excessive stimulation or environmental changes capable of reducing the membrane sodium gradient(passive) caused byhyperexcitability
School 27 Sep 2006 Taking large doses of androgens , or steroids , is knownto causehyperexcitability
PubMed ] Zhu L , Polley N , Mathews GC , Delpire E. NKCC1 and KCC2preventhyperexcitability
questions claudio m tamburrini and steroids in handy for a sports industries , 27 Sep 2006 Taking large doses of androgens , or steroids , is knownto causehyperexcitability
environmental changes or excessive stimulation capable of reducing membrane sodium gradient(passive) caused byhyperexcitability
excessive stimulation or en(passive) caused byhyperexcitability
Publication - NKCC1 and KCC2preventhyperexcitability
2008 ) NKCC1 and KCC2preventhyperexcitability
brain injury(passive) caused byhyperexcitability
N. Polley , G. C. Mathews , , NKCC1 and KCC2preventhyperexcitability
Changes in suprathreshold currents failto causehyperexcitability
excessive stimulation or environmental changes capable of reducing membrane Na+ gradient(passive) caused byhyperexcitability
excessive stimulation or environmental changes competent of dropping membrane sodium gradient(passive) caused byhyperexcitability
incremental stimulation of the developing brain in the womb(passive) caused byhyperexcitability
the mismanagement of glutamate levels and Ca2 + homeostasis in the brain(passive) can be triggered byHyperexcitability
several inhibitory mechanisms , involving negative ions like chloride ions and inhibitory neurotransmitters(passive) is usually prevented byHyperexcitability
weak or broken and MC loss leads to insufficient activation of inhibitory neuronscausinghyperexcitability
to participate in pain enhancement , as TNF and IL-1 alter ion channels in Aplysia neuronescausinghyperexcitability
Of these neurotransmitters , the regulation of neuron excitability by γ - aminobutyric acid ( GABA ) , the predominant inhibitory neurotransmitter , is especially requiredto preventhyperexcitability
the modification of postsynaptic receptor expression , central sensitization and potentiation of presynaptic delivery of neurotransmitters , as well as the reduction of inhibitory inputs(passive) caused byHyperexcitability
initiating eventscausinghyperexcitability
Excitation of neurons along with too little inhibitioncauseshyperexcitability
Second , maybe once the nerves were unimpaired , the motor units fired up too muchcausinghyperexcitability
which would , if allowed to build up , depolarize neuronsfirst causinghyperexcitability
lesions involving the upper motor neurons of the corticospinal tract(passive) caused byhyperexcitability
However , in mice with Fragile X syndrome , activity from a single whisker activates multiple clusters of cellscreatinghyperexcitability
Tau elevationmay causehyperexcitability
Either way hypomyelination ... upregulation of sodium channels ( Na+ IIwill causehyperexcitability
excite C fiberscausinghyperexcitability
the disruption of this delicate balance at the microcircuit level(passive) caused byHyperexcitability
an effective approachto preventhyperexcitability
in CNS neurons , where TREK1 expression is a major influence on resting membrane potential , respiratory or metabolicwill causehyperexcitability
loss of HIPP cellsmight ... causehyperexcitability
Estrogencan causehyperexcitability
a dysregulation of the intracortical GABAergic inhibitory circuitries and selective alteration of glutamatergic neurotransmission(passive) might be caused byHyperexcitability
Narcoticshowever ... may causehyperexcitability
that the channel is mutated with an increase in current flowsubsequently causinghyperexcitability
Severe hypokalemiacauseshyperexcitability
to ataxia and seizures.[33 ] Mutations inleadingto ataxia and seizures.[33 ] Mutations in
to the development and perpetuation of seizuresleadingto the development and perpetuation of seizures
to seizures in heterozygous affected patientsleadingto seizures in heterozygous affected patients
to seizures and myoclonus , and neuronal degenerationleadingto seizures and myoclonus , and neuronal degeneration
the onset of spontaneous recurrent seizurescausesthe onset of spontaneous recurrent seizures
epileptic seizures ( Gustafsson and Wigström , 1988causingepileptic seizures ( Gustafsson and Wigström , 1988
to central nervous system sensitization , which can result in persistent painmay leadto central nervous system sensitization , which can result in persistent pain
to seizure genesiscan contributeto seizure genesis
to withdrawal seizureleadingto withdrawal seizure
in hidden seizure activityresultingin hidden seizure activity
to cytotoxicity and cell deathcan leadto cytotoxicity and cell death
to spontaneous firing , neuropathic pain , and paresthesias ( Devor 1994 ; Zimmermann 2001may leadto spontaneous firing , neuropathic pain , and paresthesias ( Devor 1994 ; Zimmermann 2001
withdrawal symptoms to affect you much differently than the reaction you get from drinking alcoholcauseswithdrawal symptoms to affect you much differently than the reaction you get from drinking alcohol
to runaway excitation resulting in epileptic dischargecan leadto runaway excitation resulting in epileptic discharge
to hypersynchrony that normally leads to neuropathologynormally leadsto hypersynchrony that normally leads to neuropathology
to convulsions which could overload the myocardiummay leadto convulsions which could overload the myocardium
tetanic contractions – Hypercalcemic tetany [ Ca 2 +causestetanic contractions – Hypercalcemic tetany [ Ca 2 +
in uncontrolled reflex emptyingresultingin uncontrolled reflex emptying
in excess statesresultingin excess states
muscle fatiguabilitycan causemuscle fatiguability
calcium overload to activate calpain ... leading to Tau hyperphosphorylationmay causecalcium overload to activate calpain ... leading to Tau hyperphosphorylation
in rapid firing of action potentialsresultingin rapid firing of action potentials
tetanic contractions Hypercalcemic tetany [ Ca2+]cyt Three definable fractions of calcium in serumcausestetanic contractions Hypercalcemic tetany [ Ca2+]cyt Three definable fractions of calcium in serum
from any other mechanism , such as loss of other K+ conductances , or gain of excitatory currentresultingfrom any other mechanism , such as loss of other K+ conductances , or gain of excitatory current
from peripheral and central sensitization ( Figure 6resultingfrom peripheral and central sensitization ( Figure 6
tetanic contractions Hypocalcemic tetany Extracellular Calcium Three definable fractions of calcium in serumcausestetanic contractions Hypocalcemic tetany Extracellular Calcium Three definable fractions of calcium in serum
to release of excess glutamate , a known problem in the diseaseleadsto release of excess glutamate , a known problem in the disease
from mutations of K+ channel subunitsresultingfrom mutations of K+ channel subunits
tetanic contractions Hypercalcemic tetany [ Ca2+]cyt 10 Extracellular Calcium Three definable fractions of calcium in serum : Ionized calcium 50 %causestetanic contractions Hypercalcemic tetany [ Ca2+]cyt 10 Extracellular Calcium Three definable fractions of calcium in serum : Ionized calcium 50 %
oscillations in motor circuits that lead to tremorCan ... causeoscillations in motor circuits that lead to tremor
from abnormal input from suprasegmental structures or loss of inhibition by interneuronsmay resultfrom abnormal input from suprasegmental structures or loss of inhibition by interneurons
siezures from lots of AP 'scausessiezures from lots of AP 's
from deficiency of astrocytic Kir4.1resultingfrom deficiency of astrocytic Kir4.1
in higher dosesresultingin higher doses
to involuntary rather than voluntary movementleadsto involuntary rather than voluntary movement