Inhibitory and excitatory binocular convergence to visual cortical neurons of the cat.

Responses of 182 visual cortical (VC) neurons to electrical stimulation of both optic nerves (ON) were recorded intra- and extracellularly, and their eye dominance determined with visual stimuli. Many VC neurons could not be excited by ON stimulation without simultaneous activation by visual stimulation of the eye of the other side. The ON-excited units (25 simple and 71 complex cells) had essentially the same response latency from both ONs. In almost all VC neurons including those not driven from the ON, ON stimulation elicited inhibition which was shown to be post-synaptic in all neurons recorded intra- or quasi-intracellularly. The onset latency of IPSPs not preceded by an action potential or EPSP was 4.2+/-1.0 msec, suggesting that intracortical inhibition was initiated by afferent impulses mediated through fast conducting fibers. In visually monocular neurons, ON stimulation of the non-driving side also elicited primary inhibition. Visually binocular, but monocular-dominant neurons responded more reliably to ON stimulation of the dominant side than to the other. In most binocular neurons with equal visual responsiveness to both eyes, inhibition and excitation evoked from both ONs had about the same latency and magnitude.     

Pattern electroretinography and visual evoked potentials in optic nerve diseases.

BACKGROUND: To evaluate transient pattern electroretinography (PERG) and pattern visual evoked potential (VEP) for the diagnosis, differential diagnosis and follow-up of optic nerve diseases. METHODS: Twenty-nine consecutive patients (14 female, 15 male) with the diagnosis of ischaemic optic neuropathy (n=14) and optic neuritis (n=15) were included in this study. Mean age of the patients with ischaemic optic neuropathy was 63.3+/-3.3 (60-78) years and the mean age of the patients with optic neuritis was 28.3+/-8.4 (19-43) years. In each patient ophthalmological examination and systemic evaluation were done and VEP and PERG were recorded. As a control group, VEP recordings of 35 healthy subjects were included. RESULTS: In the ischaemic optic neuropathy group (group 1), mean VEP amplitude (+/-SD) (1.96+/-0.95 microV) was found to be decreased significantly in the affected eyes in comparison to the control group and the unaffected eyes. The delay in latency (116.3+/-20.14 msec in the affected eyes compared with 101.31+/-6.19 msec in unaffected eyes) was statistically significant when compared with the healthy subjects. In the optic neuritis group (group 2), VEP amplitude was decreased (4.13+/-4.04 microV vs 6.97+/-3.35 microV and 6.97+/-4.43 microV) and latency was increased (122.59+/-20.09 msec vs 101.31+/-6.19 msec and 108.76+/-13.57 msec) in affected eyes significantly in comparison to the unaffected eyes and control group, respectively. Even though there were no significant differences for P50 latency and N95/P50 ratios between affected and unaffected eyes in both groups, N95 amplitude decreased significantly in the affected eyes of the ischaemic optic neuropathy patients and N95 latency was found to be decreased in optic neuritis patients. There was no correlation between VEP and PERG findings in both groups. CONCLUSION: VEP amplitude decreased significantly in ischaemic optic neuropathies while latency delay was more significant in patients with optic neuritis. PERG findings showed decreased N95 amplitude in ischemic optic neuropathy without associated latency changes.     

Postsynaptic potentials of motor neurons in the nucleus of the hypoglossal nerve in cats, evoked by rubrofugal impulses

The effects of ipsi- and contralateral red nuclei stimulation on the hypoglossal motoneurons were studied in the cats under chloralose-nembutal anesthesia. Repetitive ipsi- and contralateral rubrofugal volleys evoked PSPs in 35 (69%) from 51 investigated motoneurons (3-5 stimuli of threshold intensity at frequency 500-600 per/s were used). EPSPs appeared in 33 motoneurons with latencies from 3.5 to 14.0 ms (mean value 5.7 +/- 0.75 ms for ipsilateral and 6.8 +/- 0.8 ms for contralateral rubral stimulations). In two motoneurons IPSPs were observed with latency 6.2 ms. Stimulation of the lingual nerve evoked EPSPs and action potentials in 31 motoneurons and IPSPs in 4 motoneurons. 16 motoneurons which could not be activated by rubral stimulation also responded by IPSPs to lingual nerve stimulation. The presented data testify to the existence of two rubrobulbar systems connected by polysynaptic pathways mainly with motoneurons of tongue retractor muscle.     

Somatosensory evoked potentials in the term newborn.

Median nerve somatosensory evoked potentials (SEPs) were recorded from surface electrodes in 40 healthy term infants (range 36.5-43 weeks postmenstrual age). Electrical stimulation at 5 Hz was used, averaging the response to several runs of 1024 stimuli to each median nerve, bandpass 10-3000 Hz, sweeptime 100 msec. Identifiable potentials were collected over the cervical cord on all runs in all 40 infants and from the cortex in at least some runs in 39 out of 40 infants. The cervical response showed little variation and consisted of a clear negative wave with up to 3 peaks, mean latency of the largest 10.2 +/- 0.7 msec, followed by a positive deflection. The cortical response was very variable in form and latency between infants and to a lesser degree within infants. Four types of cortical wave form were found, symmetrical, asymmetrical, plateau and M shaped, of increasing complexity. In 11% of trials the response was absent or indistinct but could usually be uncovered by alteration in stimulus frequency or intensity. In the whole group, the mean latency for N1 was 30.0 +/- 6.8 msec and for the central conduction time 19.8 +/- 6.5 msec. Significant differences were found between the 4 cortical wave forms in the main variables measured, which gave support for form S being the most primitive and form M the most mature response.     

Mode of activation of pyramidal neurons by mossy fiber stimulation in thin hippocampal slices in vitro

Activation of pyramidal neurons by mossy fiber stimulation was studied electrophysiologically in guinea pig hippocampal slices in vitro. In the CA3 pyramidal layer, the stimulation of mossy fibers evoked the primary response which consisted of two main components, the sharp negative deflection and the slow positive wave. Simultaneous intracellular and extracellular recordings revealed that the slow positive wave reflects the monosynaptic excitatory (EPSPs) and inhibitory postsynaptic potentials (IPSPs) generated in the pyramidal neurons. This was further supported by the shift of the sink toward the somata from the intermediate portion of the apical dendrites in the laminar field potential profiles when Cl^? was removed from the medium. Tetanized stimuli applied to the mossy fibers caused a drastic potentiation of the sharp negative deflection. The latency of the sharp negative deflection in CA3 was nearly equal to that in CA4 with a latency delay of within 1 msec and, in both regions, latencies of the sharp negative deflections remained almost constant throughout tetanic stimuli. On the other hand, the field potential in CA2 was mainly composed of the IPSPs, and the sharp negative deflection was not observed. From these findings, it was concluded that the primary response is the summed extracellular manifestation of EPSPs, IPSPs, and action potentials which are evoked monosynaptically. The current-density analysis (the second derivative of the potential profiles) also brought about results consistent with the above notions, though its validity may be questioned in several respects.     

Modulation of bistratified cell IPSPs and basket cell IPSPs by pentobarbitone sodium, diazepam and Zn2+: dual recordings in slices of adult rat hippocampus

Simultaneous intracellular recordings from presynaptic Stratum pyramidale interneurons and postsynaptic pyramidal cells in adult rat hippocampal slices were performed to investigate the strength of the modulation of single-axon inhibitory postsynaptic potentials (IPSPs) by the GABAA receptor modulators pentobarbitone, diazepam and zinc. The processing of biocytin-filled interneurons for light microscopy revealed that these single-axon IPSPs were generated by basket cells (n = 33), bistratified cells (n = 18) and axo-axonic cells (n = 2). The IPSPs generated by these three groups of interneurons had amplitudes and widths at half amplitude with similar ranges, but when bistratified cell IPSPs were compared with basket cell IPSPs with similar half widths their rise times were slower. Pentobarbitone sodium (250 microM) powerfully enhanced 13 tested IPSPs generated by all three cell types. Amplitudes were enhanced by 82 +/- 56%, 10-90% rise times by 150 +/- 101% and the widths at half amplitude by 71 +/- 29%. Diazepam (1-2 microM) also increased all IPSPs tested, although the changes were more moderate in basket cell IPSPs (amplitudes increased by 19 +/- 11%, n = 8) than in bistratified cell IPSPs (amplitudes increased by 66 +/- 48%, n = 5). Basket cell IPSP 10-90% rise times and widths at half amplitude were not significantly increased. Bistratified cell IPSP 10-90% rise times were increased by 44 +/- 24% and the widths at half amplitude by 32 +/- 35%. The one tested IPSP generated by an axo-axonic cell was also diazepam-sensitive. Zinc, 250 microM, decreased four out of 10 IPSPs generated by basket cells and four out of five IPSPs generated by bistratified cells. The one tested axo-axonic cell IPSP was zinc-insensitive. These data suggest that IPSPs generated in CA1 pyramidal cells by basket and bistratified cells display different pharmacologies and may be mediated by different receptors or receptor combinations.     

A comparison of magnetic and electrical stimulation of facial nerve at the cerebello-pontine angle in the dog.

Magnetic stimulation is a painless, non-invasive technique which allows an alternative method for testing cranial nerves which were previously inaccessible. We compared the latency of muscle responses obtained by electrical stimulation of the facial nerve at the cerebello-pontine angle (CPA) to high intensity transcranial magnetic stimulation (TMS) in 6 dogs. Evoked muscle response from the levator nasolabialis during electrical stimulation had a mean latency of 6.24 +/- 0.42 msec, compared with a mean of latency of 6.13 +/- 0.50 msec obtained by magnetic stimulation. Orbicularis oculi had a mean latency of 3.65 +/- 0.34 msec compared with a mean latency of 3.53 +/- 0.36 msec for magnetic stimulation. This suggests that high intensity TMS results in direct activation of the facial nerve as it exits the brain-stem in dogs. This observation is in accord with previous clinical studies that magnetic stimulation results in activation of the intracranial segment of the facial nerve in man.     

An in vitro analysis of sound localization mechanisms in the gerbil lateral superior olive

One way in which animals localize sounds along the horizon is by detecting the level differences at the 2 ears. Neurons in the lateral superior olive (LSO) encode this cue by integrating the synaptic drive from ipsilateral excitatory and contralateral inhibitory connections. This synaptic integration was analyzed in 400-500-microns brain slices through the gerbil superior olive. Intracellular recordings from LSO neurons were obtained during the application of independent or conjoint electrical stimuli to the excitatory afferent and inhibitory afferent pathways. Stimulation of ascending fibers from the ipsilateral cochlear nucleus reliably evoked EPSPs and action potentials. Stimulation of the medial nucleus of the trapezoid body (MNTB) consistently evoked IPSPs. The evoked postsynaptic potentials differed in that IPSPs were 2 times the duration of EPSPs. An electrophysiological estimate of convergence indicated approximately 10 excitatory and 8 inhibitory afferents per LSO neuron. MNTB stimulation suppressed synaptically evoked action potentials. When stimulus amplitude was increased to the excitatory pathway, it was generally found that a greater MNTB stimulus was necessary to suppress the action potential. A similar commensurate rise in ipsilateral and contralateral acoustic stimulation was also found to be necessary to give the same criterion response. These results confirm that the LSO can integrate evoked action potentials and IPSPs to encode interaural level. Increasing stimulus voltage was found to decrease both action potential and IPSP latency, suggesting that intensity information may be encoded with temporal cues in the nervous system. It was also found that an evoked burst of action potentials could be inhibited in such a way as to yield intermediate discharge rates, dependent on contralateral stimulus level. Taken together, these results suggest that certain properties related to level-difference coding may be available for intracellular analysis using the brain-slice preparation. Several temporal characteristics of the synaptic potentials, including latency and duration, may play a critical role in this simple computation.     

A freeze-fracture study of fiber types in normal human muscle.

The sarcoplasmic reticulum (SR) and plasma membranes of Type 1 and Type 2 fibers of normal human muscle were examined by the freeze-fracture technique. Total particle counts in the SR appeared much lower than in other mammals and a packing density of about 1200 particles/micrometer 2 was found in both longitudinal and cisternal components of SR. There was no difference in particle density of Type 1 and Type 2 fibers. In freeze-fracture replicas of plasma membranes several fiber type differences were seen. The surface caveolae were uniformly distributed in Type 1 fibers whereas in Type 2 they were clustered preferentially at the I-band levels. Total density of intramembranous particles was greater in Type 1 fibers (347 +/- 68/micrometer 2 in P-face, 58 +/- 11/micrometer 2 in E face) than in Type 2 fibers (207 +/- 30/micrometer 2 in P-face, 80 +/- 9/micrometer 2 in E-face). There was a striking difference in respect to rectilinear arrays which were virtually absent in Type 1 fibers (0--2/micrometer 2) and numberous (up to 50--70/micrometer 2) in Type 2 fibers.     

Electrophysiological characterization of reciprocal connections between the parabrachial nucleus and the area postrema in the rat

Neuroanatomical studies have demonstrated reciprocal connections between the parabrachial nucleus (PBN) and both the area postrema (AP) and the nucleus tractus solitarius (NTS). To functionally characterize these projections, antidromic identification of AP and NTS neurons projecting to the PBN was attempted. Orthodromic influences on these cells, resulting from PBN stimulation, were also examined. Four percent of AP neurons tested (n = 74) were antidromically identified as projecting to the PBN [latency (L) = 26 +/- 4 msec, threshold current (T) = 79 +/- 11 microA]. Parabrachial stimulation orthodromically influenced 24% of AP cells. Equal numbers of these neurons (12%) were excited [L = 25 +/- 9 msec, duration (D) = 29 +/- 14 msec] and inhibited (L = 28 +/- 8 msec, D = 107 +/- 40 msec). Of 46 NTS neurons tested, 11% were antidromically identified as projecting to the PBN (L = 12 +/- 4 msec, T = 61 +/- 18 microA), while orthodromic influences were seen in 41% of these neurons. Initial responses of 30% of the cells were excitatory (L = 34 +/- 14 msec, D = 63 +/- 24 msec), PBN stimulation inhibited the remaining 11% of NTS neurons (L = 30 +/- 10 msec, D = 108 +/- 32 msec). These findings suggest that a functional heterogeneity exists in the PBN efferents to the AP and NTS. However, the small proportion of antidromically identified AP and NTS efferents to the PBN disagrees with neuroanatomical studies suggesting a denser projection.     

Latency differences of N20, P40/N60, P100/N140 SEP components after stimulation of proximal and distal sites of the median nerve.

The latencies of SEP N20, P40, N60, P100, and N140 components were measured after stimulation of two different sites, and the differences in relation to conduction velocity and their central functions are discussed. Subjects were 8 healthy right-handed males (age 22-31 years, height 164-184 cm). An electrical pulse of 200micro sec duration with an intensity of 2 times the motor threshold was delivered to the wrist and to the elbow alternately at a random rate of 0.1 to 0.3 Hz. Recording electrodes were Cz', C3', and C4' referenced to linked ears. Analysis time was 50 msec before and 450 msec after the stimulus. The band pass was 0.5 Hz to 2 kHz. Subjects were asked to mentally count the number of stimuli. The averaging was interrupted after every 16 to 24 stimuli and checked to determine whether the subject was attentive to the stimuli by verifying the number of stimuli counted. A total of 100 responses each from elbow and wrist stimuli were averaged. Differences in peak latency between elbow and wrist stimuli for N20, P40, N60, P100, and N140 were 3.7 +/- 0.7 msec, 5.0 +/- 1.8, 4.3 +/- 1.2, 8.1 +/- 6.3, and 7.4 +/- 2.6 msec, respectively. According to the latency differences, SEP components can be divided into 3 groups: the shortest difference for N20, medium difference for P40 and N60 and longest difference for P100 and N140. Similar latency differences and similar potential distribution for P40 and N60, and for P100 and N140, and their differences from N20 confirmed that each of N20, P40/N60, and P100/N140 has a different function centrally. In addition, central processing time was longer with the more distal site stimulation.     

Corneal reflex in normal and pathological subjects

The orbicularis oculi response can be evoked both by mechanical stimulation of the cornea (corneal reflex) and by electrical stimulation of the skin overlying the supraorbital nerve (blink reflex). Mechanical stimuli to the cornea activate A delta and C free nerve endings of the corneal mucosa. Electrical stimuli to the supraorbital nerve activate A beta, A delta and C fibers of the nerve trunk. Both reflexes present a bilateral late response, but the blink reflex shows in addition an early ipsilateral component (R1), which has never been observed with the corneal stimulation in man. We have developed a simple technique of electrical stimulation of the cornea which provides stable responses and allows precise measurements of threshold and latency of the reflex. In normal subjects, the threshold ranged from 50 to 350 microA, and the maximal stimulus that the subject could bear (tolerance level) ranged from 1000 to 2500 microA. The minimal latency to tolerance level stimuli was 39 +/- 3 msec. The latency difference between the direct responses evoked from the two opposite corneas never exceeded 8 msec and the difference between the direct and consensual responses elicited from the same cornea never exceeded 5 msec. An early ipsilateral component similar to the R1 response of the blink reflex was not observed, even with supramaximal stimulation. The electrically evoked corneal reflex was normal in 10 cases of essential trigeminal neuralgia, while the responses showed significant abnormalities in 18 subjects submitted to thermocoagulation of the Gasserian ganglion as a treatment of neuralgic pain, as well as in 2 cases of symptomatic neuralgia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Simultaneous recording of late and ultra-late pain evoked potentials in fibromyalgia.

OBJECTIVE: To characterize laser evoked potentials (LEP), pain psychophysics and local tissue response in fibromyalgia patients. METHODS: LEP were recorded in 14 women with fibromyalgia in response to bilateral stimulation of tender and control points in upper limbs by 4 blocks of 20 stimuli at each point. Subsequently, heat pain thresholds were measured and supra-threshold magnitude estimations of heat pain stimuli were obtained on a visual analogue scale. Finally, the extent of the local tissue response induced by the previous stimuli was evaluated. RESULTS: Laser stimuli elicited two long latency waves: A late wave (mean latency 368.9+/-66.9 ms) in most patients (13/14) from stimuli at all points, and an ultra-late wave (mean latency 917.3+/-91.8 ms) in 78.5% of the patients at the control points and in 71.4% at the tender points. Amplitude of ultra-late waves was higher at the tender points (20.67+/-11.1 microV) than at the control points (10.47+/-4.1 microV) (P=0.016). Pain thresholds were lower in the tender (41.2+/-2.7 degrees C) than the control points (43.9+/-3.2 degrees C) (P=0.008). Local tissue response was significantly more intense at tender than control points (P=0.004). CONCLUSIONS: Ultra-late laser evoked potentials can be recorded simultaneously with late potentials. Our findings are compatible with presence of peripheral C-fiber sensitization, mostly at tender points, probably combined with generalized central sensitization of pain pathways in fibromyalgia.     

Projection of thenar muscle afferents to frontal and parietal cortex of human subjects.

There is some controversy about the projection of muscle afferents from the human upper limb to cerebral cortex and about their contribution to somatosensory evoked potentials. In 8 normal volunteers, the somatosensory projections of muscle and cutaneous afferents from the hand were recorded at 21 scalp sites, using a non-cephalic reference. Low-threshold thenar muscle afferents were selectively activated by intramuscular microstimulation. In addition, the averaged data for the projections were mapped for each individual. In each subject a focal parietal negativity was detected over the contralateral parietal cortex at a mean latency of 20.8 msec (S.D. 1.15 msec) following stimulation of thenar muscle afferents. The amplitude of the parietal 'N20-P25' was relatively small (mean 0.49 microV, range 0.18-1.56 microV). A small focal positivity was detected, maximal over contralateral frontal cortex at 22.8 msec (S.D. 2.05 msec) but recorded bilaterally. In all subjects subcortical positive waves (P9 and P14) were defined for the muscle afferent volley. This pattern of cortical activity was similar to that for the projection from the digital nerves of the index finger. For the cutaneous input the latency of the parietal 'N20' was 21.7 msec (S.D. 1.17 msec) and of the frontal 'P22' was 24.2 msec (S.D. 3.09 msec). The amplitude of the parietal 'N20-P25' was larger for the cutaneous projection (mean 1.59 microV; range 0.65-4.28 microV).     

Caudate evoked synaptic activities in nigral neurons

Intracellular recordings from neurons in the substantia nigra have revealed three varieties of monosynaptic PSPs in response to stimulation of the ipsilateral head of the caudate nucleus: short (3–5 msec) latency EPSPs; short (3–5 msec) latency IPSPs; and long (15–20 msec) latency IPSPs. The data indicate that at least three efferent fiber systems link the caudate to the nigra: two fast conducting axonal systems of comparable diameters mediate the short-latency PSPs whereas a slow conducting axonal system mediates the long-latency PSPs. The caudate evoked long-latency IPSPs in nigral neurons were preceded by antidromic and orthodromic potentials in the motor cortex; these cortical potentials are regarded as epiphenomena. The dual, facilitatory-inhibitory control of caudate on nigral neurons is consonant with the proposal that the caudate self-regulates its input from the nigra. The caudate-evoked EPSPs in nigral neurons are sine qua non for the operation of the caudato-nigrothalamic projection system.     

Relationships between physiological and morphological properties of retinocollicular axons in the hamster

Intracellular recording and HRP injection were used to characterize retinocollicular axons in the hamster. Eighteen retinotectal axons were filled with HRP. The type of axon recovered most often (N = 10) had a receptive field with center-surround organization, gave sustained responses to flashed spots, had linear spatial summation, and responded only to more slowly moving stimuli. These fibers had a mean axonal diameter of 0.58 microns (SD = 0.21) and an average conduction latency of 3.4 msec (SD = 1.2) to optic chiasm (OX) stimulation. They gave rise to circular or vertically elongated arbors with an average cross-sectional area of 33,238 microns2 (SD = 12,763) and were almost completely restricted to the stratum griseum superficiale (SGS). We recovered 6 fibers with very different structural and functional properties. The receptive fields of these axons also had center-surround organization, but gave phasic responses to flashed stimuli, had nonlinear spatial summation, and responded to rapidly moving stimuli. These axons had an average diameter of 0.84 micron (SD = 0.09) and an average latency of 2.1 msec (SD = 0.40) to OX stimulation. They had elongated arbors with an average cross-sectional area of 78,045 microns2 (SD = 14,252) and innervated the SGS, the stratum opticum (SO), and upper stratum griseum intermediale (SGI). We also recovered 2 fibers that had thin (0.3 and 0.6 micron) axons and latencies of 4.2 and 3.6 msec to OX stimulation. They both gave rise to horizontally oriented arbors in the stratum zonale (SZ) and upper SGS.     

Intracellular synaptic potentials of primate motor cortex neurons during voluntary movement

An intracellular recording technique was applied to the precentral motor cortex of the unanesthetized, chronically behaving monkey. Postsynaptic potentials, responsible for an initiation of the voluntary movement, were recorded. In total, 22 pyramidal tract neurons (PTNs) and 40 non-pyramidal tract neurons (non-PTNs) were successfully penetrated in 5 monkeys while the monkey was performing a flexion-extension wrist movement after a visual cue (reaction time, 200--350 msec). The neurons showed a negative membrane potential shift of at least 30 mV for more than 30 sec. A slowly rising PSP appeared 80--180 msec after the visual cue, and was 70--180 msec prior to an onset of the movement. Spike activities were superimposed upon this slow PSP with 20--80 msec rise time and 2--6 mV depolarization (8 PTNs and 6 non-PTNs). Since these depolarizations were variable in magnitude and latency, these were considered to be summated potentials of small EPSPs and hidden IPSPs. Membrane resistance was measured from an IR drop by a hyperpolarizing current (1.2 X 10(-9) A) passed through a recording electrode, and was 3.5 +/- 1.7 Momega in 18 PTNs and 4.5 +/- 2.5 Momega in 28 non-PTNs. There was a linear relationship in PTNs between membrane resistance and antidromic latency from the pontine pyramid. Because of the time course of PSPs, their possible dendritic origins were discussed.     

Reticulospinal vasomotor neurons of the rat rostral ventrolateral medulla: relationship to sympathetic nerve activity and the C1 adrenergic cell group

Neurons projecting from the rostral ventrolateral medulla (RVL) to the spinal cord were antidromically identified in rats anesthetized with urethane, paralyzed, and ventilated. The sites of lowest antidromic threshold were concentrated in the intermediolateral nucleus (IML). Their axonal conduction velocities were distributed bimodally, with the mean of the rapidly conducting fibers (greater than 1 m/sec) being 3.1 +/- 0.1 m/sec (n = 105), and of the slower axons being 0.8 +/- 0.03 m/sec (n = 25). Single-shock electrical stimulation of RVL elicited 2 bursts of excitation in splanchnic sympathetic nerve activity (SNA), which resulted from activation of 2 descending pathways with conduction velocities comparable to those of antidromically excited RVL-spinal neurons. The probability of discharge of RVL-spinal cells was synchronized both with the cardiac-related bursts in SNA with functional baroreceptor reflexes and with the free-running 2-6 Hz bursts in SNA following baroreceptor afferent denervation. On the average, their spontaneous discharges occurred 67 +/- 2 msec (n = 31) prior to the peak of the spontaneous bursts in splanchnic SNA. This time corresponded to the latency to the peak of the early excitatory potential in splanchnic SNA following electrical stimulation of RVL. Baroreceptor reflex activation inhibited RVL-spinal neurons. The recording sites of RVL-spinal vasomotor neurons were consistently located within 100 micron of cell bodies (C1 neurons) immunoreactive for the adrenaline-synthesizing enzyme phenylethanolamine N-methyltransferase (PNMT). Ultrastructural analysis of the lateral funiculus of the cervical and thoracic spinal cord demonstrated PNMT immunoreactivity within myelinated (0.6-2.1 micron diameter) and unmyelinated (0.1-0.8 micron diameter) axons. Estimated conduction velocities of these fibers were comparable to the antidromic conduction velocities of the rapidly and slowly conducting populations of RVL-spinal vasomotor neurons. We conclude that in rat, the discharge of RVL-spinal vasomotor neurons strongly influences SNA: the baroreceptor-mediated inhibition of these neurons is reflected in the cardiac locking of SNA, while, in the absence of baroreceptor input, the synchronous discharge of RVL-spinal neurons maintains a free-running 2-6 Hz bursting pattern in SNA. RVL-spinal neurons are located within, and may be elements of, the C1 adrenergic cell group, and they provide a sympathoexcitatory drive to neurons in the IML over rapidly and slowly conducting pathways that correspond to myelinated and unmyelinated spinal axons containing PNMT.     

Randomized double pulse stimulation for assessing stimulus frequency-dependent conduction in injured spinal and peripheral axons.

Injury compromises the ability of axons to conduct action potentials at high frequencies. To study stimulus frequency-dependent conduction in injured spinal and peripheral axons, we developed a new stimulation paradigm which applies trains of double pulses at 5 Hz and randomly varied interpulse intervals of 3, 4, 5, 8, 10, 30, 50, and 80 msec. In each double pulse, the first pulse was used to condition the response activated by the second test pulse. Responses elicited by double pulses with 80 msec intervals served as controls. The L5 dorsal root was stimulated to activate dorsal column and dorsal root compound action potentials in pentobarbital anesthetized rats. To injure the spinal cord, we compressed the cord stepwise (0.25 mm every 5 min) until action potential conduction across the compression site was abolished and then decompressed the spinal cord 10 min later. Before injury, conditioning pulses applied 3-80 msec before the test pulses did not alter dorsal column responses except for a slight amplitude augmentation at 20 msec interpulse intervals (mean +/- S. E., + 4.2 +/- 0.8%, P less than 0.02) compared to controls. Injury had 3 effects on the responses. First, it significantly reduced response amplitudes and increased response latencies at 3-5 msec interpulse intervals, i.e., responses activated with 3 msec intervals were 26.0 +/- 7.4% (P less than 0.002, paired t test, n = 6) smaller and had 108 +/- 45 microseconds (P less than 0.04) longer latency than control responses. Second, response amplitude increases at 20 msec interpulse intervals (9.0 +/- 0.7%, P less than 0.0001) significantly exceeded those observed before injury (P less than 0.02, paired t test). Third, injury accentuated response amplitude declines during the stimulus train, most prominently at 80 msec intervals. Spinal cord injury did not affect the dorsal root responses. L5 root compression injury depressed dorsal root action potentials at 3-5 msec interpulse intervals (36.9 +/- 8.4%, n = 4, P less than 0.0001) but had no other effect on the responses. Our data indicate that randomized double pulse evoked potentials are sensitive detectors of acute axonal dysfunction and can be used to quantify stimulus frequency-dependent conduction deficits in injured central and peripheral axons.     

Seizure frequency affects event-related potentials (P300) in epilepsy.

To analyse the effect of epilepsy an P300 event-related potentials we studied 27 patients with idiopathic generalized epilepsy (IGE), 13 patients with temporal lobe epilepsy (TLE) and 60 normal controls. The prolongation of P300 latencies was highly cor related with increasing age in controls but not epileptic patients. The age-corrected P300 latency used in this study was actual P300 latency-predicted P300 latency (predicted P300 (msec)=306.20+0.79 age, P=0.001, R2=0.32). By using ANOVA analysis, the age-corrected latencies of P300 were significantly longer in TLE patients (19.72+/-47.82 msec, mean+/-SD) than in IGE patients (10.97+/-36.97 msec) and controls (0.23+/-20.28 msec). Likewise, significantly prolonged P300 latencies were seen in the epileptic patients with a seizure frequency more than 400 times (37.21+/-47.50 msec). The multivariate-adjusted odds ratio for those who had TLE was 10.97 (95% CI=3.99 - 30.14 ) in the prolonged latencies of P300 compared with that of IGE patients. The odds ratio of longer latencies of P300 was 7.43 (95% CI=2.75 - 20.08) among those who had a high seizure frequency (> or =400 times) compared with those who had a low seizure frequency. No interaction between TLE and high frequency of attacks was found. The age at onset of seizure and duration of illness was not associated with P300 latency prolongation. From the above results, we might infer that the seizure type of TLE and a high frequency of seizure are two major independent precipitate factors for abnormal latencies of P300 in the epileptic patients.