Receptive properties of mouse sensory neurons innervating hairy skin

Using an in vitro nerve skin preparation and controlled mechanical or thermal stimuli, we analyzed the receptive properties of 277 mechanosensitive single primary afferents with myelinated (n = 251) or unmyelinated (n = 26) axons innervating the hairy skin in adult or 2-wk-old mice. Afferents were recorded from small filaments of either sural or saphenous nerves in an outbred mice strain or in the inbred Balb/c strain. On the basis of their receptive properties and conduction velocity, several receptor types could be distinguished. In adult animals (>6 wk old), 54% of the large myelinated fibers (Abeta, n = 83) showed rapidly adapting (RA) discharges to constant force stimuli and probably innervated hair follicles, whereas 46% displayed a slowly adapting (SA) response and probably innervated Merkel cells in touch domes. Among thin myelinated fibers (Adelta, n = 91), 34% were sensitive D hair receptors and 66% were high-threshold mechanoreceptors (AM fibers). Unmyelinated fibers had high mechanical thresholds and nociceptive functions. All receptor types had characteristic stimulus-response functions to suprathreshold force stimuli. Noxious heat stimuli (15-s ramp from 32 to 47 degrees C measured at the corium side of the skin) excited 26% (5 of 19) of AM fibers with a threshold of 42.5 +/- 1.4 degrees C (mean +/- SE) and an average discharge of 15.8 +/- 9.7 action potentials and 41% (7 of 17) C fibers with a mean threshold of 37.6 +/- 1.9 degrees C and an average discharge of 22.0 +/- 6.0 action potentials. Noxious cold stimuli activated 1 of 10 AM fibers and 3 of 10 C fibers. One of 10 C units responded to both heat and cold stimuli. All types of afferent fibers present in adult mice could readily be recognized in mice at postnatal day 14. However, fibers had reduced conduction velocities and the stimulus-response function to mechanical stimuli was more shallow in all fibers except for the D hairs. In juvenile mice, 22% of RA units also displayed an SA response at high stimulus intensities; these units were termed RA/SA units. We conclude that all types of cutaneous afferent fibers are already committed to their phenotype 2 wk after birth but undergo some maturation over the following weeks. This preparation has great potential for the study of transgenic mice with targeted mutations of genes that code factors that are involved in the specification of sensory neuron phenotypes.     

Normal abomasal electromyography and emptying in sheep and the effects of intraabomasal volatile fatty acid infusion

Electromyographic activity and emptying of the abomasum were studied in 3 sheep. Pacesetter potentials (PP), with a frequency of 6.06 +/- 0.05 (X +/- SEM) cycles/minute and propagated distally with an increased conduction velocity approaching the pylorus, were recorded from the distal 11 cm of the antrum. Spike burst and fused action potentials (AP) were superimposed on a variable percentage of PP. The aborad propagation of both types of AP was associated with abomasal emptying at the net rate of 12.61 +/- 1.38 (X +/- SEM) ml/minute. Intraabomasal infusion of 50 ml of a 300 mM solution of either acetic, propionic, or butyric acid was associated with a marked decrease in abomasal AP activity and in the emptying rate. Butyric acid was most effective, followed by propionic and acetic acids. The importance of the results in relation to the pathogenesis of left displaced abomasum (LDA) in dairy cows was noted.     

The delayed depolarization in rat cutaneous afferent axons is reduced following nerve transection and ligation, but not crush: implications for injury-induced axonal Na+ channel reorganization

Two distinct populations of Na+ channels (kinetically fast and slow) are present on the cell bodies and axons of cutaneous afferent neurons; the fast current is increased and the slow current reduced in amplitude following nerve injury. The present study was undertaken to determine if similar changes occur on the axons of these neurons following peripheral nerve injury. The compound action potentials from rat sural nerves were recorded in a sucrose gap chamber. Following application of 4-aminopyridine, a prominent and well-characterized depolarization (the delayed depolarization) followed the action potential. This potential, only present on cutaneous afferent axons, has been correlated with activation of a slow Na+ current. The delayed depolarization was reduced after nerve transection. The refractory period of transmission of the action potential was shortened in the transected nerves, but that of the delayed depolarization was prolonged. The changes were largest when the sural nerve was cut and ligated [control: 38.1 +/- 1.7% (n = 5); injury: 24.5 +/- 2.8% (n = 5), P < 0.05], which prevented reconnection to its peripheral target. When the nerve was crushed and allowed to reestablish peripheral target connections, the delayed depolarization was minimally effected. These results indicate that the changes in Na+ channel organization following peripheral target disconnection observed on cutaneous afferent cell bodies also occur on their axons.     

Dendrite classification in rat hippocampal neurons according to signal propagation properties. Observation by multichannel optical recording in cultured neuronal networks

Two-dimensional neuronal networks were formed using a dissociated culture of rat hippocampal neurons on glass plates. Neural activity in response to pulse stimuli applied to the neurons by whole-cell clamp electrodes was observed with a 128-channel optical recording apparatus using a voltage-sensitive dye, RH482. Dendrites emerging from the somata of single neurons were classified according to two signal-transmission properties, those with lower conduction velocities (0.12+/-0.034 m/s, n=24) and those with very fast conduction velocity (faster than 1.0 m/s), by evaluating the conduction velocities of pulse responses. The distinction between these two properties seemed to be related to the morphological differences in input connectivity with the axons of neighboring neurons.     

Inhibitory effects of centrally administered somatostatin on the adrenal zona glomerulosa in male rats

Segmental zoster paresis (SZP) is the focal, asymmetrical neurogenic weakness which may occur in a limb affected by cutaneous zoster. We have summarized the features of this syndrome, based on a retrospective review of 8 personal and 96 published cases. Limb SZP becomes apparent in at least 3-5% of patients with cutaneous zoster, who are usually over the age of sixty and weak proximally (C5,6,7 or L2,3,4 innervated muscles). Functional motor recovery occurs in about 75% of cases, generally by 1-2 years. Limb weakness is probably due to a lesion of the ventral nerve root, in close proximity to the initiating dorsal ganglionitis. The electrodiagnostic findings, scarce in the literature, typically consist of absent compound sensory nerve action potentials in the involved limb, with less frequent reduction or loss of compound muscle action potentials. Fibrillations and positive sharp waves become detectable within 1-4 months in limb and related paraspinal muscles, decreasing or disappearing later. In addition to this radiculopathy, peripheral nerves may also occasionally become involved, manifest as mononeuropathies of the median, ulnar, long thoracic, recurrent laryngeal, and phrenic nerves. The zoster infection or consequent inflammatory response appears able to affect motor axons distally as well as proximally.     

Axonal structure and function after axolemmal leakage in the squid giant axon

Membrane leakage is a common consequence of traumatic nerve injury. In order to measure the early secondary effects of different levels of membrane leakage on axonal structure and function we studied the squid giant axon after electroporation at field strengths of 0.5, 1.0, 1.6, or 3.3 kV/cm. Immediately after mild electroporation at 0.5 kV/cm, 40% of the axons had no action potentials, but by 1 h all of the mildly electroporated axons had recovered their action potentials. Many large organelles (mitochondria) were swollen, however, and their transport was reduced by 62% 1 h after this mild electroporation. One hour after moderate electroporation at 1.0 kV/cm, most of the axons had no action potentials, most large organelles were swollen, and their transport was reduced by 98%, whereas small organelle transport was reduced by 75%. Finally at severe electroporation levels of 1.65-3.0 kV/cm all conduction and transport was lost and the gel-like axoplasmic structure was clumped or liquefied. The structural damage and transport block seen after severe and moderate poration were early secondary injuries that could be prevented by placing the porated axons in an intracellular-type medium (low in Ca2+, Na+, and Cl-) immediately after poration. In moderately, but not severely, porated axons this protection of organelle transport and structure persisted, and action potential conduction returned when the axons were returned to the previously injurious extracellular-type medium. This suggests that the primary damage, the axolemmal leak, was repaired while the moderately porated axons were in the protective intracellular-type medium.     

Diaphragm EMG measured by cervical magnetic and electrical phrenic nerve stimulation

The purpose of the study was to compare electrical stimulation (ES) and cervical magnetic stimulation (CMS) of the phrenic nerves for the measurement of the diaphragm compound muscle action potential (CMAP) and phrenic nerve conduction time. A specially designed esophageal catheter with three pairs of electrodes was used, with control of electrode positioning in 10 normal subjects. Pair A and pair B were close to the diaphragm (pair A lower than pair B); pair C was positioned 10 cm above the diaphragm to detect the electromyogram from extradiaphragmatic muscles. Electromyograms were also recorded from upper and lower chest wall surface electrodes. The shape of the CMAP measured with CMS (CMS-CMAP) usually differed from that of the CMAP measured with ES (ES-CMAP). Moreover, the latency of the CMS-CMAP from pair B (5.3 +/- 0.4 ms) was significantly shorter than that from pair A (7.1 +/- 0.7 ms). The amplitude of the CMS-CMAP (1.00 +/- 0.15 mV) was much higher than that of ES-CMAP (0.26 +/- 0.15 mV) when recorded from pair C. Good-quality CMS-CMAPs could be recorded in some subjects from an electrode positioned very low in the esophagus. The differences between ES-CMAP and CMS-CMAP recorded either from esophageal or chest wall electrodes make CMS unreliable for the measurement of phrenic nerve conduction time.     

Electrophysiological properties of neurons in intact rat dorsal root ganglia classified by conduction velocity and action potential duration

1. L4 and L5 dorsal root ganglia of rats aged 4-5 wk were isolated in vitro with their dorsal roots and sciatic nerves intact. With the use of intracellular microelectrodes, conduction velocity (CV) was determined along both peripheral and central axons and active and passive membrane properties were investigated with the use of a single-electrode switching clamp. 2. Neurons were classified into one of the three subgroups, A alpha/beta, A delta, and C, on the basis of a combination of axonal CV and action potential duration. Soma diameters overlapped between these groups. 3. Action potentials elicited by nerve stimulation in all cells and by a somatic current step in A alpha/beta-cells were always blocked by tetrodotoxin (TTX) 0.1-1 microM), whereas somatic action potentials in a proportion of A delta-cells and all C cells were TTX-resistant. 4. Passive electrical properties differed significantly between A alpha/beta-, A delta-, and C cells. The contribution of the additional membrane of the axons to the recorded electrical properties was analyzed with the use of a compartmental model of the neurons (see APPENDIX). 5. Most neurons discharged only a single action potential at the onset of a depolarizing current step, but 33% of A alpha/beta-cells fired repetitively throughout the step. This was associated with a lower threshold for action potential initiation by depolarizing current and a shorter afterhyperpolarization than in other A alpha/beta-cells. 6. Afterhyperpolarizations varied in size and duration between neurons and most were either not or only slightly affected by replacing Ca2+ in the bathing solution with Co2+ or Ba2+ or by adding tetraethylammonium (1 and 10 mM). Outward tail currents following an active response could be fitted with one fast exponential (time constant = 13 +/- 1 ms, mean +/- SE) and, in 65% of cells, one to three slower time course currents (to which exponentials with time constants of approximately 50, 300, or 1,500 ms could be fitted). A very slow late-onset current (detected in 33% of C cells) resembled a Ca(2+)-dependent K+ conductance described in several other neurons. 7. Voltage transients showed "sag" during maintained hyperpolarizing current steps in 90% of A alpha/beta-cells and 70% of A delta-cells but only 13% of C cells. Time-dependent inward currents were recorded when membrane potential was hyperpolarized. These currents had mean activation time constants of approximately 40 ms at -120 mV and were Cs+ sensitive and Ba2+ insensitive. 8. The proportion of neurons with a transient outward current, IA, increased as CV decreased (36% of A alpha/beta-cells, 56% of A delta-cells, 63% of C cells). Outward currents in cells of all subgroups had either one or two of three inactivation time constants (means approximately 22, 120, and 800 ms). 9. This study shows that many of the electrical characteristics of isolated dorsal root ganglion neurons can be demonstrated in intact ganglia in which the neurons can be better identified functionally. The currents underlying the afterhyperpolarization in these cells are diverse across all subgroups and require further investigation. The electrical effects of retaining the axonal projections of the cells and the use of microelectrodes filled with 0.5 M KC1 are discussed in relation to the differences from data recorded in dissociated neurons.     

Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics

BACKGROUND: Previous work has demonstrated that cells with AV nodal-type action potentials are not confined to Koch's triangle but may extend along the AV orifices. The aim of this study was to examine the histological and electrophysiological characteristics of this tissue. METHODS AND RESULTS: Studies were performed in isolated, blood-perfused dog and pig hearts. Microelectrode recordings revealed cells with nodal-type action potentials around the tricuspid and mitral valve rings. These cells were found within 1 to 2 mm of the valve annuli. A zone of cells with intermediate action potentials, approximately 1 cm wide, separated cells with nodal-type action potentials from cells with atrial-type action potentials in the body of the atria. In cells with nodal-type action potentials, adenosine caused a reduction in action potential amplitude (49 +/- 2 versus 33 +/- 2 mV, mean +/- SE; P < .001), upstroke velocity (2.5 +/- 0.2 versus 2.0 +/- 0.2 V/s, P < .05), and duration (150 +/- 4 versus 96 +/- 8 ms, P < .001). The light microscopic appearance of AV junctional cells was similar to that of myocytes in the body of the atrium. A polyclonal antibody raised against connexin-43 bound to atrial and ventricular tissue but not to the AV junctional tissue or AV nodal region. The absence of connexin-43 correlated with the sites of cells with nodal-like action potentials. With pacing techniques, the AV junctional tissue in the region of the posterior AV nodal approaches could be electrically dissociated from atrial, AV nodal, and ventricular tissue. AV nodal echoes were induced with ventricular pacing in three dog hearts. In each case, retrograde conduction was through the slow pathway, and anterograde conduction was through the fast pathway. During echoes, activation of AV junctional cells preceded atrial activation during retrograde slow pathway conduction, but these cells were not activated during anterograde fast pathway conduction. CONCLUSIONS: AV junctional cells around both annuli are histologically similar to atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43. The light microscopic appearance of AV junctional cells is a poor guide to their action potential characteristics. The AV junctional cells in the posterior AV nodal approaches appear to participate in slow pathway conduction. These cells may be the substrate of the slow "AV nodal" pathway.     

Resistance to anoxic injury in the dorsal columns of adult rat spinal cord following demyelination

In order to examine the relationship between myelination and sensitivity to anoxia in adult white matter, we studied action potential conduction in the spinal cord dorsal column of adult rats in which focal demyelinating lesions had been produced using ethidium bromide/X-irradiation. Acutely isolated spinal cords from control rats and following demyelination were maintained in vitro at 36 degrees C and compound action potentials were studied following supramaximal stimulation. The compound action potential was totally abolished within 12 min of the onset of anoxia in normal dorsal columns, but was not abolished until 50 min following the onset of anoxia in demyelinated dorsal columns. Compound action potentials showed significantly greater recovery (to 58.1 +/- 12.2% of control amplitude) in demyelinated dorsal columns compared to controls (30.8 +/- 5.3%) following 120 min of reoxygenation. These results show that focal demyelination is associated with reduced sensitivity to anoxia within white matter of the adult spinal cord.     

Actions of halothane and isoflurane on Purkinje fibers in the infarcted canine heart: conduction, regional refractoriness, and reentry

The actions of halothane (HAL) and isoflurane (ISO) on conduction and regional refractoriness were studied in infarcted canine hearts to compare their effects on reentry in vitro. In two anesthetic groups of 8 hearts, high and low dose effects were assessed using action potentials recorded from Purkinje fibers located in the nonischemic and ischemic regions. An extrastimulus technique was used to determine the relationship between delay of conduction of premature impulses into the more refractory ischemic region and induction of reentrant responses. At high doses (HAL 0.60 mM and ISO 0.64 mM, approximately 2.3 minimum alveolar anesthetic concentration [MAC]) both anesthetics decreased (P < or = 0.05) the effective refractory period for direct intracellular stimulation of nonischemic fibers (local ERP, initial control: 294 +/- 8 ms); the decrease with HAL (-29 +/- 6 ms) was smaller (P < or = 0.05) than with ISO (-50 +/- 7 ms). HAL and ISO also decreased (P < or = 0.05) the coupling interval of the earliest premature impulse which conducted into the infarct (system effective refractory period [SERP], control: 301 +/- 7 ms) by -31 +/- 11 and -44 +/- 8 ms, respectively. In contrast, the functional refractory period (FRP) in the ischemic region (control:354 +/- 4 ms) was increased by HAL (26 +/- 8 ms; P < or = 0.05) but decreased by ISO (-14 +/- 4 ms, P < or = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Granulomatous orchitis. A case report and review of the literature

We developed a method for determination of motor conduction along the mandibular and sensory conduction along the lingual and inferior alveolar nerves in 10 controls and 6 patients with lingual neuropathy following lower wisdom tooth extraction. Patients with lingual neuropathy had reduced/absent or delayed compound sensory action potentials and normal conduction along the fibers of the inferior alveolar nerve and mandibular nerve. The method provides a useful electrophysiological means of evaluating lingual nerve lesions.     

An electrophysiological and histological study on the neurotoxicity of lidocaine in excised rabbit cervical vagus nerve

We studied the neurotoxic effect of lidocaine at different concentrations on the desheathed rabbit vagus nerve by measuring the amplitudes of evoked compound action potentials and the histological changes of the nerve by means of the electron microscopy after incubation in lidocaine-Ringer's bicarbonate (RB) solution. The following results were obtained. 1) Minimum concentrations of lidocaine for producing complete conduction block (minimum blocking concentration, MBC) were 0.02% for A beta and A delta fibers, and 0.03% for C fibers. 2) Irreversible conduction blocks of compound action potentials were observed in relation with lidocaine concentrations and the duration of incubation: e.g. 0.5% for 2 hours incubation was equivalent to the block with 1% for 1 hour. 3) Degenerative change of axons was revealed morphologically in the preparations exposed to 2% or a higher concentration of lidocaine. 4) Risk ratio, which means a numerical value calculated as clinical concentration/irreversible concentration with 2 hr exposure, was similar to other local anesthetics except dibucaine HCl, which shows an higher risk ratio. However, it should be noted that lidocaine has an risk of producing irreversible changes in nerve fibers, when applied to the nervous tissue at higher concentrations for longer durations.     

Acoustic neuroma surgery and delayed facial palsy

The Prader-Willi syndrome (PWS) is associated with a tendency to self-injury and a reduced sensitivity to painful stimuli. Somatosensory functions were studied in 5 children aged 11-13 years with PWS. Tactual perception in the hands (stereognosis) was apparently normal in 4 of them. Sensory nerve conduction velocities in the median nerve and latencies for sensory evoked potentials were similar in the PWS subjects and in 10 healthy controls indicating a preserved myelinisation of sensory nerve fibers in PWS. Sensory nerve action potential amplitudes in the PWS group were on an average only 40-50% of normal size (p = 0.03), suggesting a reduced number of normal axons in the median nerve. The results may be relevant for the impaired pain sensitivity in PWS because similar neurographic findings and a low density of peripheral nerve fibers have been reported in patients with hereditary or congenital insensitivity to pain.     

Intermediate nerve conduction velocities define X-linked Charcot-Marie-Tooth neuropathy families

Three genetic loci for the Charcot-Marie-Tooth (CMT) syndromes with slow motor nerve conduction velocities (hereditary motor and sensory neuropathy: HMSN type I) have been mapped to chromosomes 1 (CMT1B), 17 (CMT1A), and the X chromosome (CMTX). The clinical features of these three CMT subgroups are similar. To determine whether any clinical features distinguish CMTX families, the range of clinical findings and motor nerve conduction velocities were examined in two large CMTX families, the range of clinical findings and motor nerve conduction velocities were examined in two large CMTX families with CMTX proven by linkage to X-chromosome markers. CMTX males had more wasting and weakness than CMTX females or individuals with CMT1A. Patellar reflexes were more often retained in CMTX. Motor nerve conduction velocities were faster than in CMT1A. Intermediate-range median nerve conduction velocities were present in CMTX females (45 +/- 9 m/sec; range, 26 to 61 m/sec). These velocities were significantly faster than those for CMT1A females (22 +/- 8 m/sec, p < 0.0001). Median nerve conduction velocities in CMTX males (31 +/- 6 m/sec) were significantly slower than in CMTX females and faster than in CMT1A males (20 +/- 6 m/sec, p < 0.0001). The combination of slow conduction velocities in affected males (< 40 m/sec) and intermediate-range median motor conduction velocity results (> 40 m/sec) in affected or obligate carrier females is a useful distinguishing feature to separate CMTX from CMT1A, as intermediate conduction velocities are not present in autosomal-dominant dominant CMT1A families. This feature defines possible CMTX families for linkage studies. Families with no male-to-male inheritance of the syndrome, slow motor nerve conductions in affected males, and normal or intermediate-range conduction velocities in carrier females should be considered to be X-linked CMT families.     

Compression injury of mammalian spinal cord in vitro and the dynamics of action potential conduction failure

1. White matter strips from the ventral spinal cord of adult guinea pigs were isolated in vitro, and their electrophysiological characteristics and response to controlled focal compression injury were examined. A double sucrose gap technique was used for stimulation and recording at opposite ends of a 12.5 mm-diam central well superfused with oxygenated Krebs solution. 2. The compound action potential recorded with the sucrose gap was similar in form to single fiber potentials recorded with intra-axonal electrodes, including the presence of a prolonged depolarizing afterpotential. 3. Three types of conduction block resulting from compression were identified: an immediate, spontaneously reversible component, which may result from a transient increase in membrane permeability and consequent disturbance of ionic distribution; a second component that was irreversible within 1-2 h of recording, perhaps resulting from complete axolemmal disruption; and a third component, which may have been due to disruption of the myelin sheath, that appeared to be reversible with application of 10-100 microM of the potassium channel blocker 4-aminopyridine. 4. Conduction deficits--decreased amplitude and increased latency of the compound potential--were stable between 5 and 60 min postinjury, and their intensity corellated with the extent of initial compression over a full range of severity. 5. Stimulus-response data indicate that mechanical damage to axons in compression was evenly distributed across the caliber spectrum, suggesting that the susceptibility of large caliber axons seen histopathologically after injury in vivo may be based on delayed, secondary processes. 6. The model provides the ability to monitor changes in the properties of central myelinated axons after compression injury in the absence of pathological variables related to vascular damage. This initial investigation found no evidence of secondary deterioration of axons in the 1st h after injury, although there was evidence of both transient and lasting mechanical damage to axons and their myelin sheaths.     

Cancer incidence of sulfite pulp workers in Denmark

A follow-up clinical study, peripheral motor and sensory nerve conduction velocities and central motor conduction by magnetic stimulation of the cortex were performed in 13 patients with classical Friedreich's ataxia (FA) phenotype, for a period of 9-12 years. Clinical worsening was unrelated to peripheral nerve abnormalities. The amplitude of the nerve action potentials and delayed conduction velocity remained unchanged for several years. Central motor conduction times were abnormal in all patients. Clinical conditions worsened significantly between successive examinations with significant increments in threshold and significant decrement of the amplitude of motor evoked potentials. The results are consistent with progressive pyramidal and cerebellar pathways involvement as the cause of clinical worsening in FA.     

Multiple action potential waveforms of single units in man as signs of variability in conductivity of their myelinated fibres

Percutaneous microneurography was performed with concentric needle electrodes to record neural activity from myelinated fibres in human peripheral nerves. Template matching techniques were used together with interspike interval analysis and studies on functional class, receptive field characteristics, conduction velocities and other single fibre properties to classify single units. Sometimes the same fibres exhibited different action potentials at the same time. The potentials had some common features, but differed either in their waveform types or only in duration. There was a correlation between the occurrence of the different potential shapes and firing frequency of the studied unit. The outcome of the studies suggested that there was a common denominator which could explain the observations. Most likely, momentary fluctuations in excitability of the myelinated fibres occurring during the relative refractory period or the supernormal period were responsible for the variations in complexity of the studied units due to a partial block of fibre propagation probably caused by the recording electrode. Thus, action potentials deriving from the same axon may not always have the same shapes. Methods for unit classification, such as template matching, are discussed in the light of our findings.     

Increased spike-frequency adaptation and tea sensitivity in dorsal root fibers after sciatic nerve injury

Excitability of rat dorsal root axons were studied 3 weeks after injury to the sciatic nerve. Whole nerve recordings were obtained from injured and control nerves in a sucrose gap chamber. Constant current depolarization pulses (30-200 ms) applied approximately 50% above the stimulus strength required for maximal amplitude compound action potentials (CAPs) evoked a burst of action potentials in the dorsal root which displayed spike adaptation. The depolarization-induced burst response of the dorsal roots was greatly reduced after crush or transection of the sciatic nerve. However, application of the potassium channel blocker, tetraethylammonium (TEA), restored the burst discharge in injured dorsal root axons. Brief tetanic stimulation of the dorsal root also induced an afterhyperpolarization (AHP) that was twice as large in the transection group as compared to the control group, and which was blocked by TEA. There were no changes seen in the amplitude of the compound action potential, frequency-following characteristics, refractory properties, or 4-AP sensitivity in the dorsal roots after peripheral nerve injury. These results suggest that there is enhanced spike adaptation that occurs at the same time as an increase in the sensitivity to the potassium channel blocker, TEA, in axon regions proximal to the site of nerve injury and have implications for the pathophysiology of nerve injury.     

Action potential conduction and sodium channel content in the optic nerve of the myelin-deficient rat

Compound action potential (CAP) conduction and Na+ channel content were studied in optic nerves from control and myelin-deficient (md) rats. Action potential propagation was approximately five times slower in the md rat, but the action potentials propagated securely and had frequency-following and refractory properties equivalent to control myelinated axons. Tritium-labelled saxitoxin ([3H]-STX) binding in md optic nerve was approximately 30% greater, per wet mass of tissue, than in the control optic nerve. However, calculations of channel density per axon based on previously published anatomical data from md and control optic nerves (Dentinger et al. 1985) show an equivalent number of sodium channels per axon, with an average density of 10 channels micron-2 in md and 11 channels micron-2 in control optic nerve axons. The amplitude of the CAP in both control and md optic nerves was significantly attenuated by 50 nM TTX, precluding the possibility that TTX-insensitive channels are responsible for the action potential in myelinated or amyelinated axons. In addition, the amplitudes of voltage-activated Na+ currents in type I and type II astrocytes cultured from control and md optic nerves were similar, suggesting that the glial component of Na+ channels is not abnormal in the optic nerve of the md rat. These results suggest that myelination (or its absence) may not directly regulate the number of axonal Na+ channels.