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by Na+(passive) caused bydepolarization / Na+ entry Action potential
When K channelscontributeto the repolarization of action potentials
in turncausesprolongation of action potentials
by the previous action potential(passive) were caused bynondriven action potentials
the previous action potential(passive) were caused bynondriven action potentials
The congenital long QT syndrome ... cardiac K and Na channelsresultin prolongation of the ventricular action potential
cardiac ion channelsresultin prolongation of ventricular action potential
Na+ channelsresultin prolongation of the ventricular action potential
one or more ion currentsleadingto prolongation of the ventricular action potential
the cell ... it more likelyto setup a nerve impulse ( action potential
can activate dendritic sodium channelsthereby causingdendritic action potentials
Quinidines effect of inhibiting the outward flow of potassiumadditionally causesan elongation of the action potentials
Persistent currents have been foundto ... influenceaction potential thresholds in axons
These chemical molecule or ' ligand - triggered ' ion gates ... the ' voltage - triggered ' ion gatessetoff action potentials
All types of high - voltage activated ( HVA ) VGCCs ( L - type , N - type and P / Q typecontributeto the kinetics of action potentials
4 Decreased conductance of sodiumcausesinactivation of the action potential
also(passive) can ... be causedProlongation of the action potential of cardiomyocytes
This inactivation autotraxing the Na channels and activation of K channelsresultin repolarization of the action potential
Drugs blocking these channelscan leadto a prolongation of the action potential
This blocks the passage of nerve stimulusresultingin inactivation of the action potential
A gain of function mutation in the sodium channelwould resultin prolongation of the action potential
the cardiac ion channelsleadingto prolongation of the action potential
mislocalization of VGSC(passive) caused byimpaired action potential
a persistent inward current or by a reduction in outward K currents(passive) can therefore be caused byProlongation of the action potential
Depolarizationcan resultin prolongation of the action potential
Instead , they inhibit Nav channel fast inactivationresultingin a prolongation of the action potential
Reduction in IKrmay causethe prolongation of the action potential
therefore(passive) can ... be causedProlongation of the action potential
Hypomagnesemia , like hypokalemia and hypocalcemiacan leadto prolongation of the action potential
by neural stimulation in one embodiment(passive) caused bythe action potential of the neuron
transmembrane ion channelscausingpropagation of the action potential
K+ channels in the sensory neuroncausingbroadening of the action potential
a subset of K+ channels in the sensory neuroncausingbroadening of the action potential
the sensory neuroncausingbroadening of the action potential
the currentresultingfrom the regenerative action potential
triggers a large postsynaptic response in distal IN dendriteeffectively resultingin a dendritic action potential
an abilityto originatepropagate action potential
AND k+to setoff the action potential Action potential
As a result , inactivation of the channel becomes slowerleadingto a broadened action potential
inward calcium currents which produce prolonged action potentials and increased cytoplasmic calcium concentrationscontributinginward calcium currents which produce prolonged action potentials and increased cytoplasmic calcium concentrations
chain reactionscan causechain reactions
in Ca2 +resultin Ca2 +
from an area around the electrode tiporiginatingfrom an area around the electrode tip
to the opening of the voltage - gated calcium channels resulting in an inward currentleadsto the opening of the voltage - gated calcium channels resulting in an inward current
to the workledto the work
calcium currents which produce prolonged action potentials and increased cytoplasmic calcium concentrationscontributing inwardcalcium currents which produce prolonged action potentials and increased cytoplasmic calcium concentrations
from activation of voltage - operated calcium channelsresultfrom activation of voltage - operated calcium channels
to the release of neurotransmitterwould no longer leadto the release of neurotransmitter
to the release of neurotransmitterwould no longer leadto the release of neurotransmitter
at any pointoriginateat any point
synaptic depressioncausesynaptic depression
the release of neurotransmitters from the synaptic terminal into the synaptic cleft , where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end platecausethe release of neurotransmitters from the synaptic terminal into the synaptic cleft , where they can then diffuse across the synaptic cleft and bind to a receptor molecule on the motor end plate
to depolarizationleadsto depolarization
to regulation of neuronal excitabilitycontributingto regulation of neuronal excitability
to the generation of subsequent action potentialscontributeto the generation of subsequent action potentials
the intrinsic cardiac nervous system and the heartinfluencethe intrinsic cardiac nervous system and the heart
the intrinsic cardiac nervous system and the heart and other organ systemsinfluencethe intrinsic cardiac nervous system and the heart and other organ systems
in larger calcium transientsresultin larger calcium transients
the release of the neurotransmitter acetylcholinecausesthe release of the neurotransmitter acetylcholine
depolarization of the cellcausesdepolarization of the cell
the calcium channels to opencausesthe calcium channels to open
to mimic native input at frequencies associated with stress , 15 Hz , and the basal sympathetic tone , 0.5 Hzdesignedto mimic native input at frequencies associated with stress , 15 Hz , and the basal sympathetic tone , 0.5 Hz
activation of calcium currentcausesactivation of calcium current
eventuallycauseseventually
the releasecausesthe release
symptomscausingsymptoms
voltage - gated calcium channelscausesvoltage - gated calcium channels
Shortening of the atrial refractory period and(passive) may be causedShortening of the atrial refractory period and
in the motor - end plates and is initiated from an afferent nervous impulse to neuromuscular jointoriginatesin the motor - end plates and is initiated from an afferent nervous impulse to neuromuscular joint
an electrical currentcausesan electrical current
a conformational change in voltage gated Calcium channels allowing Calcium ions ( Ca++ ) to flow into the neuron ( at the terminal portion of the axon ) from the extracellular fluidcausesa conformational change in voltage gated Calcium channels allowing Calcium ions ( Ca++ ) to flow into the neuron ( at the terminal portion of the axon ) from the extracellular fluid
another twitchto causeanother twitch
firing(passive) caused byfiring
to QT prolongationleadsto QT prolongation
to at least part of the underlying mechanism of stretch - initiated contractionscontributesto at least part of the underlying mechanism of stretch - initiated contractions
from a decrease in a specific K+ current and an enhancement of the Ca2 + transients elicited by depolarizationresultingfrom a decrease in a specific K+ current and an enhancement of the Ca2 + transients elicited by depolarization
early afterdepolarizations in a Ca - independent mannercausesearly afterdepolarizations in a Ca - independent manner
to its anesthetic effectsleadingto its anesthetic effects
in a contraction of the myocardium ( i.e. , an excitatory stimulationresultingin a contraction of the myocardium ( i.e. , an excitatory stimulation