bluuebunny/crossref_metadata_2025 huggingface dataset:
Ontogenesis of Presynaptic GABAB Receptor-Mediated Inhibition in the CA3 Region of the Rat Hippocampus
Authors: Caillard Olivier , McLean Heather A. , Ben-Ari Yehezkel , Gaïarsa Jean-Luc
Published: December 2017

Caillard, Olivier, Heather A. McLean, Yehezkel Ben-Ari, and Jean-Luc Gaı̈arsa. Ontogenesis of presynaptic GABAB receptor-mediated inhibition in the CA3 region of the rat hippocampus. J. Neurophysiol. 79: 1341–1348, 1998. γ-Aminobutyric acid-B(GABAB) receptor-dependent and -independent components of paired-pulse depression (PPD) were investigated in the rat CA3 hippocampal region. Intracellular and whole cell recordings of CA3 pyramidal neurons were performed on hippocampal slices obtained from neonatal (5–7 day old) and adult (27–34 day old) rats. Electrical stimulation in the hilus evoked monosynaptic GABAA postsynaptic currents (eIPSCs) isolated in the presence of the ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 μM) and d(−)2-amino-5-phosphovaleric acid (d-AP5, 50 μM) with 2(triethylamino)- N-(2,6-dimethylphenyl) acetamine (QX314) filled electrodes. In adult CA3 pyramidal neurons, when a pair of identical stimuli was applied at interstimulus intervals (ISIs) ranging from 50 to 1,500 ms the amplitude of the second eIPSC was depressed when compared with the first eIPSC. This paired-pulse depression (PPD) was partially blockedb y  P - 3 - a m i n o p r o p y l - P - d i e t h o x y m e t h y l  p h o s p h o r i c  a c i d(CGP35348, 0.5 mM), a selective GABAB receptor antagonist. In neonates, PPD was restricted to ISIs shorter than 200 ms and was not affected by CGP35348. The GABAB receptor agonist baclofen reduced the amplitude of eIPSCs in a dose-dependent manner with the same efficiency in both adults and neonates. Increasing the probability of transmitter release with high Ca2+ (4 mM)/low Mg2+ (0.3 mM) external solution revealed PPD in neonatal CA3 pyramidal neurons that was 1) partially prevented by CGP35348, 2) independent of the membrane holding potential of the recorded cell, and 3) not resulting from a change in the reversal potential of GABAA eIPSCs. In adults the GABA uptake blocker tiagabine (20 μM) increased the duration of eIPSCs and the magnitude of GABAB receptor-dependent PPD. In neonates, tiagabine also increased duration of eIPSCs but to a lesser extent than in adult and did not reveal a GABAB receptor-dependent PPD. These results demonstrate that although GABAB receptor-dependent and -independent mechanisms of presynaptic inhibition are present onGABAergic terminals and functional, they do not operate at the level of monosynaptic GABAergic synaptic transmission at early stages of development. Absence of presynaptic autoinhibition of GABA release seems to be due to the small amount of transmitter that can access presynaptic regulatory sites.
Long-Term Effects of Axotomy on Excitability and Growth of IsolatedAplysiaSensory Neurons in Cell Culture: Potential Role of cAMP
Authors: Bedi Supinder S. , Salim Ali , Chen Shanping , Glanzman David L.
Published: December 2017

Bedi, Supinder S., Ali Salim, Shanping Chen, and David L. Glanzman. Long-term effects of axotomy on excitability and growth of isolated Aplysia sensory neurons in cell culture: potential role of cAMP. J. Neurophysiol. 79: 1371–1383, 1998. Crushing nerves, which contain the axons of central sensory neurons, in Aplysia causes the neurons to become hyperexcitable and to sprout new processes. Previous experiments that examined the effects of axonal injury on Aplysia sensory neurons have been performed in the intact animal or in the semi-intact CNS of Aplysia. It therefore has been unclear to what extent the long-term neuronal consequences of injury are due to intrinsic or extrinsic cellular signals. To determine whether injury-induced changes in Aplysia sensory neurons are due to intrinsic or extrinsic signals, we have developed an in vitro model of axonal injury. Isolated central sensory neurons grown for 2 days in cell culture were axotomized. Approximately 24 h after axotomy, sensory neurons exhibited a greater excitability—reflected, in part, as a significant reduction in spike accommodation—and greater neuritic outgrowth than did control (unaxotomized) neurons. Rp diastereoisomer of the cyclic adenosine 3′,5′-monophosphorothiate (Rp-cAMPS), an inhibitor of protein kinase A, blocked both the reduction in accommodation and increased neuritic outgrowth induced by axotomy. Rp-cAMPS also blocked similar, albeit smaller, alterations observed in control sensory neurons during the 24-h period of our experiments. These results indicate that axonal injury elevates cAMP levels within Aplysia sensory neurons, and that this elevation is directly responsible, in part, for the previously described long-term electrophysiological and morphological changes induced in Aplysia sensory neurons by nerve crush. In addition, the results indicate that control sensory neurons in culture are also undergoing injury-related electrophysiological and structural changes, probably due to cellular processes triggered when the neurons are axotomized during cell culturing. Finally, the results provide support for the idea that the cellular processes activated within Aplysia sensory neurons by injury, and those activated during long-term behavioral sensitization, overlap significantly.
Habituation of Odor Responses in the Rat Anterior Piriform Cortex
Authors: Wilson Donald A.
Published: December 2017

Wilson, Donald A. Habituation of odor responses in the rat anterior piriform cortex. J. Neurophysiol. 79: 1425–1440, 1998. Simultaneous recordings of main olfactory bulb (MOB) and anterior piriform cortex (aPCX) neuron responses to repeated and prolonged odor pulses were examined in freely breathing, urethan-anesthetized rats. Comparisons of odor responses were made between multi-unit recordings of MOB activity and single-unit extracellular and intracellular recordings of Layer II/III aPCX neurons. Odor stimuli consisted of either 2-s pulses repeated at 30-s intervals or a single, prolonged 50-s stimulus. Respiration rate was monitored throughout. MOB and aPCX neuron responses to odor were quantified both through firing frequency and through the temporal patterning of firing over the respiratory cycle. The results demonstrate that aPCX neurons habituate significantly more (faster) than MOB neurons with both repeated and prolonged stimulation paradigms. This enhanced habituation is expressed as both a decrease in aPCX firing despite maintained odor-evoked MOB input and as a decrease in aPCX respiratory cycle entrainment despite maintained MOB cyclic input. Intracellular aPCX recordings suggest that several mechanisms may be involved in this experience-induced change in aPCX function, including 1) decreased excitatory driveof aPCX neurons, 2) decreased excitability of aPCX neurons,and/or 3) enhancement in odor-evoked inhibition of aPCX neurons. These studies provide the initial basis for understanding the mechanisms of nonassociative plasticity in olfactory cortex.
Optokinetic Eye Movements Elicited by Radial Optic Flow in the Macaque Monkey
Authors: Lappe Markus , Pekel Martin , Hoffmann Klaus-Peter
Published: December 2017

Lappe, Markus, Martin Pekel, and Klaus-Peter Hoffmann. Optokinetic eye movements elicited by radial optic flow in the macaque monkey. J. Neurophysiol. 79: 1461–1480, 1998. We recorded spontaneous eye movements elicited by radial optic flow in three macaque monkeys using the scleral search coil technique. Computer-generated stimuli simulated forward or backward motion of the monkey with respect to a number of small illuminated dots arranged on a virtual ground plane. We wanted to see whether optokinetic eye movements are induced by radial optic flow stimuli that simulate self-movement, quantify their parameters, and consider their effects on the processing of optic flow. A regular pattern of interchanging fast and slow eye movements with a frequency of 2 Hz was observed. When we shifted the horizontal position of the focus of expansion (FOE) during simulated forward motion (expansional optic flow), median horizontal eye position also shifted in the same direction but only by a smaller amount; for simulated backward motion (contractional optic flow), median eye position shifted in the opposite direction. We relate this to a change in Schlagfeld typically observed in optokinetic nystagmus. Direction and speed of slow phase eye movements were compared with the local flow field motion in gaze direction (the foveal flow). Eye movement direction matched well the foveal motion. Small systematic deviations could be attributed to an integration of the global motion pattern. Eye speed on average did not match foveal stimulus speed, as the median gain was only ∼0.5–0.6. The gain was always lower for expanding than for contracting stimuli. We analyzed the time course of the eye movement immediately after each saccade. We found remarkable differences in the initial development of gain and directional following for expansion and contraction. For expansion, directional following and gain were initially poor and strongly influenced by the ongoing eye movement before the saccade. This was not the case for contraction. These differences also can be linked to properties of the optokinetic system. We conclude that optokinetic eye movements can be elicited by radial optic flow fields simulating self-motion. These eye movements are linked to the parafoveal flow field, i.e., the motion in the direction of gaze. In the retinal projection of the optic flow, such eye movements superimpose retinal slip. This results in complex retinal motion patterns, especially because the gain of the eye movement is small and variable. This observation has special relevance for mechanisms that determine self-motion from retinal flow fields. It is necessary to consider the influence of eye movements in optic flow analysis, but our results suggest that direction and speed of an eye movement should be treated differently.
Adaptation to Visual Motion in Directional Neurons of the Nucleus of the Optic Tract
Authors: Ibbotson Michael R. , Clifford Colin W. G. , Mark Richard F.
Published: December 2017

Ibbotson, Michael R., Colin W. G. Clifford, and Richard F. Mark. Adaptation to visual motion in directional neurons of the nucleus of the optic tract. J. Neurophysiol. 79: 1481–1493, 1998. Extracellular recordings of action potentials were made from directional neurons in the nucleus of the optic tract (NOT) of the wallaby, Macropus eugenii, while stimulating with moving sine-wave gratings. When a grating was moved at a constant velocity in the preferred direction through a neuron's receptive field, the firing rate increased rapidly and then declined exponentially until reaching a steady-state level. The decline in response is called motion adaptation. The rate of adaptation increased as the temporal frequency of the drifting grating increased, up to the frequency that elicited the maximum firing rate. Beyond this frequency, the adaptation rate decreased. When the adapting grating's spatial frequency was varied, such that response magnitudes were significantly different, the maximum adaptation rate occurred at similar temporal frequencies. Hence the temporal frequency of the stimulus is a major parameter controlling the rate of adaptation. In most neurons, the temporal frequency response functions measured after adaptation were shifted to the right when compared with those obtained in the unadapted state. Further insight into the adaptation process was obtained by measuring the responses of the cells to grating displacements within one frame (10.23 ms). Such impulsive stimulus movements of less than a one-quarter cycle elicited a response that rose rapidly to a maximum and then declined exponentially to the spontaneous firing rate in several seconds. The level of adaptation was demonstrated by observing how the time constants of the exponentials varied as a function of the temporal frequency of a previously presented moving grating. When plotted as functions of adapting frequency, time constants formed a U-shaped curve. The shortest time constants occurred at similar temporal frequencies, regardless of changes in spatial frequency, even when the change in spatial frequency resulted in large differences in response magnitude during the adaptation period. The strongest adaptation occurred when the adapting stimulus moved in the neuron's preferred direction. Stimuli that moved in the antipreferred direction or flickered had an adapting influence on the responses to subsequent impulsive movements, but the effect was far smaller than that elicited by preferred direction adaptation. Adaptation in one region of the receptive field did not affect the responses elicited by subsequent stimulation in nonoverlapping regions of the field. Adaptation is a significant property of NOT neurons and probably acts to expand their temporal resolving power.
Muscarinic Inhibition of Persistent Na+ Current in Rat Neocortical Pyramidal Neurons
Authors: Mittmann Thomas , Alzheimer Christian
Published: December 2017

Mittmann, Thomas and Christian Alzheimer. Muscarinic inhibition of persistent Na+ current in rat neocortical pyramidal neurons. J. Neurophysiol. 79: 1579–1582, 1998. Muscarinic modulation of persistent Na+ current ( I NaP) was studied using whole cell recordings from acutely isolated pyramidal cells of rat neocortex. After suppression of Ca2+ and K+ currents, I NaP was evoked by slow depolarizing voltage ramps or by long depolarizing voltage steps. The cholinergic agonist, carbachol, produced an atropine-sensitive decrease of I NaP at all potentials. When applied at a saturating concentration (20 μM), carbachol reduced peak I NaP by 38% on average. Carbachol did not alter the voltage dependence of I NaP activation nor did it interfere with the slow inactivation of I NaP. Our data indicate that I NaP can be targeted by the rich cholinergic innervation of the neocortex. Because I NaP is activated in the subthreshold voltage range, cholinergic inhibition of this current would be particularly suited to modulate the electrical behavior of neocortical pyramidal cells below and near firing threshold.
Intrinsic Circuitry of the Superior Colliculus: Pharmacophysiological Identification of Horizontally Oriented Inhibitory Interneurons
Authors: Meredith M. Alex , Ramoa Ary S.
Published: December 2017

Meredith, M. Alex and Ary S. Ramoa. Intrinsic circuitry of the superior colliculus: pharmacophysiological identification of horizontally oriented inhibitory interneurons. J. Neurophysiol. 79: 1597–1602, 1998. Much of what is known about the organization of the superior colliculus is based on the arrangement of its external connections. Consequently, there is little information regarding pathways that remain intrinsic to it, even though recent data suggest that a horizontally oriented local circuit may mediate the functional reciprocity among fixation and saccade-related neurons. Therefore, the present experiments sought physiological evidence for neurons intrinsic to the superior colliculus that might participate in a horizontally oriented local circuit. Parasagittal slices of the ferret superior colliculus were prepared for in vitro recording, and 125 intermediate/deep layer neurons were examined in response to electrical stimulation rostral or caudal to the recording site. A substantial proportion (37%) of neurons responded with a prolonged period (means = 59.3 ± 30 ms) of poststimulus suppression of spontaneous action potential activity. Of the suppressed neurons, most (53%) were disinhibited when the excitatory amino acid receptor antagonists d-2-amino-5-phosphonovaleric acid (d-APV) and 6-nitro-7 sulphamoylbeno[f]-quinoxaline-2,3-dione (NBQX) were administered, indicating that excitatory input to inhibitory interneurons was blocked. Of the neurons that received inputs from inhibitory interneurons, all had their suppressive responses decreased or eliminated by the γ-aminobutyric acid antagonist, bicuculline. Finally, severing the superficial layers from the slice had no effect on intermediate layer responses to intrinsic stimulation. These data provide physiological evidence for the presence of horizontally oriented inhibitory interneurons in the superior colliculus. Furthermore, these findings are consistent with the hypothesis that an intrinsic circuit, routed through interneurons, might account for the reciprocal inhibition observed among fixation and saccade-related neurons.
Spinal NMDA Receptor Involvement in Expansion of Dorsal Horn Neuronal Receptive Field Area Produced by Intracutaneous Histamine
Authors: Jinks Steven L. , Carstens E.
Published: December 2017

Jinks, Steven L. and E. Carstens. Spinal NMDA receptor involvement in expansion of dorsal horn neuronal receptive field area produced by intracutaneous histamine. J. Neurophysiol. 79: 1613–1618, 1998. Histamine elicits the sensation of itch at the site of skin application as well as alloknesis (itch elicited by innocuous mechanical stimuli) in a surrounding area in humans and expansion of the low-threshold mechanosensitive receptive field area of spinal wide dynamic range (WDR)-type dorsal horn neurons in rats. We presently tested if the histamine-evoked expansion of neuronal receptive field area depends on a spinal N-methyl-d-aspartate (NMDA) receptor-mediated process. In pentobarbital sodium–anesthetized rats, mechanical receptive field areas of single WDR-type dorsal horn neurons were mapped with graded von Frey filaments before and 10 min after intracutaneous (ic) microinjection of histamine (1 μl; 1, 3, or 10%) at a low-threshold site within the receptive field. Intracutaneous microinjection of histamine evoked dose-related increases in firing rate, as well as a dose-dependent expansion in mean receptive field area 10 min after 3 and 10%, but not 1%, histamine doses. When a noncompetitive or competitive NMDA receptor antagonist dizocilpine [MK-801; d(-)-2-amino-5-phosphonovalerate (APV), respectively; 1 μM] was first applied topically to the surface of the spinal cord, there was no significant change in mean receptive field area after ic microinjection of 10% histamine. The mean neuronal response to histamine in the presence of spinal MK-801 or APV was not significantly different from the mean response to histamine in the absence of these drugs. These results suggest that spinal NMDA receptors are involved in histamine-induced expansion of mechanical receptive field area, a neural event possibly involved in the development of alloknesis.
Loss of Rhythmically Bursting Neurons in Rat Medial Septum Following Selective Lesion of Septohippocampal Cholinergic System
Authors: Apartis Emmanuelle , Poindessous-Jazat Frederique R. , Lamour Yvon A. , Bassant Marie H.
Published: December 2017

Apartis, Emmanuelle, Frederique R. Poindessous-Jazat, Yvon A. Lamour, and Marie H. Bassant. Loss of rhythmically bursting neurons in rat medial septum following selective lesion of septohippocampal cholinergic system. J. Neurophysiol. 79: 1633–1642, 1998. The medial septum contains cholinergic and GABAergic neurons that project to the hippocampal formation. A significant proportion of the septohippocampal neurons (SHN) exhibit a rhythmically bursting (RB) activity that is involved in the generation of the hippocampal theta rhythm. The neurochemical nature of septal RB neurons is not firmly established. To address this question, the septal unit activity has been recorded in rats after selective destruction of the cholinergic septal neurons by the immunotoxin 192 IgG-saporin. Experiments have been performed in urethan-anesthetized and unanesthetized rats, 14–21 days after lesion. Acetylcholinesterase (AChE) histochemistry revealed a near-complete loss of cholinergic septal neurons and of cholinergic fibers in the hippocampus. The recorded neurons were located in the medial septum-diagonal band of Broca area. A number of these neurons were identified as projecting to the hippocampus (SHN) by their antidromic response to the electrical stimulation of the fimbria-fornix. In urethan-anesthetized lesioned rats, the percentage of RB neurons decreased significantly as compared with controls (17 vs. 41% for SHNs and 5 vs. 19% for unidentified septal neurons). The axonal conduction velocity and the burst frequency of the SHNs that retained a RB activity were higher in lesioned as compared with control rats. The number of spikes per burst was lower and the burst duration was shorter in lesioned rats as compared with controls. The urethan-resistant hippocampal theta was altered both in terms of frequency and amplitude. In unanesthetized lesioned rats, no RB septal neurons were found during arousal, as compared with 25% in controls. Their number was also markedly reduced during paradoxical sleep (9.7 vs. 38.5%). Histochemistry in 192 IgG-saporin–treated rats showed that RB neurons were found in areas devoid of AChE-positive neurons but containing parvalbumine-positive (presumably GABAergic) neurons. These data show that RB activity is considerably reduced after selective lesion of the cholinergic medial septal neurons. They suggested that the large majority of the RB septal neurons are cholinergic and that the few neurons that display RB activity in lesioned rats are GABAergic.
Mesolimbic Component of the Ascending Cholinergic Pathways: Electrophysiological-Pharmacological Study
Authors: Brudzynski Stefan M. , Kadishevitz Ludmila , Fu Xiao-Wen
Published: December 2017

Brudzynski, Stefan M., Ludmila Kadishevitz, and Xiao-Wen Fu. Mesolimbic component of the ascending cholinergic pathways: electrophysiological-pharmacological study. J. Neurophysiol. 79: 1675–1686, 1998. The cholinergic input from the pontomesencephalic cholinergic neurons to the diencephalic and basal forebrain structures has been implicated in a number of limbically controlled overt behaviors. The cellular mechanism by which the cholinergic terminals initiate behavioral manifestations is not clear. The objective of this study was to investigate the effects of the ascending cholinergic projection from the laterodorsal tegmental nucleus (LDT) on neuronal firing in the anterior hypothalamic-medial preoptic region (AHMP), known to be involved in agonistic behavior. Experiments were performed on urethan-anesthetized rats. Iontophoretic application of carbachol (CCh) into the vicinity of single cells in the AHMP caused a dose-dependent decrease in the mean firing rate of 83% of units and an increase in 10% of units. The inhibitory effect of CCh, but not the excitatory effect, was reversed by iontophoretic pretreatment with scopolamine. The inhibition of the firing rate was repeatable for the same dose of CCh and dose dependent. Electrical stimulation of neurons in the LDT caused a comparable, current-dependent decrease in the mean firing rate of AHMP neurons that also was reversed by pretreatment of neurons in the AHMP with scopolamine. The antagonizing effects of scopolamine were reversible with time. The same units in the AHMP that inhibited their firing to stimulation of the LDT also responded with a similar inhibition to local iontophoretic CCh. Finally, the fluorescent carbocyanine dye, 4-(4-(dihexadecylamino)styryl)-N-methylpyridinium iodide, (DiA), has been used as a retrograde axonal tracer and was injected into the recording sites immediately after the electrophysiological recordings. After 1 wk, DiA dye was found in numerous neurons in the LDT as shown by the fluorescence confocal microscopy. Results of the study suggest that LDT cholinergic neurons project and terminate in the AHMP and that their activation causes a decrease in the mean firing rate of the AHMP neurons. It is postulated that this inhibitory effect is implicated in the initiation of some of the behavioral patterns like defensive or alarm vocalization and behavioral inhibition.
Enhanced Propagation of Epileptiform Activity Through the Kindled Dentate Gyrus
Authors: Behr J. , Lyson K. J. , Mody I.
Published: December 2017

Behr, J., K. J. Lyson, and I. Mody. Enhanced propagation of epileptiform activity through the kindled dentate gyrus. J. Neurophysiol. 79: 1726–1732, 1998. Extracellular recordings were performed in combined hippocampal-entorhinal cortex (HC-EC) slices obtained from control and commissural kindled rats to investigate the propagation of epileptiform activity from the entorhinal cortex (EC) to the hippocampus (HC) after chronic epilepsy. Lowering extracellular Mg2+ concentration in control slices induced epileptiform activity consisting of spontaneous epileptiform bursts in area CA3 and of electrographic seizures in the EC. In contrast, the CA3 region of HC-EC slices obtained from kindled rats displayed significantly longer lasting epileptiform bursts and electrographic seizures. The electrographic seizures that were absent in controls propagated from the EC because disconnecting the HC from the EC stopped their occurrence in the CA3, whereas epileptiform bursts persisted with an unaltered pattern and frequency. Thus the area CA3 is affected by kindling and contributes to the spread of epileptiform activity within the EC-HC complex. We developed a method to induce focal epileptiform activity in the EC by locally perfusing the γ-aminobutyric acid-A (GABA) antagonist bicuculline (50 mM) in 10 mM KCl containing artificial cerebrospinal fluid. This method enabled us to investigate the propagation of epileptiform discharges from the disinhibited EC to the DG without affecting the DG with the epileptogenic medium. We show here that kindling facilitates the propagation of epileptiform activity through the DG. These data are consistent with the normal function of the DG as a filter limiting the spread of epileptiform activity within the HC-EC complex. This gating mechanism breaks down after chronic epilepsy induced by kindling.
Morphologically Identified Cutaneous Afferent DRG Neurons Express Three Different Potassium Currents in Varying Proportions
Authors: Everill Brian , Rizzo Marco A. , Kocsis Jeffery D.
Published: December 2017

Everill, Brian, Marco A. Rizzo, and Jeffery D. Kocsis. Morphologically identified cutaneous afferent DRG neurons express three different potassium currents in varying proportions. J. Neurophysiol. 79: 1814–1824, 1998. Outward K+ currents were recorded using a whole cell patch-clamp configuration, from acutely dissociated adult rat cutaneous afferent dorsal root ganglion (DRG) neurons (L4 and L5) identified by retrograde labeling with Fluoro-gold. Recordings were obtained 16–24 h after dissociation from cells between 39 and 49 mm in diameter with minimal processes. These cells represent medium-sized DRG neurons relative to the entire population, but are large cutaneous afferent neurons giving rise to myelinated axons. Voltage-activated K+ currents were recorded routinely during 300-ms depolarizing test pulses increasing in 10-mV steps from −40 to +50 mV; the currents were preceded by a 500-ms conditioning prepulse of either −120 or −40 mV. Coexpression of at least three components of K+ current was revealed. Separation of these components was achieved on the basis of sensitivities to the K+ channel blockers, 4-aminopyridine (4-AP) and dendrotoxin (DTx), and by the current responses to variation in conditioning voltage. Changing extracellular K+ concentration from 3 to 40 mM resulted in a shift to the right of the I-V curve commensurate with K+ being the principal charge carrier. Presentation of 100 mM 4-AP revealed a rapidly activating K+ current sensitive to low concentrations of 4-AP. High concentrations of 4-AP (6 mM) extinguished all inactivating current, leaving almost pure sustained current ( I K). On the basis of the relative distribution of K+ currents neurons could be separated into three distinct categories: fast inactivating current ( I A), slow inactivating current ( I D), and sustained current ( I K); only I A and I K; and slow inactivating current and I K. However, I K was always the dominant outward current component. These results indicate that considerable variation in K+ currents is present not only in the entire population of DRG neurons, as previously reported, but even within a restricted size and functional group (large cutaneous afferent neurons).
Modulation of Pre- and Postsynaptic Calcium Dynamics by Ionotropic Glutamate Receptors at a Plastic Synapse
Authors: Schwartz Neil E. , Alford Simon
Published: December 2017

Schwartz, Neil E. and Simon Alford. Modulation of pre- and postsynaptic calcium dynamics by ionotropic glutamate receptors at a plastic synapse. J. Neurophysiol. 79: 2191–2203, 1998. This study was conducted to assess the role of ionotropic glutamate receptors in the modulation of calcium dynamics on both sides of a vertebrate plastic synapse. Retrograde labeling of neuronal elements with high-affinity calcium-sensitive dyes was used in conjunction with confocal imaging techniques in an in vitro lamprey brain stem preparation. A prolonged calcium transient was measured both pre- and postsynaptically in response to a period of high-frequency (“tetanic”) stimulation to the vestibulospinal-reticulospinal synapse. The ionotropic glutamate receptor antagonists 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM) and d,l−2-amino-5-phosphonopentanoate (d,l-AP5; 100 μM) reduced the calcium signal in both compartments of the synapse. The presynaptic d,l-AP5–sensitive component was enhanced markedly by the removal of Mg2+ from the superfusate. Increasing the extracellular stimulus intensity progressively augmented the presynaptic calcium signal, suggesting the recruitment of excitatory axo-axonic inputs onto these fibers. Further, the presence of an excitatory amino acid-mediated presynaptic potential underlying a component of the Ca2+ signal was demonstrated by electrophysiological recordings from vestibulospinal axons. Bath application of agonist, in the presence of tetrodotoxin (1 μM), confirmed the existence of N-methyl-d-aspartate receptors at the presynaptic element capable of modulating calcium levels. The postsynaptic Ca2+ response, which is known to be necessary for long-term potentiation (LTP) induction at this synapse, was localized to areas of the dendritic tree that correlated with the location of known synaptic inputs; thus the synaptically activated rise in postsynaptic calcium may confer the synapse specificity of LTP induction previously demonstrated. In summary, we have demonstrated the existence of physiologically activated presynaptic ionotropic glutamate receptors that are capable of modulating levels of intracellular calcium and have highlighted the importance of receptor-mediated increases in postsynaptic calcium for neuronal plasticity in the lamprey.
Attention-Regulated Activity in Human Primary Visual Cortex
Authors: Watanabe Takeo , Sasaki Yuka , Miyauchi Satoru , Putz Benno , Fujimaki Norio , Nielsen Matthew , Takino Ryosuke , Miyakawa Satoshi
Published: December 2017

Watanabe, Takeo, Yuka Sasaki, Satoru Miyauchi, Benno Putz, Norio Fujimaki, Matthew Nielsen, Ryosuke Takino, and Satoshi Miyakawa. Attention-regulated activity in human primary visual cortex. J. Neurophysiol. 79: 2218–2221, 1998. Effects of attention to a local contour of a moving object on the activation of human primary visual cortex (area V1) were examined. Local cerebral oxygenation changes (an index of neuronal activity) in human area V1 were measured with functional magnetic resonance imaging (fMRI) in conditions including the following two: 1) when attention was selectively directed toward one side of a moving wedge (the attention condition) and 2) when the wedges were viewed passively (the passive condition). Activation in area V1 was found to be higher in the attention condition than in the passive condition. To our knowledge, this is the first finding that attention to motion activates as early as area V1. We suggest that attentional activation of area V1 is task dependent.
Basilar Membrane Vibration in the Gerbil Hemicochlea
Authors: Richter Claus-Peter , Evans Burt N. , Edge Roxanne , Dallos Peter
Published: December 2017

Richter, Claus-Peter, Burt N. Evans, Roxanne Edge, and Peter Dallos. Basilar membrane vibration in the gerbil hemicochlea. J. Neurophysiol. 79: 2255–2264, 1998. Excised gerbil cochleae were cut along the mid-modiolar plane (hemicochlea). Along one-half turn of this preparation, fluorescent microbeads were placed on the basilar membrane (BM). The BM was vibrated with click stimuli (50 μs) produced mechanically by a piezo pusher. The stimulus delivery probe could be positioned either more apical or more basal from the beads. Vibration patterns were measured with a wide bandwidth photomultiplier from the movements of the beads. When the probe was positioned more basal, the responses to click stimuli were brief, damped sinusoids. According to the fast Fourier transforms (FFTs) of the averaged time wave forms, the best frequency between successive beads decreased toward the apex (0.8 octave/mm). Sharpness of tuning of the normalized FFT spectra (NQ10dB) on average was 1.5. Response amplitude at a fixed input level, measured at different beads away from the stimulation site, dropped exponentially (58 dB/mm). In addition, for each individual bead, amplitude dropped linearly with decreasing stimulus intensity. In experiments where the stimulating probe was placed more apical, two major properties were observed: first, beads revealed only the spectral components present in the motion of the probe. Second, magnitude reduction of the displacement of the cochlear partition was greater, on average 155 dB/mm, indicating a lack of significant propagation in the reverse direction.
Activity-Dependent Regulation of [Ca2+]iin Avian Cochlear Nucleus Neurons: Roles of Protein Kinases A and C and Relation to Cell Death
Authors: Zirpel Lance , Lippe William R. , Rubel Edwin W
Published: December 2017

Zirpel, Lance, William R. Lippe, and Edwin W Rubel. Activity-dependent regulation of [Ca2+]iin avian cochlear nucleus neurons: roles of protein kinases A and C and relation to cell death. J. Neurophysiol. 79: 2288–2302, 1998. Neurons of the cochlear nucleus, nucleus magnocellularis (NM), of young chicks require excitatory afferent input from the eighth nerve for maintenance and survival. One of the earliest changes seen in NM neurons after deafferentation is an increase in intracellular calcium concentration ([Ca2+]i). This increase in [Ca2+]iis due to loss of activation of metabotropic glutamate receptors (mGluR) that activate second-messenger cascades involved in [Ca2+]iregulation. Because mGluRs are known to act via the phospholipase C and adenylate cyclase signal transduction pathways, the goal of this study was to determine the roles of protein kinases A (PKA) and C (PKC) activities in the regulation of NM neuron [Ca2+]iby eighth nerve stimulation. Additionally, we sought to determine the relationship between increased [Ca2+]iand cell death as measured by propidium iodide incorporation. [Ca2+]iof individual NM neurons in brain stem slices was monitored using fura-2 ratiometric fluorescence imaging. NM field potentials were monitored in experiments in which the eighth nerve was stimulated. Five hertz orthodromic stimulation maintained NM neuron [Ca2+]iat ∼110 nM for 180 min. In the absence of stimulation, NM neuron [Ca2+]iincreased steadily to a mean of 265 nM by 120 min. This increase was attenuated by superfusion of PKC activators phorbol-12,13-myristate acetate (100 nM) or dioctanoylglycerol (50 μM) and by activators of PKA: 1 mM 8-bromoadenosine-3′,5′-cyclophosphate sodium (8-Br-cAMP), 50 μM forskolin or 100 μM Sp-adenosine 3′,5′-cyclic monophosphothioate triethylamine. Inhibition of PKA (100 μM Rp-cAMPS) or PKC (50 nM bisindolymaleimide or 10 μM U73122) during continuous orthodromic stimulation resulted in an increase in NM neuron [Ca2+]ithat exceeded 170 and 180 nM, respectively, by 120 min. Nonspecific kinase inhibition with 1 μM staurosporine during stimulation resulted in an [Ca2+]iincrease that was greater in magnitude than that seen with either PKA or PKC inhibition alone, equal to that seen in the absence of stimulation, but much smaller than that seen with inhibition of mGluRs. In addition, manipulations that resulted in a [Ca2+]iincrease ≥250 nM resulted in an increase in number and percentage of propidium iodide-labeled NM neurons. These results suggest that eighth nerve activity maintains [Ca2+]iof NM neurons at physiological levels in part via mGluR-mediated activation of PKA and PKC and that increases in [Ca2+]idue to activity deprivation or interruption of the PKA and PKC [Ca2+]iregulatory mechanisms are predictive of subsequent cell death.
GABAergic Disinhibition Affects Responses of Bat Inferior Collicular Neurons to Temporally Patterned Sound Pulses
Authors: Lu Yong , H.-S. Jen Philip , Wu Min
Published: December 2017

Lu, Yong, Philip H.-S. Jen, and Min Wu. GABAergic disinhibition affects responses of bat inferior collicular neurons to temporally patterned sound pulses. J. Neurophysiol. 79: 2303–2315, 1998. Using the big brown bat, Eptesicus fuscus, as a model mammalian auditory system, we studied the effect of GABAergic disinhibition by bicuculline on the responses of inferior collicular (IC) neurons to temporally patterned trains of sound pulses delivered at different pulse repetition rates (PRRs) under free-field stimulation conditions. All 66 neurons isolated from eight bats either discharged one to two impulses (phasic on responders, n = 41, 62%), three to eight impulses (phasic bursters, n = 19, 29%), or many impulses throughout the entire duration of the stimulus (tonicresponders, n = 6, 9%). Whereas 50 neurons responded vigorously to frequency-modulated (FM) pulses, 16 responded poorly ornot at all to FM pulses. Bicuculline application increased the number of impulses of all 66 neurons in response to 4 ms pulses by 15–1,425%. The application also changed most phasic on responders into phasic bursters or tonic responders, resulting in 12 (18%) phasic on responders, 34 (52%) phasic bursters, and 20 (30%) tonic responders. Response latencies of these neurons were either shortened ( n = 25, 38%) by 0.5–6.0 ms, lengthened ( n = 9, 14%) by 0.5–2.5 ms or not changed ( n = 32, 48%) on bicuculline application. Each neuron had a highest response repetition rate beyond which the neuron failed to respond. Bicuculline application increased the highest response repetition rates of 62 (94%) neurons studied. The application also increased the highest 100% pulse-locking repetition rates of 21 (32%) neurons and facilitated 27 (41%) neurons in response to more pulses at the same PRR than predrug conditions. According to average rate-based modulation transfer functions (average rate MTFs), all 66 neurons had low-pass filtering characteristics both before and after bicuculline application. According to total discharge rate-based modulation transfer functions (total rate MTFs), filtering characteristics of these neurons can be described as band-pass ( n = 52, 79%), low-pass ( n = 12, 18%), or high-pass ( n = 2, 3%) before bicuculline application. Bicuculline application changed the filtering characteristics of 14 (21%) neurons. According to synchronization coefficient-based modulation transfer functions, filtering characteristics of these neurons can be described as low-pass ( n = 41, 62%), all-pass ( n = 11, 17%), band-suppression ( n = 7, 10.5%), and band-suppression–band-pass filters ( n = 7, 10.5%). Bicuculline application changed filtering characteristics of 19 (29%) neurons.
Convergence Properties of Solitary Tract Neurons Responsive to Cardiac Receptor Stimulation in the Anesthetized Cat
Authors: Silva-Carvalho L. , Paton J.F.R. , Rocha I. , Goldsmith G. E. , Spyer K. M.
Published: December 2017

Silva-Carvalho, L., J.F.R. Paton, I. Rocha, G. E. Goldsmith and K. M. Spyer. Convergence properties of solitary tract neurons responsive to cardiac receptor stimulation in the anesthetized cat. J. Neurophysiol. 79: 2374–2382, 1998. The convergence pattern of cardiac receptors, pulmonary C-fibers, carotid chemoreceptor, and baroreceptor afferents onto neurons within the nucleus of the solitary tract (NTS) was studied in the anesthetized (pentobarbitone sodium, 40 mg/kg,) paralyzed and artificially ventilated cat. Extra- and intracellular recordings were made from NTS neurons while stimulating both cardiac receptors by aortic root injections of veratridine (1–3 μg/kg) and pulmonary C-fibers by a right atrial injection of phenylbiguanide (10–20 μg/kg). The ipsilateral carotid body was stimulated by using arterial injection of CO2-saturated bicarbonate solution, whereas inflation of the ipsilateral carotid sinus was used to activate baroreceptors. The ipsilateral cardiac vagal branch, cervical vagus, and carotid sinus nerves were stimulated electrically (1 Hz, 0.2–1 ms, 1–35 V). In 78 NTS neurons recorded either extracellularly ( n = 47) or intracellularly ( n = 31), electrical stimulation of the cardiac branch of the vagus nerve evoked synaptic potentials (spikes and/or excitatory postsynaptic potentials) with an onset latency between 4 and 220 ms. Some neurons displayed both short and long latency inputs(15.5 ± 1.8 and 160.0 ± 8.5 ms; n = 14). Of these 78 neurons, 24 responded to veratridine stimulation of cardiac receptors (i.e., cardioreceptive neurons) by exhibiting an augmenting–decrementing discharge of 37 ± 4 s in duration with a peak frequency of 30 ± 5 Hz. Convergence from other cardiorespiratory receptors was noted involving either carotid chemoreceptors ( n = 7) or pulmonary C-fibers ( n = 4) or from both carotid chemoreceptors and pulmonary C-fibers ( n = 6). In contrast, only one cardioreceptive NTS neuron was activated by distension of the carotid sinus. Recording sites recovered were confined to the medial NTS at the level of the area postrema and extended caudally into the commissural subnucleus. Our results indicate a convergence of carotid chemoreceptor and pulmonary C-fiber afferent inputs to cardioreceptive NTS neurons. With the paucity of baroreceptor inputs to these neurons it is suggested that sensory integration within the NTS may reflect regulatory versus defensive or protective reflex control.
Diverse Signal Transduction Pathways Mediated by Endogenous P2 Receptors in Cultured Rat Cerebral Cortical Neurons
Authors: Nishizaki Tomoyuki , Mori Masahiro
Published: December 2017

Nishizaki, Tomoyuki and Masahiro Mori. Diverse signal transduction pathways mediated by endogenous P2 receptors in cultured rat cerebral cortical neurons. J. Neurophysiol. 79: 2513–2521, 1998. The present study was conducted to assess the intracellular signaling pathways mediated by receptors for ATP, uridine triphosphate (UTP), and 2-methylthio ATP (2-MeSATP), by monitoring patch-clamp currents and intracellular calcium mobilization in cultured rat cortical cerebral neurons. All three agonists evoked potassium currents and increased the intracellular free Ca2+ concentration ([Ca2+]i), and these effects were inhibited by the broad G-protein inhibitor guanosine-5′- O-(2-thiodiphosphate) (GDPβS) but not by the Gi/o-protein inhibitor pertussis toxin (PTX). UTP-evoked currents were inhibited by either the phospholipase C inhibitor neomycin or the selective protein kinase C (PKC) inhibitor GF109203X, and the rise in cytosolic Ca2+ was inhibited by either neomycin or the inositol 1,4,5-trisphosphate (IP3) receptor antagonist heparin, indicating that the UTP receptor involved phospholipase C-mediated phosphatidylinositol signaling. In contrast, 2-MeSATP–induced currents and rise in cytosolic Ca2+ were not inhibited by either neomycin, or GF109203X, or heparin. 2-MeSATP elicited single-channel currents in the cell-attached patch-clamp configuration and also in excised patches. The G-protein activator GTPγS induced single-channel currents in a fashion that mimicked the effect of 2-MeSATP. These data suggest that 2 MeSATP activated potassium channels by a direct action of G-protein βγ subunits and increased [Ca2+]i by a mechanism independent of phospholipase C stimulation and IP3 production. ATP-evoked currents were partially inhibited by either neomycin or GF109203X, although the rise in cytosolic Ca2+ was not affected by these inhibitors. ATP produced single-channel currents with two major classes of the slope conductance (86 and 95 pS) in cell-attached patches, each of which is consistent with that achieved by 2-MeSATP (85 pS) or UTP (96 pS); the currents with the lower conductance were observed in the outside-out patch-clamp configuration. These results indicate that P2 receptors for UTP and 2-MeSATP are linked to a PTX-insensitive G-protein involving different signal transduction pathways and that ATP responses are mediated by both of these P2 receptors.
Neurotransmitter-Induced Novel Modulation of a Nonselective Cation Channel by a cAMP-Dependent Mechanism in Rat Pineal Cells
Authors: Darvish Nissim , Russell James T.
Published: December 2017

Darvish, Nissim and James T. Russell. Neurotransmitter-induced novel modulation of a nonselective cation channel by a cAMP-dependent mechanism in rat pineal cells. J. Neurophysiol. 79: 2546–2556, 1998. In the rat, circadian rhythm in melatonin is regulated by noradrenergic and neuropeptide inputs to the pineal via adenosine 3′,5′-cyclic monophosphate (cAMP)- and Ca2+-dependent mechanisms. We have identified a large conductance (170 pS), voltage-dependent, nonselective cation channel on rat pineal cells in culture that shows a novel mode of modulation by cAMP. Pituitary adenylate cyclase activating peptide (PACAP), norepinephrine, or 8-Br-cAMP increase channel open probability ( Po) with a hyperpolarizing shift in voltage dependence such that the channel becomes active at resting membrane potentials. The increase in Powas accompanied by a change in current rectification properties such that the channel was transformed from being inactive at rest to an inwardly rectifying cation conductance in the presence of agonist, which depolarizes the cell. This channel is calcium insensitive, is blocked by Cs+, and shows a permeability sequence: K+> Na+≥ NH+4> Li+. The data suggest thatPACAP and norepinephrine acting through a cAMP-dependent mechanism modulate this nonselective cation channel, resulting in a slow onset depolarization that may be important in regulation of pineal cell excitability.