bluuebunny/crossref_metadata_2025 huggingface dataset:
Noise From Voltage-Gated Ion Channels May Influence Neuronal Dynamics in the Entorhinal Cortex
Authors: White John A. , Klink Ruby , Alonso Angel , Kay Alan R.
Published: December 2017

White, John A., Ruby Klink, Angel Alonso, and Alan R. Kay. Noise from voltage-gated ion channels may influence neuronal dynamics in the entorhinal cortex. J. Neurophysiol. 80: 262–269, 1998. Neurons of the superficial medial entorhinal cortex (MEC), which deliver neocortical input to the hippocampus, exhibit intrinsic, subthreshold oscillations with slow dynamics. These intrinsic oscillations, driven by a persistent Na+ current and a slow outward current, may help to generate the theta rhythm, a slow rhythm that plays an important role in spatial and declarative learning. Here we show that the number of persistent Na+ channels underlying subthreshold oscillations is relatively small (<104) and use a physiologically based stochastic model to argue that the random behavior of these channels may contribute crucially to cellular-level responses. In acutely isolated MEC neurons under voltage clamp, the mean and variance of the persistent Na+ current were used to estimate the single channel conductance and voltage-dependent probability of opening. A hybrid stochastic-deterministic model was built by using voltage-clamp descriptions of the persistent and fast-inactivating Na+ conductances, along with the fast and slow K+ conductances. All voltage-dependent conductances were represented with nonlinear ordinary differential equations, with the exception of the persistent Na+ conductance, which was represented as a population of stochastic ion channels. The model predicts that the probabilistic nature of Na+ channels increases the cell's repertoire of qualitative behaviors; although deterministic models at a particular point in parameter space can generate either subthreshold oscillations or phase-locked spikes (but rarely both), models with an appropriate level of channel noise can replicate physiological behavior by generating both patterns of electrical activity for a single set of parameters. Channel noise may contribute to higher order interspike interval statistics seen in vitro with DC current stimulation. Models with channel noise show evidence of spike clustering seen in brain slice experiments, although the effect is apparently not as prominent as seen in experimental results. Channel noise may contribute to cellular responses in vivo as well; the stochastic system has enhanced sensitivity to small periodic stimuli in a form of stochastic resonance that is novel (in that the relevant noise source is intrinsic and voltage-dependent) and potentially physiologically relevant. Although based on a simple model that does not include all known membrane mechanisms of MEC stellate cells, these results nevertheless imply that the stochastic nature of small collections of molecules may have important effects at the cellular and network levels.
Neuronal Responses Related to Smooth Pursuit Eye Movements in the Periarcuate Cortical Area of Monkeys
Authors: Tanaka Masaki , Fukushima Kikuro
Published: December 2017

Tanaka, Masaki and Kikuro Fukushima. Neuronal responses related to smooth pursuit eye movements in the periarcuate cortical area of monkeys. J. Neurophysiol. 80: 28–47, 1998. To examine how the periarcuate area is involved in the control of smooth pursuit eye movements, we recorded 177 single neurons while monkeys pursued a moving target in the dark. The majority (52%, 92/177) of task-related neurons responded to pursuit but had little or no response to saccades. Histological reconstructions showed that these neurons were located mainly in the posterior bank of the arcuate sulcus near the sulcal spur. Twenty-seven percent (48/177) changed their activity at the onset of saccades. Of these, 36 (75%) showed presaccadic burst activity with strong preference for contraversive saccades. Eighteen (10%, 18/177) were classified as eye-position–related neurons, and 11% (19/177) were related to other aspects of the stimuli or response. Among the 92 neurons that responded to pursuit, 85 (92%) were strongly directional with uniformly distributed preferred directions. Further analyses were performed in these directionally sensitive pursuit-related neurons. For 59 neurons that showed distinct changes in activity around the initiation of pursuit, the median latency from target motion was 96 ms and that preceding pursuit was −12 ms, indicating that these neuron can influence the initiation of pursuit. We tested some neurons by briefly extinguishing the tracking target ( n = 39) or controlling its movement with the eye position signal ( n = 24). The distribution of the change in pursuit-related activity was similar to previous data for the dorsomedial part of the medial superior temporal neurons ( Newsome et al. 1988) , indicating that pursuit-related neurons in the periarcuate area also carry extraretinal signals. For 22 neurons, we examined the responses when the animals reversed pursuit direction to distinguish the effects of eye acceleration in the preferred direction from oppositely directed eye velocity. Almost all neurons discharged before eye velocity reached zero, however, only nine neurons discharged before the eyes were accelerated in the preferred direction. The delay in neuronal responses relative to the onset of eye acceleration in these trials might be caused by suppression from oppositely directed pursuit velocity. The results suggest that the periarcuate neurons do not participate in the earliest stage of eye acceleration during the change in pursuit direction, although most of them may participate in the early stages of pursuit initiation in the ordinary step-ramp pursuit trials. Some neurons changed their activity when the animals fixated a stationary target, and this activity could be distinguished easily from the strong pursuit-related responses. Our results suggest that the periarcuate pursuit area carries extraretinal signals and affects the premotor circuitry for smooth pursuit.
Decorrelating Actions of Renshaw Interneurons on the Firing of Spinal Motoneurons Within a Motor Nucleus: A Simulation Study
Authors: Maltenfort Mitchell G. , Heckman C. J. , Rymer W. Zev
Published: December 2017

Maltenfort, Mitchell G., C. J. Heckman, and W. Zev Rymer. Decorrelating actions of Renshaw interneurons on the firing of spinal motoneurons within a motor nucleus: a simulation study. J. Neurophysiol. 80: 309–323, 1998. A simulation of spinal motoneurons and Renshaw cells was constructed to examine possible functions of recurrent inhibition. Recurrent inhibitory feedback via Renshaw cells is known to be weak. In our model, consistent with this, motoneuron firing was only reduced by a few pulses per second. Our initial hypothesis was that Renshaw cells would suppress synchronous firings of motoneurons caused by shared, dynamic inputs. Each motoneuron received an identical pattern of noise in its input. Synchrony coefficients were defined as the average motoneuron population firing relative to the activity of selected reference motoneurons; positive coefficients resulted if the motoneuron population was particularly active at the same time the reference motoneuron was active. With or without recurrent inhibition, the motoneuron pools tended to show little if any synchronization. Recurrent inhibition was expected to reduce the synchrony even further. Instead, it reduced the variance of the synchrony coefficients, without a comparable effect on the average. This suggests—surprisingly—that both positive and negative correlations between motoneurons are suppressed by recurrent inhibition. In short, recurrent inhibition may operate as a negative feedback mechanism to decorrelate motoneurons linked by common inputs. A consequence of this decorrelation is the suppression of spectral activity that apparently arises from correlated motoneuron firings due to common excitatory drive. Without recurrent inhibition, the power spectrum of the total motoneuron pool firings showed a peak at a frequency corresponding to the largest measured firing rates of motoneurons in the pool. Recurrent inhibition either reduced or abolished this peak, presumably by minimizing the likelihood of correlated firing among pool elements. Renshaw cells may act to diminish physiological tremor, by removing oscillatory components from aggregate motoneuron activity. Recurrent inhibition also improved coherence between the aggregate motoneuron output and the common drive, at frequencies above the frequency of the “synchronous” peak. Sensitivity analyses demonstrated that the spectral effect became stronger as the duration of inhibitory synaptic conductance was shortened with either the magnitude or the spatial extent of the inhibitory conductances increased to maintain constant net inhibition. Overall, Renshaw inhibition appears to be a powerful way to adjust the dynamic behavior of a neuron population with minimal impact on its static gain.
Physiological Properties of Neurons in the Optic Layer of the Rat's Superior Colliculus
Authors: Lo Fu-Sun , Cork R. John , Mize R. Ranney
Published: December 2017

Lo, Fu-Sun, R. John Cork, and R. Ranney Mize. Physiological properties of neurons in the optic layer of the rat's superior colliculus. J. Neurophysiol. 80: 331–343, 1998. We made intracellular recordings from 74 neurons in the optic layer of the rat superior colliculus (SC). Resting membrane potentials were −62.3 ± 6.2 (SD) mV, and input resistances were 37.9 ± 10.1 MΩ. Optic layer neurons had large sodium spikes (74.2 ± 12.3 mV) with an overshoot of 12 mV and a half-amplitude duration of 0.75 ± 0.2 ms. Each sodium spike was followed by two afterhyperpolarizations (AHPs), one of short duration and one of longer duration, which were mediated by tetraethylammonium (TEA)-sensitive ( I C) or apamin-sensitive ( I AHP) calcium-activated potassium currents, respectively. Sodium spikes were also followed by an afterdepolarization (ADP), which was only revealed when the AHPs were blocked by TEA or apamin. In response to hyperpolarizing current pulses, optic layer neurons showed an inward rectification mediated by H channels. At the break of the current pulse, there was a rebound low-threshold spike (LTS) with a short duration of <25 ms. The LTS usually induced two sodium spikes (doublet). Most optic layer neurons (84%) behaved as intrinsically bursting cells. They responded to suprathreshold depolarization with an initial burst (or doublet) followed by a train of regular single spikes. The remaining 16% of cells acted as chattering cells with high-frequency gamma (20–80 Hz) rhythmic burst firing within a narrow range of depolarized potentials. The interburst frequency was voltage dependent and also time dependent, i.e., showed frequency adaptation. Unmasking the ADP with either TEA or apamin converted all of the tested intrinsically bursting cells into chattering cells, indicating that the ADP played a crucial role in the generation of rhythmic burst firing. Optic layer neurons receive direct retinal excitation mediated by both N-methyl-d-aspartate (NMDA) and non-NMDA receptors. Optic tract (OT) stimulation also led to γ-aminobutyric acid-A (GABAA) receptor–mediated inhibition, the main effect of which was to curtail the excitatory response to retinal inputs by shunting the excitatory postsynaptic current. Intracellular staining with biocytin showed that the optic layer neurons that we recorded from were mostly either wide-field vertical neurons or other cells with predominately superficially projecting dendrites. These cells were similar to calbindin immunoreactive cells seen in the optic layer. The characteristics of these optic layer neurons, such as prominent AHPs, strong shunting effect of inhibition, and short-lasting LTS, suggest that they respond transiently to retinal inputs. This is consistent with a function for these cells as the first relay station in the extrageniculate visual pathway.
Spatiotemporal Patterns at the Retinal Output
Authors: Jacobs Adam L. , Werblin Frank S.
Published: December 2017

Jacobs, Adam L. and Frank S. Werblin. Spatiotemporal patterns at the retinal output. J. Neurophysiol. 80: 447–451, 1998. Edge enhancement in the retina is thought to be mediated by classical center-surround antagonism, first encountered as the interactions between horizontal cells and cones. But in the salamander retina these interactions do little to enhance edges. Instead, a robust dynamic interaction between amacrine and bipolar cells appears to be responsible for a sharp edge enhancement. To demonstrate this we recorded extracellularly from a single ganglion cell and moved a flashed square, 300 μm on a side, over a 1.5 × 1.0 mm2 grid at 25-μm increments. Playing back all of these recordings simultaneously simulated the pattern of responses that would have been measured from an array of ganglion cells. The emerging pattern of ganglion cell activity first faithfully represented the flashed square, but after ∼60 ms the center of the representation collapsed, leaving a representation of only the edges. We inferred that the feedback synapse from amacrine to bipolar cells at γ-aminobutyric acid-C (GABAC) receptors mediated this effect: bicuculline and strychnine were ineffective in altering the response pattern, but in picrotoxin the center of the representation did not collapse. The GABAergic amacrine cells thought to mediate this effect have quite narrow spread of processes, so the existence of this edge-enhancing effect suggests a mechanism quite different from classical lateral inhibition, namely the delayed inhibition of a spatially expanding input pattern.
Functional Organization of Owl Monkey Lateral Geniculate Nucleus and Visual Cortex
Authors: O'Keefe Lawrence P. , Levitt Jonathan B. , Kiper Daniel C. , Shapley Robert M. , Movshon J. Anthony
Published: December 2017

O'Keefe, Lawrence P., Jonathan B. Levitt, Daniel C. Kiper, Robert M. Shapley, and J. Anthony Movshon. Functional organization of owl monkey lateral geniculate nucleus and visual cortex. J. Neurophysiol. 80: 594–609, 1998. The nocturnal, New World owl monkey ( Aotus trivirgatus) has a rod-dominated retina containing only a single cone type, supporting only the most rudimentary color vision. However, it does have well-developed magnocellular (M) and parvocellular (P) retinostriate pathways and striate cortical architecture [as defined by the pattern of staining for the activity-dependent marker cytochrome oxidase (CO)] similar to that seen in diurnal primates. We recorded from single neurons in anesthetized, paralyzed owl monkeys using drifting, luminance-modulated sinusoidal gratings, comparing receptive field properties of M and P neurons in the lateral geniculate nucleus and in V1 neurons assigned to CO “blob,” “edge,” and “interblob” regions and across layers. Tested with achromatic stimuli, the receptive field properties of M and P neurons resembled those reported for other primates. The contrast sensitivity of P cells in the owl monkey was similar to that of P cells in the macaque, but the contrast sensitivities of M cells in the owl monkey were markedly lower than those in the macaque. We found no differences in eye dominance, orientation, or spatial frequency tuning, temporal frequency tuning, or contrast response for V1 neurons assigned to different CO compartments; we did find fewer direction-selective cells in blobs than in other compartments. We noticed laminar differences in some receptive field properties. Cells in the supragranular layers preferred higher spatial and lower temporal frequencies and had lower contrast sensitivity than did cells in the granular and infragranular layers. Our data suggest that the receptive field properties across functional compartments in V1 are quite homogeneous, inconsistent with the notion that CO blobs anatomically segregate signals from different functional “streams.”
Serotonergic Neurons Differentially Modulate the Efficacy of Two Motor Neurons Innervating the Same Muscle Fibers inAplysia
Authors: Fox Lyle E. , Lloyd Philip E.
Published: December 2017

Fox, Lyle E. and Philip E. Lloyd. Serotonergic neurons differentially modulate the efficacy of two motor neurons innervating the same muscle fibers in Aplysia. J. Neurophysiol. 80: 647–655, 1998. Feeding behavior in Aplysia shows substantial plasticity. An important site for the generation of this plasticity is the modulation of synaptic transmission between motor neurons and the buccal muscles that generate feeding movements. We have been studying this modulation in the anterior portion of intrinsic buccal muscle 3 (I3a), which is innervated by two excitatory motor neurons and identified serotonergic modulatory neurons, the metacerebral cells (MCCs). We have shown previously that serotonin (5-HT) applied selectively to the muscle potently modulates excitatory junction potentials (EJPs) and contractions. All the effects of 5-HT were persistent, lasting many hours after wash out. We examined whether the release of endogenous 5-HT from the MCC could produce effects similar to the application of 5-HT. Stimulation of the MCCs did produce similar short-term effects to the application of 5-HT. MCC stimulation facilitates EJPs, potentiates contractions, and decreases the latency between the onset of a motor neuron burst and the onset of the evoked contraction. The effects of MCC stimulation reached a maximum at quite low firing frequencies, which were in the range of those previously recorded during feeding behavior. The maximal effects were similar to those produced by superfusion with ∼0.1 μM 5-HT. Although the effects of MCC stimulation on EJPs were persistent, they were less persistent than the effects of 0.1 μM 5-HT. Mechanisms that may account for differences in the persistence between released and superfused 5-HT are discussed. Thus activity in the MCCs has dramatic short-term effects on the behavioral output of motor neurons, increasing the amplitude and relaxation rate of contractions evoked by both B3 and B38 and shifting the temporal relationship between B38 bursts and evoked contractions.
Responses of Rapidly Adapting Afferent Neurons to Dynamic Stretch of Rat Hairy Skin
Authors: Prete Zaccaria Del , Grigg Peter
Published: December 2017

Del Prete, Zaccaria and Peter Grigg. Responses of rapidly adapting afferent neurons to dynamic stretch of rat hairy skin. J. Neurophysiol. 80: 745–754, 1998. Twenty-four rapidly adapting (RA) cutaneous afferents were recorded from a preparation of isolated, innervated hairy skin from the rat hindlimb for the purpose of identifying the mechanical variables associated with the initiation of afferent discharge. Neurons were studied while the skin was stretched dynamically along a single direction with the use of a linear actuator and a feedback controller. Input signals were load- or displacement-controlled stretches that followed either periodic or pseudorandom Gaussian noise control signals. When the tissue was actuated, loads and displacements were measured along the direction of stretch and neuronal responses were recorded. All RA afferents were activated by dynamic stretching. None had a sustained response to static stretch. Cross-correlation products, calculated between neuronal responses and either stress- or strain-related variables observed at the time of the spike, revealed a strong relationship between neuronal responses and tensile stress. Neuronal responses were observed at rates of change of stress between +1,000 and −800 kPa/s. Neuronal responses were poorly related to skin strain. Two loading conditions were used along the direction transverse to the stretch. In one condition the sides were unconstrained, so that on axial loading there was zero stress and negative strain along the transverse axis. In the other condition the sides were constrained so that when the tissue was loaded axially there was zero strain and positive stress along the transverse axis. In these two conditions the same level of axial stress was associated with two levels of axial strain. The neuronal responses were determined by the stress and not the strain. Neuronal responses were observed at stresses >5 kPa. It appears that RA afferents make little contribution to signaling limb movements or position in rat hindlimb on the basis of the behavior of rat hindlimb skin, as observed when the limb is rotated.
Resting Membrane Properties of Locust Muscle and Their Modulation I. Actions of the Neuropeptides YGGFMRFamide and Proctolin
Authors: Walther Christian , Zittlau Klaus E. , Murck Harald , Voigt Karlheinz
Published: December 2017

Walther, Christian, Klaus E. Zittlau, Harald Murck, and Karlheinz Voigt. Resting membrane properties of locust muscle and their modulation. I. Actions of the neuropeptides YGGFMRFamide and proctolin. J. Neurophysiol. 80: 771–784, 1998. The resting K+conductance ( GK,r) of locust jumping muscle and its modulation by two neuropeptides, proctolin (Arg-Tyr-Leu-Pro-Thr) and YGGFMRFamide (Tyr-Gly-Gly-Phe-Met-Arg-Phe-NH2), were investigated using the two-electrode voltage clamp. At a physiological [K+]oof 10 mM, GK,raccounts for ∼90% of the membrane resting conductance, and the resting membrane potential differs by ≤1 mV from EK(mean: −74 mV). There is a K+conductance that slowly activates on hyperpolarization ( GK,H) and that seems to be largely located in the transverse tubules. Steady-state activation of GK,Hwas analyzed by tail current measurements. GK,His activated partially at EKbut accounts for probably ≤50% of total resting K+conductance. Raising [K+]ocaused a large increase in GK,rand in maximal steady state GK,Hwithout shifting the voltage sensitivity of GK,H. YGGFMRFamide and proctolin reduce GK,H, mainly affecting the maximal steady-state conductance. The voltage-insensitive component of the resting K+conductance is also reduced. The conductance suppressed by the peptides exhibited an outwardly rectifying instantaneous current/voltage-characteristic that is quite similar to that of GK,H. The actions of the two peptides appeared to be identical, but proctolin was by some two orders of magnitude more potent than YGGFMRFamide. The effects of both peptides are mediated by G proteins. They are mimicked by phorbol esters but do not seem to be initiated by either branch of the phospholipase C-dependent intracellular pathways. The properties of the resting K+conductance in locust muscle and other invertebrate muscles are compared. The biological significance of peptide-induced reduction in resting K+conductance is discussed in view of the known property of proctolin to support tonic force as opposed to FMRFamide-peptides that support quick leg movements.
Shared Target Selection for Combined Version-Vergence Eye Movements
Authors: Chaturvedi Vivek , Gisbergen Jan A. M. Van
Published: December 2017

Chaturvedi, Vivek and Jan A. M. Van Gisbergen. Shared target selection for combined version-vergence eye movements. J. Neurophysiol. 80: 849–862, 1998. Primates frequently make rapid binocular eye movements to reorient gaze in both direction and depth. To explain the unequal movements made by the two eyes, it often is assumed that they result from the combined action of a conjugate saccadic system and a vergence contribution. Clearly such a scheme can only yield coordinated binocular movements if both systems are guided by a shared or coupled target selection mechanism. To investigate the degree of cooperation at this level, we studied binocular refixations to target-nontarget double-stimuli in three-dimensional (3-D) space. Binocular eye movements were recorded in seven subjects using the scleral coil technique. In the experiments, 20% of trials were composed of a green target and a red nontarget, presented at the same time, but at different locations in 3-D space. These were alternated randomly with single-target trials (80%) in which the green stimulus was presented randomly at one of eight possible positions in 3-D space. Instructions to the subject emphasized either the speed or accuracy of response. Our findings show that typical features of the saccadic response to double-stimuli (bistability, averaging, and a speed-accuracy trade-off), as found in earlier two-dimensional studies, are also prevalent for initial binocular refixations to double stimuli in 3-D space. When the first saccadic response is directed to one of the two stimuli, the vergence system almost invariably makes the same choice. Likewise, when the saccadic system makes a short-latency averaging response, the vergence system shows a similar compromise. Statistical analysis shows a high correlation between saccadic and vergence target selection, strongly suggesting that the amplitude computation process of both subsystems is due to a common target selection stage that has access to information about stimulus location in 3-D space.
Codes for Sound-Source Location in Nontonotopic Auditory Cortex
Authors: Middlebrooks John C. , Xu Li , Eddins Ann Clock , Green David M.
Published: December 2017

Middlebrooks, John C., Li Xu, Ann Clock Eddins, and David M. Green. Codes for sound-source location in nontonopic auditor cortex. J. Neurophysiol. 80: 863–881, 1998. We evaluated two hypothetical codes for sound-source location in the auditory cortex. The topographical code assumed that single neurons are selective for particular locations and that sound-source locations are coded by the cortical location of small populations of maximally activated neurons. The distributed code assumed that the responses of individual neurons can carry information about locations throughout 360° of azimuth and that accurate sound localization derives from information that is distributed across large populations of such panoramic neurons. We recorded from single units in the anterior ectosylvian sulcus area (area AES) and in area A2 of α-chloralose–anesthetized cats. Results obtained in the two areas were essentially equivalent. Noise bursts were presented from loudspeakers spaced in 20° intervals of azimuth throughout 360° of the horizontal plane. Spike counts of the majority of units were modulated >50% by changes in sound-source azimuth. Nevertheless, sound-source locations that produced greater than half-maximal spike counts often spanned >180° of azimuth. The spatial selectivity of units tended to broaden and, often, to shift in azimuth as sound pressure levels (SPLs) were increased to a moderate level. We sometimes saw systematic changes in spatial tuning along segments of electrode tracks as long as 1.5 mm but such progressions were not evident at higher sound levels. Moderate-level sounds presented anywhere in the contralateral hemifield produced greater than half-maximal activation of nearly all units. These results are not consistent with the hypothesis of a topographic code. We used an artificial-neural–network algorithm to recognize spike patterns and, thereby, infer the locations of sound sources. Network input consisted of spike density functions formed by averages of responses to eight stimulus repetitions. Information carried in the responses of single units permitted reasonable estimates of sound-source locations throughout 360° of azimuth. The most accurate units exhibited median errors in localization of <25°, meaning that the network output fell within 25° of the correct location on half of the trials. Spike patterns tended to vary with stimulus SPL, but level-invariant features of patterns permitted estimates of locations of sound sources that varied through 20-dB ranges. Sound localization based on spike patterns that preserved details of spike timing consistently was more accurate than localization based on spike counts alone. These results support the hypothesis that sound-source locations are represented by a distributed code and that individual neurons are, in effect, panoramic localizers.
Requirement of Protein Synthesis for Group I mGluR-Mediated Induction of Epileptiform Discharges
Authors: Merlin Lisa R. , Bergold Peter J. , Wong Robert K. S.
Published: December 2017

Merlin, Lisa R., Peter J. Bergold, and Robert K. S. Wong. Requirement of protein synthesis for group I mGluR-mediated induction of epileptiform discharges. J. Neurophysiol. 80: 989–993, 1998. Picrotoxin (50 μM) elicited rhythmic synchronized bursting in CA3 pyramidal cells in guinea pig hippocampal slices. Addition of the selective group I metabotropic glutamate receptor (mGluR) agonist ( S)-3,5-dihydroxyphenylglycine (25 μM) elicited an increase in burst frequency. This was soon followed by a slowly progressive increase in burst duration (BD), converting the brief 250–520 ms picrotoxin-induced synchronized bursts into prolonged discharges of 1–5 s in duration. BD was significantly increased within 60 min and reached a maximum after 2–2.5 h of agonist exposure. The protein synthesis inhibitors anisomycin (15 μM) or cycloheximide (25 μM) significantly impeded the mGluR-mediated development of the prolonged bursts; 90–120 min of agonist application failed to elicit the expected burst prolongation. By contrast, the mGluR-mediated enhancement of burst frequency progressed unimpeded. Furthermore, protein synthesis inhibitors had no significant effect on the frequency or duration of fully developed mGluR-induced prolonged discharges. These results suggest that the group I mGluR-mediated prolongation of synchronized bursts has a protein synthesis-dependent mechanism.
Contrast Enhancement and Distributed Encoding by Bipolar Cells in the Retina
Authors: Burkhardt Dwight A. , Fahey Patrick K.
Published: December 2017

Burkhardt, Dwight A. and Patrick K. Fahey. Contrast enhancement and distributed encoding by bipolar cells in the retina. J. Neurophysiol. 80: 1070–1081, 1998. Responses of bipolar cells, cone photoreceptors, and horizontal cells were recorded intracellularly in superfused eyecup preparations of the tiger salamander ( Ambystoma tigrinum). Contrast flashes of positive and negative polarity were applied at the center of the receptive field while the entire retina was light adapted to a background field of 20 cd/m2. For small contrasts, many bipolar cells showed remarkably high contrast gain: up to 15–20% of the bipolar response was evoked by a contrast step of 1%. There was considerable variation from cell to cell but, on average, no striking differences in contrast gain were found between the depolarizing (Bd) and hyperpolarizing (Bh) bipolar cells. Quantitative comparisons of contrast/response measurements for cone photoreceptors and cone-driven bipolars suggest that the high contrast gain of bipolars is the consequence of a 5–10 × amplification of small signals across the cone → bipolar synapse. Bipolar cells had a very restricted linear range of response and tended to saturate at stimulus levels that were within the linear range of the cone response. The contrast/response of horizontal cells was similar to that of cones and differed markedly from that of Bh cells. For steps of equal contrast, the latency of the Bh cells was ∼20 ms shorter than that of the Bd cells regardless of the contrast magnitude. For both bipolar cells and cones, the effect of contrast polarity on latency seems largely due to the absolute value of the light step, Δ L. In the large signal domain, properties of the contrast responses of bipolar cells varied appreciably, both within and between the Bd and Bh classes. Cells of either class could be positive- or negative-contrast dominant. These and additional results show that in the light-adapted retina, the bipolar population is functionally diverse and has the potential to provide a rich substrate for distributed encoding of visual images.
Ionic Mechanism of the Slow Afterdepolarization Induced by Muscarinic Receptor Activation in Rat Prefrontal Cortex
Authors: Haj-Dahmane Samir , Andrade Rodrigo
Published: December 2017

Haj-Dahmane, Samir and Rodrigo Andrade. Ionic mechanism of the slow afterdepolarization induced by muscarinic receptor activation in rat prefrontal cortex. J. Neurophysiol. 80: 1197–1210, 1998. The mammalian prefrontal cortex receives a dense cholinergic innervation from subcortical regions. We previously have shown that cholinergic stimulation of layer V pyramidal neurons of the rat prefrontal cortex results in a depolarization and the appearance of a slow afterdepolarization (sADP). In the current report we examine the mechanism underlying the sADP with the use of sharp microelectrode and whole cell recording techniques in in vitro brain slices. The ability of acetylcholine (ACh) and carbachol to induce the appearance of an sADP in pyramidal cells of layer V of prefrontal cortex is antagonized in a surmountable manner by atropine and is mimicked by application of muscarine or oxotremorine. These results indicate that ACh acts on muscarinic receptors to induce the sADP. In many cell types afterpotentials are triggered by calcium influx into the cell. Therefore we examined the possibility that calcium influx might be the trigger for the generation of the sADP. Consistent with this possibility, buffering intracellular calcium reduced or abolished the sADP but had little effect on the direct muscarinic receptor-induced depolarization also seen in these cells. These results, coupled to the previous observation that calcium channel blockers inhibit the sADP, indicated that the sADP results from a rise in intracellular calcium secondary to calcium influx into the cell. The ionic basis for the current underlying the sADP ( I sADP) was examined with the use of ion substitution experiments. The amplitude of I sADP was found to be reduced in a graded fashion by replacement of extracellular sodium with N-methyl-d-glucamine (NMDG). In contrast no clear evidence for the involvement of potassium or chloride channels in the generation of the sADP or I sADP could be found. This result indicated that I sADP is carried by sodium ions flowing into the cell. However, the dependence of I sADP on extracellular sodium was less pronounced than expected for a pure sodium current. We interpret these results to indicate that the sADP is most likely mediated by nonselective cation channels. Examination of the current underlying the sADP at different voltages indicated that this current was also voltage dependent, turning off with hyperpolarization. We conclude that the sADP elicited by muscarinic receptor activation in rat cortex is mediated predominantly by a calcium- and voltage-sensitive nonselective cation current. This current could represent an important mechanism through which ACh can regulate neuronal excitability in prefrontal cortex.
Serum From Diabetic BB/W Rats Enhances Calcium Currents in Primary Sensory Neurons
Authors: Ristic Helen , Srinivasan Shanthi , Hall Karen E. , Sima Anders A. F. , Wiley John W.
Published: December 2017

Ristic, Helen, Shanthi Srinivasan, Karen E. Hall, Anders A. F. Sima, and John W. Wiley. Serum from diabetic BB/W rats enhances calcium currents in primary sensory neurons. J. Neurophysiol. 80: 1236–1244, 1998. We examined the hypothesis that exposure of nondiabetic rat dorsal root ganglion (DRG) neurons to sera from diabetic BB/W rats would produce an increase in calcium currents associated with impaired regulation of the inhibitory G protein–calcium channel complex. Acutely dissociated rat DRGs were incubated for 18–24 h in medium supplemented with sera (10% vol/vol) from either diabetic rats with neuropathy or age-matched, nondiabetic controls. Exposure of DRG neurons to sera from diabetic BB/W rats resulted in a surface membrane immunofluorescence pattern when treated with an anti-rat light-chain antibody that was not observed in neurons exposed to control sera. Calcium current density ( I DCa) was assessed with the use of the whole cell variation of the patch-clamp technique. I DCa in neurons exposed to diabetic sera was significantly increased compared with neurons exposed to control sera. Guanine nucleotide-binding (G) protein regulation of calcium channel function was examined with the use of a two-pulse “facilitation” or I DCa enhancement protocol in the presence of activators [guanosine 5′-O-(3-thiotriphosphate) (GTPγS)] or antagonists [guanosine 5′-O-(2-thiodiphosphate) (GDPβS) and pertussis toxin (PTX)] of G protein function. Facilitation was significantly decreased in neurons exposed to diabetic sera. Intracellular diffusion of neurons with GDPβs blocked facilitation, whereas dialysis with GTPγs increased facilitation to a similar magnitude in neurons exposed to either diabetic or control sera. Treatment with PTX resulted in a significant increase in I DCa and ∼50% decrease in facilitation in neurons treated with control sera but no significant changes in neurons exposed to diabetic sera. We conclude that serum from diabetic BB/W rats with neuropathy contains an autoimmune immunoglobulin that impairs regulation of the inhibitory G protein–calcium channel complex, resulting in enhanced calcium influx. Regulation of the inhibitory G protein–calcium channel complex involves PTX-sensitive and -insensitive G proteins.
Changes in Membrane and Synaptic Properties of Thalamocortical Circuitry Caused by Hydrogen Peroxide
Authors: Frantseva Marina V. , Velazquez Jose L. Perez , Carlen Peter L.
Published: December 2017

Frantseva, Marina V., Jose L. Perez Velazquez, and Peter L. Carlen. Changes in membrane and synaptic properties of thalamocortical circuitry caused by hydrogen peroxide. J. Neurophysiol. 80: 1317–1326, 1998. Free radical (FR) production was linked to the generation of epileptiform activity. We performed electrophysiological recordings in rat thalamocortical slices to investigate the effects of FRs on the intrinsic and synaptic properties of thalamic and cortical neurons. Whole cell recordings from identified cortical pyramidal neurons and thalamic neurons of the ventrobasal nucleus revealed that exposure to the FR-forming agent H2O2 (2.5 mM) decreased γ-aminobutyric acid-A– and γ-aminobutyric acid-B–mediated inhibition to 35.3 ± 13.4% and 13.7 ± 4.4% (means ± SE) of control in cortical neurons and to 41.8 ± 14.8% and 33.6 ± 11.6% of control in thalamic neurons. H2O2 application increased excitatory transmission in thalamic neurons to 162.9 ± 29.6% of control but caused no change in cortical neurons. H2O2 altered significantly the characteristic low-pass filter behavior of cortical and thalamic cells as determined by their input impedances. After 35 min of superfusion, the impedance of cortical neurons decreased by 67.0 ± 14.5%, and thalamic decreased by 76.3 ± 2.7% for the frequencies in the range 1–50 Hz while remaining constant for frequencies >200 Hz. Neuronal hyperexcitability was manifested during H2O2 exposure by continuous firing and long depolarizing shifts in response to extracellular stimulation in both thalamocortical and cortical neurons only in slices preserving thalamocortical connections. In slices with severed thalamocortical connections, cortical neurons did not show signs of hyperexcitability. These observations indicate that FRs could promote hyperexcitability of thalamocortical circuits by altering the balance between excitation and inhibition and by transforming the characteristic low-pass filter behavior into a flat band-pass filter.
Involvement of Ras/MAP Kinase in the Regulation of Ca2+Channels in Adult Bullfrog Sympathetic Neurons by Nerve Growth Factor
Authors: Lei Saobo , Dryden William F. , Smith Peter A.
Published: December 2017

Lei, Saobo, William F. Dryden, and Peter A. Smith. Involvement of Ras/MAP kinase in the regulation of Ca2+channels in adult bullfrog sympathetic neurons by nerve growth factor. J. Neurophysiol. 80: 1352–1361, 1998. The cellular mechanisms that underlie nerve growth factor (NGF) induced increase in Ca2+-channel current in adult bullfrog sympathetic B-neurons were examined by whole cell recording techniques. Cells were maintained at low density in neuron-enriched, defined-medium, serum-free tissue culture for 6 days in the presence or absence of NGF (200 ng/ml). The increase in Ba2+current ( IBa) density induced by NGF was attenuated by the RNA synthesis inhibitor cordycepin (20 μM), by the DNA transcription inhibitor actinomycin D (0.01 μg/ml), by inhibitors of Ras isoprenylation (perillic acid 0.1–1.0 mM or α-hydroxyfarnesylphosphonic acid 10–100 μM), by tyrosine kinase inhibitors genistein (20 μM) or lavendustin A (1 μM), and by PD98059 (10–100 μM), an inhibitor of mitogen-activated protein kinase kinase. Inhibitors of the phosphatidylinositol 3-kinase (PI3K) pathway (wortmannin, 100 nM, or LY29400, 100 μM) were ineffective as were inhibitors of phospholipase Cγ (U73122 or neomycin, both 100 μM). The effect of NGF persisted in Ca2+-free medium that contained 1.8 mM Mg2+and 2 mM ethylene glycol-bis(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid. It was mimicked by a Trk antibody that was capable of inducing neurite outgrowth in explant cultures of bullfrog sympathetic ganglion. Antibodies raised against the low-affinity p75 neurotrophin receptor were ineffective in blocking the effect of NGF on IBa. These results suggest that NGF-induced increase in Ca2+channel current in adult sympathetic neurons results, at least in part, from new channel synthesis after Trk activation of Ras and mitogen activated protein kinase by a mechanism that is independent of extracellular Ca2+.
Computer Simulation of Post-Spike Facilitation in Spike-Triggered Averages of Rectified EMG
Authors: Baker S. N. , Lemon R. N.
Published: December 2017

Baker, S. N. and R. N. Lemon. Computer simulation of post-spike facilitation in spike-triggered averages of rectified EMG. J. Neurophysiol. 80: 1391–1406, 1998. When the spikes of a motor cortical cell are used to compile a spike-triggered average (STA) of rectified electromyographic (EMG) activity, a post-spike facilitation (PSF) is sometimes seen. This is generally thought to be indicative of direct corticomotoneuronal (CM) connections. However, it has been claimed that a PSF could be caused by synchronization between CM and non-CM cells. This study investigates the generation of PSF using a computer model. A population of cortical cells was simulated, some of which made CM connections to a pool of 103 motoneurons. Motoneurons were simulated using a biophysically realistic model. A subpopulation of the cortical cells was synchronized together. After a motoneuron discharge, a motor unit action potential was generated; these were summed to produce an EMG output. Realistic values were used for the corticospinal and peripheral nerve conduction velocity distribution, for slowing of impulse conduction in CM terminal axons, and for the amount of cortical synchrony. STA of the rectified EMG from all cortical neurons showed PSF; however, these were qualitatively different for CM versus non-CM cells. Using an epoch analysis to determine reliability in a quantitative manner, it was shown that the onset latency of PSF did not distinguish the two classes of cells after 10,000 spikes because of high noise in the averages. The time of the PSF peak and the peak width at half-maximum (PWHM) could separate CM from synchrony effects. However, only PWHM was robust against changes in motor unit action-potential shape and duration and against changes in the width of cortical synchrony. The amplitude of PSF from a CM cell could be doubled by the presence of synchrony. It is proposed that, if a PSF has PWHM <7 ms, this reliably indicates that the trigger is a CM cell projecting to the muscle whose EMG is averaged. In an analysis of experimental data where macaque motor cortical cells facilitated hand and forearm muscle EMG, 74% of PSFs fulfilled this criterion. The PWHM criterion could be applied to other STA studies in which it is important to exclude the effects of synchrony.
Spike-Wave Complexes and Fast Components of Cortically Generated Seizures. II. Extra- and Intracellular Patterns
Authors: Steriade Mircea , Amzica Florin , Neckelmann Dag , Timofeev Igor
Published: December 2017

Steriade, Mircea, Florin Amzica, Dag Neckelmann, and Igor Timofeev. Spike-wave complexes and fast components of cortically generated seizures. II. Extra- and intracellular patterns. J. Neurophysiol. 80: 1456–1479, 1998. In the previous paper we have demonstrated, by means of field potential and extracellular unit recordings, that bicuculline-induced seizures, which include spike-wave (SW) or polyspike-wave (PSW) complexes, are initiated intracortically and survive ipsilateral thalamectomy. Here, we used multisite field potential and extracellular recordings to validate the patterns of cortical SW/PSW seizures in chronically implanted, behaving cats. To investigate the cellular patterns and excitability during spontaneously occurring and electrically elicited cortical seizures, we used single and dual intracellular recordings from regular-spiking (RS) and fast-rhythmic-bursting (FRB) cortical neurons, in conjunction with field potential recordings from neocortex and related thalamic nuclei, in cats maintained under ketamine-xylazine anesthesia. 1) Invariably, the spontaneous or electrically induced seizures were initiated within the cortex of both behaving and anesthetized animals. Spontaneously occurring, compound seizures consisting of SW/PSW complexes at 2–4 Hz and fast runs at 10–15 Hz, developed without discontinuity from the slow (mainly 0.5–0.9 Hz), sleeplike, cortically generated oscillation. 2) During SW/PSW complexes, RS neurons discharged spike trains during the depth-negative component of the cortical “spike” component of field potentials and were hyperpolarized during the depth-positive field wave. The FRB neurons fired many more action potentials than RS cells during SW/PSW complexes. Averaged activities triggered by the spiky field potentials or by the steepest slope of depolarization in cortical neurons demonstrated similar relations between intracellular activities and field potentials during sleep and seizure epochs, the latter being an exaggeration of the depolarizing and hyperpolarizing components of the slow sleep oscillation. 3) During the fast runs, RS cells were tonically depolarized and discharged single action potentials or spike doublets (usually with pronounced spike inactivation), whereas FRB cells discharged rhythmic spike bursts, time locked with the depth-negative field potentials. 4) Neuronal excitability, tested by depolarizing current pulses applied throughout the seizures and compared with pre- and postseizure epochs, showed a decreased number of evoked action potentials during both seizure components (SW/PSW complexes and fast runs), eventually leading to null responses during the postictal depression. 5) Data suggest that interconnected FRB neurons may play an important role in the initiation of cortical seizures. We discuss the similarities between the electrographic patterns described in this study and those found in different forms of clinical seizures.