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Compound Action Potential (compound + action_potential)
Selected AbstractsConduction block and glial injury induced in developing central white matter by glycine, GABA, noradrenalin, or nicotine, studied in isolated neonatal rat optic nerveGLIA, Issue 11 2009Stavros Constantinou Abstract The damaging effects of excessive glutamate receptor activation have been highlighted recently during injury in developing central white matter. We have examined the effects of acute exposure to four other neurotransmitters that have known actions on white matter. Eighty minutes of Glycine or GABA-A receptor activation produced a significant fall in the compound action potential recorded from isolated post-natal day 10 rat optic nerve. This effect was largely reversed upon washout. Nicotinic acetylcholine receptor (nAChR) or adrenoreceptor activation with noradrenalin resulted in an ,35% block of the action potential that did not reverse during a 30-min washout period. While the effect of nAChR activation was blocked by a nAChR antagonist, the effect of noradrenalin was not ablated by ,- or ,-adrenoreceptor blockers applied alone or in combination. In the absence of noradrenalin, co-perfusion with ,- and ,-adrenoreceptor blockers resulted in nonreversible nerve failure indicating that tonic adrenoreceptor activation is required for nerve viability, while overactivation of these receptors is also damaging. Nerves exposed to nAChR + adrenoreceptor activation showed no axon pathology but had extensive glial injury revealed by ultrastructural analysis. Oligodendroglia exhibited regions of membrane vacuolization while profound changes were evident in astrocytes and included the presence of swollen and expanded mitochondria, vacuolization, cell processes disintegration, and membrane breakdown. Blinded assessment revealed higher levels of astrocyte injury than oligodendroglial injury. The findings show that overactivation of neurotransmitter receptors other than those for glutamate can produce extensive injury to developing white matter, a phenomenon that may be clinically significant. © 2009 Wiley-Liss, Inc. [source] Motoneurons: A preferred firing range across vertebrate species?MUSCLE AND NERVE, Issue 5 2002T. George Hornby PhD Abstract The term "preferred firing range" describes a pattern of human motor unit (MU) unitary discharge during a voluntary contraction in which the profile of the spike-frequency of the MU's compound action potential is dissociated from the profile of the presumed depolarizing pressure exerted on the unit's spinal motoneuron (MN). Such a dissociation has recently been attributed by inference to the presence of a plateau potential (PP) in the active MN. This inference is supported by the qualitative similarities between the firing pattern of human MUs during selected types of relatively brief muscle contraction and that of intracellularly stimulated, PP-generating cat MNs in a decerebrate preparation, and turtle MNs in an in vitro slice of spinal cord. There are also similarities between the stimulus-response behavior of intracellularly stimulated turtle MNs and human MUs during the elaboration of a slowly rising voluntary contraction. This review emphasizes that there are a variety of open issues concerning the PP. Nonetheless, a rapidly growing body of comparative vertebrate evidence supports the idea that the PP and other forms of non-linear MN behavior play a major role in the regulation of muscle force, from the lamprey to the human. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000,000, 2002 [source] Electrosurgery after Cochlear Implantation: Eighth Nerve Electrophysiology,THE LARYNGOSCOPE, Issue 12 2004David M. Poetker MD Abstract Hypothesis: Monopolar electrosurgery below the neck in cochlear implant recipients can be performed without damage to the internal cochlear stimulator, electrode array, and the cochlear nerve. Study Design: Prospective pre- and postintervention electrically evoked compound action potential (ECAP) study of cochlear nerve function and behavioral sound perception assessment. Methods: Neural response telemetry (NRT) was used to measure ECAPs before and after the use of monopolar electrosurgery during coronary artery bypass surgery to assess prosthetic device function and electrophysiologic function of the cochlear nerve. In addition, electrode voltage impedances and behavioral sound perception was measured at the same time intervals. Results: ECAPs, behavioral sound perception, and electrode voltage impedances were within the normal range, within compliance, and similar preoperatively and on postoperative day 6. Conclusion: The studies reported herein were a series of measurements designed to test neural integrity and prosthetic device function before and after the use of monopolar electrosurgery. With appropriate precautions, use of monopolar electrosurgery below the neck in cochlear implant recipients can be performed safely. [source] Metabotropic glutamate receptor 1 activity generates persistent, N -methyl- d -aspartate receptor-dependent depression of hippocampal pyramidal cell excitabilityEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2009J. P. Clement Abstract Metabotropic glutamate receptors (mGluRs) are involved in many forms of neuronal plasticity. In the hippocampus, they have well-defined roles in long-lasting forms of both synaptic and intrinsic plasticity. Here, we describe a novel form of long-lasting intrinsic plasticity that we call (S)-3,5-dihydroxyphenylglycine (DHPG)-mediated long-term depression of excitability (DHPG-LDE), and which is generated following transient pharmacological activation of group I mGluRs. In extracellular recordings from hippocampal slices, DHPG-LDE was expressed as a long-lasting depression of antidromic compound action potentials (cAPs) in CA1 or CA3 cells following a 4-min exposure to the group I mGluR agonist (S)-DHPG. A similar phenomenon was also seen for orthodromic fibre volleys evoked in CA3 axons. In single-cell recordings from CA1 pyramids, DHPG-LDE was manifest as persistent failures in antidromic action potential generation. DHPG-LDE was blocked by (S)-(+)- a -amino-4-carboxy-2-methylbenzeneacetic acid (LY367385), an antagonist of mGluR1, but not 2-methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP), an mGluR5 inhibitor. Although insensitive to antagonists of ,-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate/kainate and ,-aminobutyric acidA receptors, DHPG-LDE was blocked by antagonists of N -methyl- d -aspartate (NMDA) receptors. Similarly, in single-cell recordings, DHPG-mediated antidromic spike failures were eliminated by NMDA receptor antagonism. Long after (S)-DHPG washout, DHPG-LDE was reversed by mGluR1 antagonism. A 4-min application of (S)-DHPG also produced an NMDA receptor-dependent persistent depolarization of CA1 pyramidal cells. This depolarization was not solely responsible for DHPG-LDE, because a similar level of depolarization elicited by raising extracellular K+ increased the amplitude of the cAP. DHPG-LDE did not involve HCN channels or protein synthesis, but was eliminated by blockers of protein kinase C or tyrosine phosphatases. [source] Complex interplay between glutamate receptors and intracellular Ca2+ stores during ischaemia in rat spinal cord white matterTHE JOURNAL OF PHYSIOLOGY, Issue 1 2006Mohamed Ouardouz Electrophysiological recordings of propagated compound action potentials (CAPs) and axonal Ca2+ measurements using confocal microscopy were used to study the interplay between AMPA receptors and intracellullar Ca2+ stores in rat spinal dorsal columns subjected to in vitro combined oxygen and glucose deprivation (OGD). Removal of Ca2+ or Na+ from the perfusate was protective after 30 but not 60 min of OGD. TTX was ineffective with either exposure, consistent with its modest effect on ischaemic depolarization. In contrast, AMPA antagonists were very protective, even after 60 min of OGD where 0Ca2++ EGTA perfusate was ineffective. Similarly, blocking ryanodine receptor-mediated Ca2+ mobilization from internal stores (0Ca2++ nimodipine or 0Ca2++ ryanodine), or inositol 1,4,5-trisphosphate (IP3)-dependent Ca2+ release (block of group 1 metabotropic glutamate receptors with 1-aminoindan-1,5-dicarboxylic acid, inhibition of phospholipase C with U73122 or IP3 receptor block with 2APB; each in 0Ca2+) were each very protective, with the combination resulting in virtually complete functional recovery after 1 h OGD (97 ± 32% CAP recovery versus 4 ± 6% in artificial cerebrospinal fluid). AMPA induced a rise in Ca2+ concentration in normoxic axons, which was greatly reduced by blocking ryanodine receptors. Our data therefore suggest a novel and surprisingly complex interplay between AMPA receptors and Ca2+ mobilization from intracellular Ca2+ stores. We propose that AMPA receptors may not only allow Ca2+ influx from the extracellular space, but may also significantly influence Ca2+ release from intra-axonal Ca2+ stores. In dorsal column axons, AMPA receptor-dependent mechanisms appear to exert a greater influence than voltage-gated Na+ channels on functional outcome following OGD. [source] | |||||||||||||