Ringo, Doty, Demeter and Simard, Cerebral Cortex 1994;4:331-343: a proof of the need for the spatial clustering of interneuronal connections to enhance cortical computation.
It has been argued that an important principle driving the organization of the cerebral cortex towards local processing has been the need to decrease time lost to interneuronal conduction delay. In this paper, I show for a simplified model of the cerebral cortex, using analytical means, that if interneuronal conduction time increases proportional to interneuronal distance, then the only way to increase the numbers of synaptic events occurring in a fixed finite time period is to spatially cluster interneuronal connections. (+info)
Spinal cord-evoked potentials and muscle responses evoked by transcranial magnetic stimulation in 10 awake human subjects.
Transcranial magnetic stimulation (TCMS) causes leg muscle contractions, but the neural structures in the brain that are activated by TCMS and their relationship to these leg muscle responses are not clearly understood. To elucidate this, we concomitantly recorded leg muscle responses and thoracic spinal cord-evoked potentials (SCEPs) after TCMS for the first time in 10 awake, neurologically intact human subjects. In this report we provide evidence of direct and indirect activation of corticospinal neurons after TCMS. In three subjects, SCEP threshold (T) stimulus intensities recruited both the D wave (direct activation of corticospinal neurons) and the first I wave (I1, indirect activation of corticospinal neurons). In one subject, the D, I1, and I2 waves were recruited simultaneously, and in another subject, the I1 and I2 waves were recruited simultaneously. In the remaining five subjects, only the I1 wave was recruited first. More waves were recruited as the stimulus intensity increased. The presence of D and I waves in all subjects at low stimulus intensities verified that TCMS directly and indirectly activated corticospinal neurons supplying the lower extremities. Leg muscle responses were usually contingent on the SCEP containing at least four waves (D, I1, I2, and I3). (+info)
Multiple point electrical stimulation of ulnar and median nerves.
A computer-assisted method of isolating single motor units (MUs) by multiple point stimulation (MPS) of peripheral nerves is described. MPS was used to isolate 10-30 single MUs from thenar and hypothenar muscles of normal subjects and patients with entrapment neuropathies, with the original purpose of obtaining a more representative mean motor unit potential for estimating the number of MUs in a muscle. The two important results that evolved from MPS however, were: (1) in the absence of 'alternation' MUs were recruited in an orderly pattern from small to large, and from longer to shorter latencies by graded electrical stimulation in both normal and pathological cases, (2) a comparison of the sizes of MUs recruited by stimulation proximal and distal to the elbow suggested that axonal branching can occur in the forearm 200 mm or more proximal to the motor point in intrinsic hand muscles. (+info)
Acute conduction velocity changes in guinea-pigs after administration of diphenylhydantoin.
Motor nerve conduction velocity was measured after dosing guinea-pigs with 200-400 mumol/kg diphenylhydantoin (DPH) daily for three to four days. Conduction velocity fell by a mean value of 13% in animals that achieved plasma DPH levels over 200 mumol/l. There was no change in velocity with DPH levels below this value. (+info)
Electrophysiological evidence for tetrodotoxin-resistant sodium channels in slowly conducting dural sensory fibers.
A tetrodotoxin (TTX)-resistant sodium channel was recently identified that is expressed only in small diameter neurons of peripheral sensory ganglia. The peripheral axons of sensory neurons appear to lack this channel, but its presence has not been investigated in peripheral nerve endings, the site of sensory transduction in vivo. We investigated the effect of TTX on mechanoresponsiveness in nerve endings of sensory neurons that innervate the intracranial dura. Because the degree of TTX resistance of axonal branches could potentially be affected by factors other than channel subtype, the neurons were also tested for sensitivity to lidocaine, which blocks both TTX-sensitive and TTX-resistant sodium channels. Single-unit activity was recorded from dural afferent neurons in the trigeminal ganglion of urethan-anesthetized rats. Response thresholds to mechanical stimulation of the dura were determined with von Frey monofilaments while exposing the dura to progressively increasing concentrations of TTX or lidocaine. Neurons with slowly conducting axons were relatively resistant to TTX. Application of 1 microM TTX produced complete suppression of mechanoresponsiveness in all (11/11) fast A-delta units [conduction velocity (c.v.) 5-18 m/s] but only 50% (5/10) of slow A-delta units (1.5 +info)
Diaphragm electromyogram measured with unilateral magnetic stimulation.
The purpose of this study was to establish the phrenic nerve conduction time (PNCT) for magnetic stimulation and further assess the relatively new technique of anterior unilateral magnetic stimulation (UMS) of the phrenic nerves in evaluating the diaphragm electromyogram (EMG). An oesophageal electrode was used to record the diaphragm compound muscle action potential (CMAP) elicited by supramaximal percutaneous electrical phrenic nerve stimulation (ES) and UMS from eight normal subjects. The oesophageal electrode used for recording the CMAP was positioned at the level of the hiatus and 3 cm below. The diaphragm CMAP was also recorded from chest wall surface electrodes in five subjects. All of the phrenic nerves could be maximally stimulated with UMS. A clear plateau of the amplitude of the CMAP was achieved for the right and left phrenic nerves. The mean amplitudes of the CMAP recorded from the oesophageal electrode were, for the right side, 0.74+/-0.29 mV (mean+SD) for ES and 0.76+/-0.30 mV for UMS with maximal power output, and for the left side 0.88+/-0.33 mV for ES and 0.80+/-0.24 mV for UMS. PNCT measured by the oesophageal electrode with ES and UMS with maximal output were, for the right side, 7.0+/-0.8 ms and 6.9+/-0.8 ms, respectively, and for the left side 7.8+/-1.2 ms and 7.7+/-1.3 ms, respectively. However, the CMAP recorded from chest wall surface electrodes with UMS was unsuitable for the measurement of PNCT. The results suggest that unilateral magnetic stimulation of the phrenic nerves combined with an oesophageal electrode can be used to assess diaphragmatic electrical activity and measure the phrenic nerve conduction time. (+info)
Activity-dependent slowing of conduction differentiates functional subtypes of C fibres innervating human skin.
1. The effects of impulse activity on conduction in cutaneous C fibres have been examined in 46 microneurographic recordings from 11 normal subjects and 11 diabetic patients with normal nerve conduction. A tungsten microelectrode was inserted into a cutaneous nerve, usually the superficial peroneal close to the ankle, and intraneural microstimulation was used to identify an area of skin innervated. Three minute trains of 0.25 ms stimuli at 1, 2 and 4 Hz were then delivered to the surface of the skin, separated by intervals of 6 min with stimulation at 0.25 Hz. Slowing and block of conduction were measured from the nerve responses for up to seven C units per stimulation sequence. 2. Three types of C unit were distinguished by their responses to repetitive stimulation: type 1 units slowed progressively during the 3 min trains; slowing of type 2 units reached a plateau within 1 min; while type 3 units hardly slowed at all. Data from normal and diabetic subjects did not differ and were pooled. After 3 min at 2 Hz, the percentage increases in latency were for type 1, 28.3 +/- 9.7 (n = 63 units, mean +/- s.d.); for type 2, 5.2 +/- 1.6 (n = 14); and for type 3, 0.8 +/- 0.5 (n = 5), with no overlap. After 3 min at 4 Hz, 58 % of type 1 units (but no type 2 or 3 units) blocked intermittently. Recovery of latency after stimulation was faster for type 2 than for type 1 units, but conduction velocities of the three types were similar. 3. Type 1 units were identified as nociceptors and 7 type 2 units were identified as 'cold' fibres, activated by non-noxious cold, with no overlap in modality. None of the units tested was activated by weak mechanical stimuli or reflex sympathetic activation. 4. Spike waveforms were averaged for 18 type 1, 10 type 2 and 6 type 3 units. All units had predominantly triphasic action potentials with a major negative peak, but those of type 3 units were on average both smaller and briefer than those of type 1 and type 2 units. 5. It is concluded that repetitive electrical stimulation reliably differentiates nociceptive from cold-specific C fibres innervating human hairy skin, as has previously been shown for the rat. Cold fibres can propagate impulses continuously at much higher rates than nociceptive fibres. The nature of the type 3 units is unclear. (+info)
Thapsigargin inhibits a potassium conductance and stimulates calcium influx in the intact rat lens.
1. An increase in lens cell calcium has long been associated with cortical cataract. Recently, it has been shown that thapsigargin induces a rise in lens cell calcium by release from endoplasmic reticulum stores. The effects of this rise on the optical and membrane characteristics of the lens were studied in the isolated rat lens. 2. The electrical characteristics of the isolated, perifused rat lens were measured using a two-internal microelectrode technique that permits measurement of plasma membrane conductance (Gm), membrane potential (Vm) and junctional conductance in the intact lens. 3. Thapsigargin (1 microM) induced a rapid overall depolarization of Vm that was accompanied by first a decrease and then an increase in Gm. 4. Replacing external Na+ with tetraethylammonium (TEA) abolished the decrease in Gm. However, a transient increase phase was still observed. 5. The changes in conductance were further characterized by measuring 22Na+ and 45Ca2+ influxes into the isolated lens. Thapsigargin (1 microM) induced a transient increase in 45Ca2+, but did not affect Na+ influx. 6. The Ca2+ channel blocker La3+ (10 microM) totally inhibited the thapsigargin-induced Ca2+ influx. It also blocked the increase in Gm observed in control and in Na+-free-TEA medium. In the absence of external calcium, thapsigargin induced a small depolarization in Vm. 7. These data indicate that thapsigargin induces both a decrease in K+ conductance and an increase in Ca2+ conductance. These probably result from release of stored Ca2+ and subsequent activation of store-operated Ca2+ channels (capacitative Ca2+ entry). 8. Thapsigargin application over the time course of these experiments (24 h) had no effect on junctional conductance or on the transparency of the lens. (+info)