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At least 1,531 records · Page 85Linked to original sources
PubMed1975

[Classification of the vestibulospinal neurons of the cat Deiter's nucleus].

The antidromic activation of neurons in the cat Deiters nucleus to stimulation of spinal cerevical segments was studied using the intracellular microelectrode recording technique. Separate components of the antidromic action potential and its after-deflections were analyzed in fast- and slow-conducting neurons. A direct dependence between the parameters of the after-deflections and duration of the refractory period was revealed for these neurons. Variable responsivity of neurons with the same axonal conductance velocity is shown to be dependent on the after-depolarizing potential.

Action Potentials↗
PubMed1996

Monitoring the integrity of somatosensory pathways with evoked electroencephalographic bursts.

During isoflurane-induced electroencephalographic (EEG) suppression, external stimuli evoke high-amplitude cortical responses (bursts). We tested whether bursts evoked by somatosensory stimuli would reliably distinguish intact somatosensory pathways from pathways in which peripheral nerve conduction had been blocked by local anesthetic. Ten subjects were anesthetized with isoflurane until burst suppression was achieved. During EEG suppression, they were given somatosensory stimulation, consisting of 3-s episodes of 60 electric pulses (20 mA, 0.2 ms), to the tips of the left and right fifth fingers alternately for 10 min. One finger was then anesthetized at the base of the proximal phalanx with prilocaine and the other finger was injected with saline in a double-blind manner. The stimulation was continued for 20 min. In nine patients, the disappearance of bursts in response to stimuli applied to the anesthetized finger clearly indicated the side of the conduction block. After the injection of local anesthetic, there was a predominance of offset bursts over onset bursts in response to stimuli applied to the anesthetized finger (P < 0.05) before the responses disappeared. We conclude that evoked bursts merit further investigation for potential use in monitoring the integrity of neural pathways.

Anesthesia, Inhalation↗
PubMed1990

The electrophysiologic profile of Dejerine-Sottas disease (HMSN III).

Electrophysiologic studies in 11 patients with Dejerine-Sottas disease (hereditary motor and sensory neuropathy type III, HMSN III) showed median and ulnar motor nerve conduction velocities less than 6 m/sec in all but 1 patient. Marked temporal dispersion without conduction block was present in all patients. Uniform slowing in adjacent motor nerves was consistent with other studies of inherited neuropathies, although marked temporal dispersion may make HMSN III more difficult to distinguish from acquired neuropathies than other hereditary conditions. The electrophysiologic features of HMSN III patients were significantly different from a series of patients with other hereditary neuropathies chosen because of very slow nerve conduction velocity.

Adolescent↗
PubMed1988

Responses in human intercostal and truncal muscles to motor cortical and spinal stimulation.

Percutaneous electrical stimulation of the human motor cortex (up to 750 V) has been used to study the cortical projections to intercostal and truncal muscles. The latencies of electromyographic (EMG) responses were measured to motor cortical stimuli and also to spinal stimulation of the appropriate nerve roots. Following single anodal stimuli at (or near) the vertex, short-latency responses were recorded in pectoralis major (mean 9.6 msec), latissimus dorsi (9.7 msec), paravertebral muscles (11.1 msec), 3rd/4th parasternal intercostals (11.1 msec), and 6th/7th intercostal muscles (12.3 msec). Responses in each muscle group were potentiated by background voluntary respiratory and truncal manoeuvres which activated the muscles. The mean estimated central conduction times from motor cortex to spinal segmental level were 4.8 msec for pectoralis major, 5.8 msec for parasternal intercostals and 6.2 msec for 6th/7th intercostal muscles. The central conduction times and properties of the cortically evoked responses are consistent with a rapidly conducting, oligosynaptic pathway from the human motor cortex to accessory respiratory muscles and to truncal muscles.

Adult↗
PubMedDate not supplied

States of high conductance in a large-scale model of the visual cortex.

This paper reports on the consequences of large, activity dependent, synaptic conductances for neurons in a large-scale neuronal network model of the input layer 4Calpha of the Macaque primary visual cortex (Area V1). This high conductance state accounts for experimental observations about orientation selectivity, dynamics, and response magnitude (D. McLaughlin et al. (2000) Proc. Natl. Acad. Sci. USA 97: 8087-8092), and the linear dependence of Simple cells on visual stimuli (J. Wielaard et al. (2001) J. Neuroscience 21: 5203-5211). The source of large conductances in the model can be traced to inhibitory corticocortical synapses, and the model's predictions of large conductance changes are consistent with recent intracellular measurements (L. Borg-Graham et al. (1998) Nature 393: 369-373; J. Hirsch et al. (1998) J. Neuroscience 15: 9517-9528; J.S. Anderson et al. (2000) J. Neurophysiol. 84: 909-926). During visual stimulation, these conductances are large enough that their associated time-scales become the shortest in the model cortex, even below that of synaptic interactions. One consequence of this activity driven separation of time-scales is that a neuron responds very quickly to temporal changes in its synaptic drive, with its intracellular membrane potential tracking closely an effective reversal potential composed of the instantaneous synaptic inputs. From the effective potential and large synaptic conductance, the spiking activity of a cell can be expressed in an interesting and simplified manner, with the result suggesting how accurate and smoothly graded responses are achieved in the model network. Further, since neurons in this high-conductance state respond quickly, they are also good candidates as coincidence detectors and burst transmitters.

Animals↗
PubMed2002

Uniform range of conduction times from the lateral amygdala to distributed perirhinal sites.

Much data indicate that the perirhinal (PRH) cortex plays a critical role in declarative memory and that the amygdala facilitates this process under emotionally arousing conditions. However, assuming that the amygdala does so by promoting Hebbian interactions in the PRH cortex is hard to reconcile with the fact that variable distances separate amygdala neurons from their PRH projection sites. Indeed, to achieve a synchronized activation of distributed PRH sites, amygdala axons should display a uniform range of conduction times, irrespective of distance to target. To determine if amygdala axons meet this condition, we measured the antidromic response latencies of lateral amygdala (LA) neurons to electrical stimuli delivered at various rostrocaudal levels of the PRH cortex in cats anesthetized with isoflurane. Although large variations in antidromic response latencies were observed, they were unrelated to the distance between the PRH stimulation sites and LA neurons. To determine whether this result was an artifact due to current spread, two control experiments were performed. First, we examined the antidromic response latency of intrinsic PRH neurons. Although we used the same methods as in the first experiment, the antidromic response latency of PRH neurons to electrical stimuli applied in the PRH cortex increased linearly with the distance between the stimulating and recording sites. Second, we measured the antidromic response latency of PRH neurons projecting to the LA. In this pathway, we also found a statistically significant correlation between conduction times and distance to target. Thus these results support the intriguing possibility that the conduction velocity and/or trajectory of LA axons are adjusted to compensate for variations in distance between the LA and distinct rostrocaudal PRH sites. We hypothesize that because of their uniform range of conduction times to the PRH cortex, LA neurons can generate short time windows of depolarization facilitating Hebbian associations between coincident, but spatially distributed, activity patterns in the PRH cortex. In this context, the temporal scatter of conduction times in the LA to PRH pathway is conceived as a mechanism used to lengthen the period of depolarization to compensate for conduction delays within intrinsic PRH pathways. In part, this mechanism might explain how the amygdala promotes memory storage in emotionally arousing conditions.

Amygdala↗
PubMed1997

Synaptic and synaptically activated intrinsic conductances underlie inhibitory potentials in cat lateral amygdaloid projection neurons in vivo.

The companion paper demonstrated that the responses of lateral amygdaloid (LAT) projection neurons to the stimulation of major input and output structures are dominated by monophasic hyperpolarizing potentials of large amplitude. To characterize the mechanisms underlying these inhibitory potentials, intracellular recordings of cortically evoked responses were obtained from morphologically and/or physiologically identified LAT projection neurons in barbiturate anesthetized cats. The reversal potential of the cortically evoked hyperpolarization was measured at its peak, and 115 ms later (tail), an interval corresponding to the peak latency of the gamma-aminobuturic acid-B (GABAB) response previously recorded in vitro. When recorded with K-acetate (KAc) pipettes, these reversal potentials were -86.9 +/- 1.6 mV (peak; mean +/- SE) and -90.7 +/- 1.7 mV (tail), suggesting that both Cl- and K+ conductances contribute throughout the cortically evoked hyperpolarization. The small, but consistent, difference between the two reversal potentials suggested that an additional slowly activating K(+)-mediated component contributed to the inhibitory postsynaptic potential (IPSP) tail. To determine whether Cl- conductances contributed to the evoked hyperpolarization, recordings were performed with KCl; the peak (-57.8 +/- 2.2 mV) and tail (-61.3 +/- 2.1 mV) reversal potentials were approximately 15-20 mV more depolarized than those recorded with KAc pipettes. However, the difference between the peak and tail reversals remained. In an attempt to block the Cl- conductance, recordings were obtained with pipettes filled with KAc or KCl and 4,4'-diisothiocyanostilbene-2,2'-disulphonic acid (DIDS), a Cl- pump blocker that also was reported to block GABAA responses. With KAc and DIDS, the initial depolarization was prolonged and the amplitude of the hyperpolarization decreased relative to that seen with KAc alone. However, with KCl and DIDS, the reversal potential was shifted to an even greater extent than with KCl pipettes with the evoked response consisting entirely of a large depolarization, which produced a spike burst. These results suggest that LAT neurons have a Cl- pump that is blocked by DIDS, but that their Cl- channels are not blocked by DIDS. To assess the contribution of K+ conductances to cortically evoked hyperpolarizing potentials, recordings were obtained with Cs-acetate pipettes. Under these conditions, the response reversed at more depolarized potentials (peak, -71.9 +/- 1.0 mV; tail, -72.0 +/- 0.9 mV) compared with KAc recordings, with no difference between the peak and tail reversal potentials. These cells also had depolarized resting potentials (-66.2 +/- 1.8 mV) compared with those of cells recorded with KAc pipettes (-73.6 +/- 1.8 mV); however, this difference was too small to attribute the shift in reversals to a redistribution of Cl- ions across the membrane. The action potentials generated by LAT neurons under Cs+ had a shoulder that prolonged their falling phase. The increased duration of the spikes was presumably due to a dendritic Ca2+ conductance because LAT amygdaloid neurons are known to possess such conductances and Cs+ blocks the delayed rectifier and some Ca(2+)-dependent K+ currents. The dramatic reduction of this shoulder by spontaneous and evoked IPSPs suggests that the activation of dendritic conductances by back-propagating somatic action potentials is regulated tightly by synaptic events. Intracellular injection of the Ca2+ chelating agent, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (100 mM) caused a depolarization of the peak (-75.3 +/- 1.3 mV) and tail (-77.7 +/- 1.7 mV) reversal potentials during a time course of 15-45 min. Concurrently, the amplitude of the excitatory postsynaptic potential increased whereas that of the hyperpolarization decreased, suggesting that a Ca(2+)-dependent K+ conductance contributes significantly to the evoked hyperpolarization. (ABSTRACT TRUNCATED)

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1999

[The electrophysiological properties of the conduction pathways of the stellate ganglion in the cat in postnatal ontogeny].

In new-born, 10-, and 20-day-old kittens and in adult cats, the stellate ganglia branches contained both continuous and synaptically interrupted fibres. In the course of postnatal ontogenesis, the average conduction velocity of excitation and average amplitude of the responses increased. In new-born and 10-day old kittens, these are C-fibres. Apart from the latter, A delta and B fibres appeared in 20-day old kittens. In adult cats, two subgroups of all types of the fibres appeared. Since the 10-day age, synaptically interrupted responses have been recorded in anastomoses and inferior cardiac nerve following stimulation of cranial and caudal branches of the subclavian loop, the responses being conducted in both directions in adult cats.

Aging↗
PubMed1992

"Backfiring" in spinal cord monitoring. High thoracic spinal cord stimulation evokes sciatic response by antidromic sensory pathway conduction, not motor tract conduction.

Spinal cord stimulation has been advocated as an alternative to motor cortex stimulation for motor tract activation. To test this theory, evoked responses were recorded from lumbar spinal cord (L2; n = 14), spinal roots (L4-L7; n = 112), peripheral nerves (sciatics; n = 28), and hind limb muscles (n = 28) after epidural stimulation of the T1-T2 segment of the spinal cord in dogs (n = 12), cats (n = 2), and monkeys (n = 2). The spinal response evoked by spinal cord stimulation was resistant to a dorsal hemisectioning (depth, 7-8 mm) of the midthoracic spinal cord. A minimal attenuation of latency and amplitude occurred with dorsal hemisectioning, suggesting signal transmission through descending or ascending pathways in the ventrolateral and ventral quadrants of the spinal cord. The sciatic nerve response was abolished by a dorsal column transection (depth, 3-4 mm) or ipsilateral lumbar dorsal rhizotomy (four dorsal roots). This shows that the evoked response recorded from the sciatic nerve in our animals was not travelling, as we expected, through the ventral roots, but rather was conducted antidromically through sensory fibers in dorsal roots.

Animals↗
PubMed1991

Cerebellar evoked potentials and motor evoked potentials in the spinal cord of rats.

In rats, the cerebellar evoked potentials (CEPs) were monitored along the spinal cord following the electrical stimulation of cerebellar cortex. The CEPs monitored at thoracic and lumbar cord consisted of from 1 to 3 waves with conduction velocities of 16-20.28 m/sec. The amplitudes of these waves declined dramatically as the frequency of the stimulation increased above 50 Hz, indicating that the CEPs were either evoked or conducted polysynaptically. The pathway conducting CEPs were studied using acute spinal cord lesioning and intracord recording methods. The pathways conducting CEP and MEP were also compared in the same preparation in controlled spinal-cord-lesioned animals. The CEPs were mainly conducted along the ventral and lateral funiculi where the reticulospinal tracts and the vestibulospinal tracts are located. Simultaneous disappearance of both MEP and CEP after controlled spinal cord section seems to suggest the 2 different evoked potentials are conducted along the same pathways in the spinal cord of rats. Species difference in conduction pathways of MEP and CEP were compared and discussed.

Animals↗
PubMed1964

TETRODOTOXIN BLOCKAGE OF SODIUM CONDUCTANCE INCREASE IN LOBSTER GIANT AXONS.

Previous studies suggested that tetrodotoxin, a poison from the puffer fish, blocks conduction of nerve and muscle through its rather selective inhibition of the sodium-carrying mechanism. In order to verify this hypothesis, observations have been made of sodium and potassium currents in the lobster giant axons treated with tetrodotoxin by means of the sucrose-gap voltage-clamp technique. Tetrodotoxin at concentrations of 1 x 10(-7) to 5 x 10(-9) gm/ml blocked the action potential but had no effect on the resting potential. Partial or complete recovery might have occurred on washing with normal medium. The increase in sodium conductance normally occurring upon depolarization was very effectively suppressed when the action potential was blocked after tetrodotoxin, while the delayed increase in potassium conductance underwent no change. It is concluded that tetrodotoxin, at very low concentrations, blocks the action potential production through its selective inhibition of the sodium-carrying mechanism while keeping the potassium-carrying mechanism intact.

Action Potentials↗
PubMed1965

BOTULINUM TOXIN, TYPE A: EFFECTS ON CENTRAL NERVOUS SYSTEM.

This study has demonstrated that type A botulinum toxin has a depressant effect on the cortical electrical activity of anesthetized and unanesthetized monkeys. Simultaneous recordings of vital signs indicated a relative lack of change in the electrocardiogram, respiration, blood pressure, and heart rate during this time. The change in the electroencephalogram appeared cyclic in nature and independent of dose or time. All animals exhibited signs of respiratory failure characterized by a gradual interference with neuromuscular transmission at the diaphragm, and subsequently died an anoxic death.

Animals↗
PubMed2006

An algorithmic method for reducing conductance-based neuron models.

Although conductance-based neural models provide a realistic depiction of neuronal activity, their complexity often limits effective implementation and analysis. Neuronal model reduction methods provide a means to reduce model complexity while retaining the original model's realism and relevance. Such methods, however, typically include ad hoc components that require that the modeler already be intimately familiar with the dynamics of the original model. We present an automated, algorithmic method for reducing conductance-based neuron models using the method of equivalent potentials (Kelper et al., Biol Cybern 66(5):381-387, 1992) Our results demonstrate that this algorithm is able to reduce the complexity of the original model with minimal performance loss, and requires minimal prior knowledge of the model's dynamics. Furthermore, by utilizing a cost function based on the contribution of each state variable to the total conductance of the model, the performance of the algorithm can be significantly improved.

Action Potentials↗