
• saltatory conduction: myelinated axons
• nodes of Ranvier – unmyelinated segment in between myelin o high Na channel density
o increased Cm
o conduction slows
• internodes - myelin
o thin layers of cell membrane
▪ virtually no charge in the inner layers myelin
▪ very little interaction between charges inside and
outside
o charges on inside of cell very separated form charges on outside of myelin
o fewer Na channels
o decreased Cm
o charges “jump” to next node
o rapid conduction
• demyelinating diseases:
• multiple sclerosis: multiple CNS sites
o “many scars”
o one of the most common diseases in CNS
o inflammatory demyelinating condition
o disrupts conduction of electrical impulses to and from brain o effects speed and efficiency with which impulses are conducted
o effects smooth, rapid and coordinated movement
o sites where myelin is los ???? plaques or lesions
▪ scars in brain and spinal cord
• Guillain-Barre disease: PNS
o sensory and motor nerves
9/25/15 4:13 PM
9/25/15 4:13 PM