Journal of Neurophysiology

Gurtu, S.; Smith, P. A.

doi: N/Apmid: 3351568

Abstract 1. The active and passive membrane properties of neurons in the lower lumbar (L6, L7) or sacral (S1) dorsal root ganglia from golden hamsters were examined in vitro by means of conventional intracellular recording techniques. Data were collected from neurons exhibiting action potentials (AP) of 70 mV or more in amplitude. 2. Cells with axonal conduction velocities (CV) greater than 20 m/s were termed fast-A-cells, those with CVs between 2.5 and 20 m/s were termed A-delta-cells, and those with CVs less than 1 m/s were termed C-cells. 3. Fast-A-cells usually exhibited short-duration APs (2.51 +/- 0.41 ms, n = 19) followed by short (less than 50 ms) afterhyperpolarizations (AHPs). C-cells usually exhibited long-duration APs (10.5 +/- 0.69 ms, n = 18) followed by long-duration AHPs (much greater than 50 ms). The characteristics of APs in A-delta-cells (AP mean duration 3.34 +/- 0.42 ms, n = 32) were intermediate between those of fast-A- and C-cells. Long AHPs (duration much greater than 50 ms) were manifest in 43.8% of A-delta-cells. 4. A time-dependent sag in hyperpolarizing electrotonic potentials (rectification) was found in 68.8% of fast-A-cells, 45.5% of A-delta-cells, and 62.5% of C-cells. 5. To examine neuronal properties 1-6 wk after transection of the sciatic nerve (axotomy), cells were reclassified as SAP (short action potential) cells and LAP (long action potential) cells. Cells in the SAP category had AP durations less than 5 ms and included all fast-A-cells and the majority of A-delta-cells. The LAP category included cells with AP durations greater than 8 ms contained only C-cells. 6. Axotomy failed to decrease the CV of LAP cells or A-delta-cells in the SAP group. The CV of LAP cells may have increased (P less than 0.05), whereas that of SAP cells was unchanged. 7. The duration of the AP and AHP of SAP cells were slightly increased (0.1 greater than P greater than 0.05), whereas AP and AHP duration of LAP cells were unchanged after axotomy. AHP amplitudes of all cell types tended to be smaller (0.1 greater than P greater than 0.05). Axotomy did not alter the resting membrane potential or reduce the incidence of rectification in any cell type. 8. Invasion of the soma by axonally evoked APs was impeded in all cell types after axotomy even though a decrease (P less than 0.05) in rheobase of SAP cells occurred.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1988 the American Physiological Society

Weiss, D. S.; Barnes, E. M.; Hablitz, J. J.

doi: N/Apmid: 2450972

Abstract 1. gamma-Aminobutyric acid (GABA) (10-500 microM) was applied to cultured chick cerebral neurons by pressure ejection, and the resulting currents (IGABA) were recorded using standard whole-cell voltage-clamp techniques. Plots of the peak IGABA as a function of membrane potential were nonlinear with an outwardly rectifying appearance. 2. IGABA decayed during a prolonged application of GABA. This decay was associated with a decline in the conductance of the cell, suggesting that the decline in IGABA was principally due to receptor desensitization. 3. After 5-7 days in culture, whole-cell recordings revealed the presence of spontaneous synaptic currents. These currents were presumed to be GABA-gated inhibitory postsynaptic currents (IPSCs) because they reversed at the Cl- equilibrium potential (ECl-), were blocked by picrotoxin (25 microM), and were prolonged by pentobarbital (50 microM). 4. Synaptic currents were analyzed by fitting exponential functions to their decay. In normal recording saline, 68% of the decays analyzed could be adequately described by a single exponential function. Two exponentials were necessary to describe the decay of the other 32%. The time constant of the decay (for those adequately fitted by a single exponential) increased with depolarization, from an average value of 15 ms at -80 mV to 60 ms at +40 mV. 5. A relationship was noted between IPSC amplitude and decay time constant; IPSCs with larger peak amplitudes had a slower decay. One possible explanation considered for this finding was that transmitter persists in the synaptic cleft and rebinds to the receptors, thus prolonging the decay of the IPSC. 6. Consistent with the above hypothesis was the observation that the decays of miniature IPCSs (examined under conditions of reduced transmitter release) were faster, showed less variability, and were all adequately described by a single exponential function. Furthermore, the decay times were independent of the membrane potential, suggesting that the kinetic parameters of the GABA channel which shape the decay of these miniature IPSCs are independent of voltage. 7. Single-channel activity underlying whole-cell GABA responses could be recorded in isolated outside-out and inside-out patches of membrane. In isotonic choline chloride, single-channel amplitudes were linearly related to voltage and reversed at -1.8 +/- 11.0 mV (n = 12). Under these conditions, the channel had a main conductance state of 20.8 +/- 3.4 pS (n = 12). Transitions were observed from this main conductance state to other conductance states, e.g., two subconductance states of 6 and 12 pS and one supraconductance state of 30 pS.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1988 the American Physiological Society

Heinzel, H. G.

doi: N/Apmid: 3351573

Abstract 1. The gastric central pattern generator (CPG) driving the three teeth of the gastric mill inside the lobster stomach has often been used as a model for the study of central nervous systems, but the actual functioning of the mill has never been observed directly. By using a small endoscope inserted through the esophagus a video analysis of the tooth movements was performed with restrained, but otherwise intact lobsters. 2. The teeth show spontaneous periodic chewing (cycle duration from 4 to 70 s) in two different basic modes. In the squeeze mode only the cusps of the three teeth move together simultaneously. In the cut-and-grind mode the lateral teeth close first with not only their cusps, but also their serrated edges. After this cut phase the lateral teeth grind backward along the file of the medial tooth, which simultaneously moves forward. 3. Simultaneous endoscope recordings of the teeth, filming of stomach muscles and ossicles combined with electrical stimulation of selected muscles reveal that muscle gm3c is responsible for this hitherto unknown backward grinding of the lateral teeth. 4. The complete behavioral repertoire includes the following modifications of the two basic modes. 1) The lateral teeth can perform chewing movements while the medial tooth stays still and vice versa, forms of chewing regarded even weaker than the squeeze. 2) There do not appear to be intermediates between the squeeze and cut-and-grind movements, with the latter as the strongest form of chewing. Transitions only occur as switching on a cycle-by-cycle basis. 3) A gradual change of the cut-and-grind chewing was observed as the gradual development of an additional opening over the time course of several periods. 4) After their grind phase, the lateral teeth can even move further back beyond the medial tooth. This can serve to push food into the pyloric filter apparatus. 5. Inflation of the cardiac sac can elicit single bites in a resting gastric mill. 6. The behavioral repertoire is compared with the in vivo activity of the gastric oscillator represented by simultaneous intracellular recording from 7 representative cells of the 11 CPG neurons. Copyright © 1988 the American Physiological Society

Fetter, M.; Zee, D. S.; Proctor, L. R.

doi: N/Apmid: 3258363

Abstract 1. We investigated the influence of visual experience upon vestibular compensation in monkeys. Two paradigms were used to elicit vestibular adaptation: artificially imposed motion of images upon the retina during head rotation and unilateral labyrinthectomy. Two groups of animals were investigated: monkeys that underwent a bilateral occipital lobectomy and intact monkeys without a cortical lesion. Occipital lobectomy alone caused only a minor change in the vestibuloocular reflex (VOR); the gain (eye vel/head vel) decreased slightly (10-15%) for high speeds of rotation (180-300 degrees/s). 2. In response to a 4-h period of continuous oscillation of the head (0.25 Hz, 30 degrees/s) with the visual scene made to move in phase with the head (X0 viewing) or out of phase with the head (X2 viewing), intact monkeys showed an average 40% decrease or increase, respectively, of the VOR gain measured in darkness. After occipital lobectomy this adaptive capability was diminished, primarily for increasing the VOR gain after X2 viewing (42% preop to 13% postop). 3. Unilateral labyrinthectomy in either occipital-lobectomized or in otherwise intact monkeys led to a static imbalance with initial (18- to 20-h postlesion) values of spontaneous nystagmus of 22-62 degrees/s measured in darkness and to a dynamic disturbance with an approximately 50% decrease of VOR gain. Compensation for both abnormalities was studied in three groups of animals: previously occipital-lobectomized monkeys kept in the light after labyrinthectomy, intact monkeys kept in the light after labyrinthectomy, and intact monkeys kept in the dark for 4 days after labyrinthectomy and then exposed to light. Spontaneous nystagmus disappeared at the same rate in each group of animals. VOR gain increased in the intact monkeys kept in the light after labyrinthectomy but not in the intact monkeys kept in the dark after labyrinthectomy until they were exposed to light. The occipital-lobectomized monkeys showed some recovery of VOR gain (approximately 25-40%), but only at low speeds of rotation (30-60 degrees/s). Occipital lobectomy performed in monkeys after they had already compensated for a labyrinthectomy caused the VOR gain to drop to values approximately 0.5 but without any recurrence of spontaneous nystagmus. 4. Our results indicate that visual experience after labyrinthectomy is essential for recovery of VOR gain but not for resolution of spontaneous nystagmus. Furthermore, geniculostriate pathways play a major role in providing information about high velocities of retinal image motion that is necessary for the acquisition of VOR gain adaptation.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1988 the American Physiological Society

Kang, Y.; Endo, K.; Araki, T.

doi: N/Apmid: 3351578

Abstract 1. By spike-triggered averaging, we documented recurrent individual excitatory postsynaptic potentials (EPSPs) produced in 33 pyramidal tract (PT) cells (target) by the activity of axon collaterals of neighboring single PT cells (reference) in the motor cortex of the cat. 2. The computer was triggered by the spontaneous activity of reference PT cells or by current pulses applied to reference PT cells through the extracellular recording electrode. 3. The threshold for direct activation of PT cells was less than 0.1 microA with an anodal current pulse and 0.2-0.3 microA with a cathodal current pulse. 4. Application of an anodal current pulse directly activated only a single reference PT cell, the surface membrane of which was presumably touched by and sucked with the extracellular recording electrode. 5. When a cathodal current pulse was used, simultaneous activation of neurons or axons other than the reference PT cell was checked by changing the stimulus parameters along the characteristic strength-duration curve for the reference PT cell and/or by comparing averaged EPSPs obtained by cathodal stimulation with those obtained from spontaneous spikes of the reference PT cell. 6. Recurrent individual EPSPs were produced in fast PT cells by activation of neighboring slow PT cells and also of neighboring fast PT cells. Some recurrent individual EPSPs were also observed in slow PT cells. 7. The mean latencies of recurrent individual EPSPs produced by the spontaneous activity of reference slow and fast PT cells were 1.61 (n = 12) and 1.12 ms (n = 8), respectively. Their amplitudes ranged between 30 and 390 microV (n = 33). The rise time observed in fast PT cells with activation of slow and fast PT cells ranged from 1.6 to 3.6 ms (n = 20) and from 0.8 to 1.9 ms (n = 10), respectively. 8. The average conduction velocity of axon collaterals of slow and fast PT cells was estimated to be as slow as that of unmyelinated fibers in the cat. 9. It is suggested that axon collaterals of slow PT cells synapse onto more distal dendrites of fast PT cells than axon collaterals of fast PT cells. Copyright © 1988 the American Physiological Society

Snyder, L. H.; King, W. M.

doi: N/Apmid: 3351563

Abstract 1. We studied eye velocity during the first 2 s of the vertical vestibuloocular reflex (VOR) elicited from cats placed on their sides (90 degrees roll position) and rotated about an earth vertical axis. Vestibular stimuli were presented in the dark and consisted of brief trapezoidal velocity profiles. Eye movements were recorded with a magnetic search coil, and eye velocity was analyzed with high temporal resolution. 2. The first 2 s of upward or downward eye velocity after the onset of head rotation was characterized and compared. Adaptive changes in VOR gain (eye/head velocity) were then induced, and upward and downward eye velocity responses were again compared. 3. The early time course of the vertical VOR was complex. After a latency of approximately 15 ms, eye velocity increased rapidly until it was equal in magnitude and opposite in direction to head velocity. The peak eye velocity decayed within less than 1 s to a plateau of slow-phase eye velocity (SPEV) equal to approximately -0.6 times the head velocity. Peak upward and downward eye velocity was symmetric. The transition from peak to plateau was more rapid for the downward VOR (slow phases downward) than for the upward VOR (slow phases upward). The plateau attained by upward SPEV was approximately 15% higher than the plateau attained by downward SPEV. 4. VOR gain adaptation was symmetric. The percentage change in adapted upward eye velocity equalled the percentage change in adapted downward eye velocity. Both peak and plateau SPEV adapted, but peak eye velocity adapted less than plateau eye velocity. VOR latency was unchanged by adaptation. 5. The trajectory of the VOR response to steps of head velocity could be divided into an invariant and a variant interval. The invariant interval consisted of the initial approximately 15 ms of the eye movement. Neither direction of head movement (upward vs. downward) nor adaptation of the VOR gain effected the eye movement trajectory during the invariant interval. The variant interval began approximately 30 ms after the onset of head movement and approximately 15 ms after the onset of eye movement. In unadapted animals, downward eye speed exceeded upward eye speed during the variant interval. In adapted animals, eye speed during the variant interval, but not during the invariant interval, diverged from eye speed in the unadapted state. We suggest that the initial invariant interval (approximately 15 ms) of the eye movement response trajectory may represent the direct response of the classically described three-neuron arc.(ABSTRACT TRUNCATED AT 400 WORDS) Copyright © 1988 the American Physiological Society

Carpenter, D. O.; Briggs, D. B.; Knox, A. P.; Strominger, N.

doi: N/Apmid: 2895167

Abstract 1. Multiple-barreled microelectrodes were used to record from neurons in the area postrema of anesthetized dogs and to test the responses of the neurons to a variety of substances in this structure, which is known to function as the chemoceptive trigger zone for emesis. 2. The neurons in area postrema were silent at rest but could be "found" by virtue of their response to ionophoretic glutamate. The glutamic response was brief and of short latency with high frequency of discharge. 3. Dog area postrema neurons were also excited by over 20 other substances, including acetylcholine, the biogenic amines, several peptides, and at least two hormones. Not all agents were excitatory, however. 4. The responses to all excitatory agents except glutamate were similar and unusual. All responses showed a relatively long latency (3-20 s), a long duration of excitation (30 s to many minutes), and a low discharge frequency (1-3 Hz). 5. There was a good correlation between substances that were excitatory on area postrema neurons and substances known to cause emesis. Because emesis due to intravenous application of these substances is known to be abolished in animals with ablation of the area postrema, it is very likely that recordings were from the neurons which trigger the response. 6. Because so many substances elicit the same type of response there is a possibility that all utilize a common second messenger. Neurons were not excited by ionophoresis of guanosine 3',5'-cyclic monophosphate (cGMP) but were excited by 8-bromo-adenosine 3',5'-cyclic monophosphate (cAMP) and by forskolin, an activator of adenylate cyclase. 7. Behavioral studies were performed looking for emetic responses in awake dogs following intravenous injection of apomorphine, insulin, angiotensin II, and leucine enkephalin. For each a threshold concentration could be determined, which would consistently evoke emesis. 8. Dogs pretreated with phosphodiesterase inhibitors (theophylline, 3-isobutyl-1-methylxanthine, or RO 1724) showed a shift in the threshold concentration of the above substances that triggered emesis, such that emesis was evoked by lower concentrations than in the control. 9. These results suggest that neurons of the dog area postrema trigger the emetic reflex in response to specific receptors for a great variety of transmitters, peptides, and hormones, and that these receptors act through a common second messenger, cAMP. Copyright © 1988 the American Physiological Society

Weiss, D. S.

doi: N/Apmid: 2450973

Abstract 1. The activity of single gamma-aminobutyric acid (GABA)-gated Cl- channels (GABA = 0.5-2.0 microM) was recorded in inside-out patches of membrane from cultured chick cerebral neurons. 2. The distribution of open intervals of the GABA channel was described by the sum of two exponentials, which suggests the presence of at least two open states of the channel. The time constants of these two components were 0.39 +/- 0.1 and 2.1 +/- 0.9 ms (+/- SD, n = 9). 3. The distribution of shut intervals was described by the sum of either three (n = 5) or four (n = 3) exponentials. This suggests the presence of at least three or four shut states. 4. At all GABA concentrations examined, the activity of the GABA channel decreased over time. This decline in activity was most likely the result of desensitization of the GABA channels. 5. The distribution of open intervals was unchanged during desensitization of the GABA channel. Thus desensitization is not associated with an alteration in either the mean lifetime of the two open states or the relative number of transitions to these two states. Rather, desensitization results from a decrease in the probability of channel opening. 6. There was an e-fold increase in the probability of finding a GABA channel open for every 80 +/- 43 mV (n = 4) of depolarization. The degree of voltage dependence decreased as the GABA channels desensitized. 7. The depolarization-induced increase in open channel probability was not associated with any change in the distribution of open intervals. Thus depolarization does not affect the mean open time of the channel but rather increases the likelihood that it will open. 8. A simple model with three or four shut and two open states is considered for the gating of the GABA channel by the agonist. Possible sites for the voltage dependence within this proposed model are discussed. Copyright © 1988 the American Physiological Society

O'Mara, S.; Rowe, M. J.; Tarvin, R. P.

doi: N/Apmid: 3351576

Abstract 1. Peripheral and central neural contributions to vibrotactile adaptation were investigated in decerebrate or anesthetized cats by recording from sensory nerve fibers associated with Pacinian corpuscle (PC) receptors and from central neurons of the dorsal column nuclei that receive their input from vibration-sensitive receptors of the forelimb footpads. Responsiveness of units was assessed using 1-s duration, test vibration stimuli delivered with 1- to 2-mm-diam probes at different times following adapting trains of vibration (usually 300 Hz) that lasted from less than 1 min up to 50 min. 2. Cuneate neuron responsiveness underwent marked depression following prior vibration. The extent of the depression and the time course of recovery in responsiveness were dependent on the intensity and duration of the adapting vibratory stimulus. The recovery time course (often several minutes) was approximately exponential and resembled the reported time course of subjective vibrotactile adaptation obtained in psychophysical experiments. 3. Response depression in PC fibers was only seen at low amplitudes of the test vibration and displayed a brief time course of recovery in comparison with that seen in cuneate neurons. It is therefore unlikely to account for the adaptation time course either in cuneate neurons or at a subjective level. Furthermore, as the adaptation seen in PC fiber responses had a similar time course in both cutaneous and mesenteric PC fibers it is unlikely that mechanical changes in the skin contribute significantly to the adaptation in PC fiber responses to vibration. 4. The time course of afferent-induced inhibition following long periods of prior vibration was too brief to account for the response adaptation in cuneate neurons. 5. As the long-term response depression in cuneate neurons following their prior activation was seen for inputs from unconditioned sites within the neuron's excitatory receptive field, as well as from the conditioned site, it appears that the response adaptation is attributable to changes in the central neuron or in synaptic processes associated with the central neuron. It is proposed that this adaptation may be due to an increase in extracellular potassium ion concentration that alters the responsiveness of the central neurons. Copyright © 1988 the American Physiological Society

Heinzel, H. G.; Selverston, A. I.

doi: N/Apmid: 3351574

Abstract 1. The response of the isolated gastric central pattern generator (CPG) to bath application of proctolin is characterized and compared with the previously analyzed behavioral response. 2. Proctolin had an excitatory effect on the ongoing spontaneous rhythm of "combined" preparations, in which the stomatogastric ganglion (STG) is connected to the esophageal and commissural ganglia by the stomatogastric nerve (STN). The effect started between 20 s and 5 min and was characterized by strongly increased burst durations as well as increased spike rates in all units except the two lateral posterior gastric (LPG) motoneurons. The effect was strongest in the dorsal gastric (DG) and lateral gastric (LG) motoneurons and was accompanied by a phase change of the DG burst. DG continued spiking throughout large parts of the burst of LG and of the gastric mill (GM) motoneurons, which are antagonists of DG. 3. The threshold concentration was approximately 10(-10) M, and the effects were dose dependent and reversible. 4. LG and DG were identified as target cells for the action of proctolin. In LG regenerative plateau properties were induced, as revealed by its long-lasting plateau potentials, sensitivity for triggering inputs, and the occurrence of oscillatory prepotentials. An induction of endogenous bursting in DG was concluded from preparations, in which DG was cycling alone or bursting with a much shorter period duration than other gastric neurons. Hyperpolarization of DG, which normally has no or weak driving power within the gastric network, demonstrated that under the influence of proctolin, firing of DG can accelerate the gastric rhythm from a 27- to a 9-s period duration. 5. Proctolin does not only have a modulatory influence on an ongoing rhythm, but it also can trigger gastric activity. This function was first concluded from proctolin-treated STGs, which, unlike normal preparations, continue bursting if inputs via the STN are blocked. Finally, triggering was demonstrated directly, since isolated STGs that were not oscillating started a gastric rhythm after 20-30 min of perfusion with proctolin. 6. The proctolin-induced changes of the CPG activity in isolated preparations are in agreement with the effect on gastric mill chewing in the intact animal, in which, depending on the dose, different modes of chewing could be elicited. Copyright © 1988 the American Physiological Society