bluuebunny/crossref_metadata_2025 huggingface dataset:
Functional Properties of Neurons in the Primate Tongue Primary Motor Cortex During Swallowing
Authors: Martin Ruth E. , Murray Gregory M. , Kemppainen Pentti , Masuda Yuji , Sessle Barry J.
Published: December 2017

Martin, Ruth E., Gregory M. Murray, Pentti Kemppainen, Yuji Masuda, and Barry J. Sessle. Functional properties of neurons in the primate tongue primary motor cortex during swallowing. J. Neurophysiol. 78: 1516–1530, 1997. Recent studies conducted in our laboratory have suggested that the tongue primary motor cortex (i.e., tongue-MI) plays a critical role in the control of voluntary tongue movements in the primate. However, the possible involvement of tongue-MI in semiautomatic tongue movements, such as those in swallowing, remains unkown. Therefore the present study was undertakein in attempts to address whether tongue-MI plays a role in the semiautomatic tongue movements produced during swallowing. Extracellular single neuron recordings were obtained from tongue-MI, defined by intracortical microstimulation (ICMS), in two awake monkeys as they performed three types of swallowing (swallowing of a juice reward after successful tongue task performance, nontask-related swallowing of a liquid bolus, and nontask-related swallowing of a solid bolus) as well as a trained tongue-protrusion task. Electromyographic activity was recorded simultaneously from various orofacial and laryngeal muscles. In addition, the afferent input to each tongue-MI neuron and ICMS-evoked motor output characteristics at each neuronal recording site were determined. Neurons were considered to show swallow and/or tongue-protrusion task-related activity if a statistically significant difference in firing rate was seen in association with these behaviors compared with that observed during a control pretrial period. Of a total of 80 neurons recorded along 40 microelectrode penetrations in the ICMS-defined tongue-MI, 69% showed significant alterations of activity in relation to the swallowing of a juice reward, whereas 66% exhibited significant modulations of firing in association with performance of the trained tongue-protrusion task. Moreover, 48% showed significant alterations of firing in relation to both swallowing and the tongue-protrusion task. These findings suggest that the region of cortex involved in swallowing includes MI and that tongue-MI may play a role in the regulation of semiautomatic tongue movement, in addition to trained motor behavior. Swallow-related tongue-MI neurons exhibited a variety of swallow-related activity patterns and were distributed throughout the ICMS-defined tongue-MI at sites where ICMS evoked a variety of types of tongue movements. These findings are consistent with the view that multiple efferent zones for the production of tongue movements are activated in swallowing. Many swallow-related tongue-MI neurons had an orofacial mechanoreceptive field, particularly on the tongue dorsum, supporting the view that afferent inputs may be involved in the regulation of the swallowing synergy.
Responses of Intraparietal Neurons to Saccadic Targets and Visual Distractors
Authors: Platt Michael L. , Glimcher Paul W.
Published: December 2017

Platt, Michael L. and Paul W. Glimcher. Responses of intraparietal neurons to saccadic targets and visual distractors. J. Neurophysiol. 78: 1574–1589, 1997. Current evidence suggests that neuronal activity in the lateral intraparietal area (LIP) reflects sensory-motor processes, but it remains unclear whether LIP activation participates directly in the planning of future eye movements or encodes data about both sensory events and the behavioral significance of those sensory events. To examine this issue, 31 intraparietal neurons were studied in awake, behaving monkeys trained to perform two tasks that independently controlled the location of a saccadic target and the location and behavioral relevance of a visual distractor. In both of these tasks, two eccentric light-emitting diodes (LEDs) were illuminated yellow, one above and one below a fixation stimulus. Shortly after the eccentric LEDs were illuminated, a change in the color of the fixation stimulus indicated which of these LEDs served as the saccadic goal and which served as a visual distractor. In the first or distractor-irrelevant task, fixation offset indicated that the subject must initiate a saccade shifting gaze to the saccadic goal. In the second or distractor-relevant task, distractor offset served as the saccade initiation cue. Intraparietal neurons responded more strongly in association with an LED that served as a saccadic target than in association with the same LED when it served as a visual distractor. Neuronal responses in association with either target or distractor stimuli on distractor-relevant and distractor-irrelevant blocks of trials were statistically indistinguishable. When the location of either the target or the distractor was varied across trials, the response of each neuron in association with a particular stimulus location was always greater for targets than for distractors and the magnitude of this response difference was independent of distractor relevance; however, distractors were nearly always associated with some intraparietal neuronal activity. A target/distractor selectivity index was computed for each neuron as the difference between responses associated with targets minus responses associated with distractors divided by the sum of these values. When the selectivity of each neuron on the distractor-relevant task was plotted against the selectivity of the same neuron on the distractor-irrelevant task, activity in the population of intraparietal neurons was found to be independent of distractor relevance. These data suggest that LIP neuronal activation represents saccadic targets and, at a lower level of activity, visual distractors, but does not encode the relevance of distractor stimuli on these tasks.
Viewer-Centered Frame of Reference for Pointing to Memorized Targets in Three-Dimensional Space
Authors: McIntyre J. , Stratta F. , Lacquaniti F.
Published: December 2017

McIntyre, J., F. Stratta, and F. Lacquaniti. Viewer-centered frame of reference for pointing to memorized targets in three-dimensional space. J. Neurophysiol. 78: 1601–1618, 1997. Pointing to a remembered visual target involves the transformation of binocular visual information into an appropriate motor output. Errors generated during pointing tasks may indicate the reference frames used by the CNS for the transformation and storage of the target position. Previous studies have proposed eye-, shoulder-, or hand-centered reference frames for various pointing tasks, depending on visual conditions. We asked subjects to perform pointing movements to remembered three-dimensional targets after a fixed memory delay. Pointing movements were executed under dim lighting conditions, allowing vision of the fingertip against a uniform black background. Subjects performed repeated movements to targets distributed uniformly within a small (radius 25 mm) workspace volume. In separate blocks of trials, subjects pointed to different workspace regions that varied in terms of distance and direction from the head and shoulder. Additional blocks were performed that differed in terms of starting position, effector hand, head rotation, and memory delay duration. Final pointing positions were quantified in terms of the constant and variable errors in three dimensions. The orientation of these errors was examined as a function of workspace location to identify the underlying reference frames. Subjects produced anisotropic patterns of variable error, with greater variability for endpoint distances from the body. The major axes of the variable-error tolerance ellipsoids pointed toward the eyes of the subject, independent of workspace region, effector hand (left or right), initial hand position, and head rotations. Constant errors were less consistent across subjects, but also tended to point toward the head and body. Both overshoots and undershoots of the target position were observed. Increasing the duration of the memory delay period increased the size but did not alter the orientation of the variable-error ellipsoids. Variability of the endpoint positions increased equally in all three Cartesian directions as the memory delay increased from 0.5 to 8.0 s. The anisotropy of variable errors indicates a viewer-centered reference frame for pointing to remembered visual targets with vision of the finger. The anisotropy of pointing variability stems from variability in egocentric binocular cues as opposed to reliance on allocentric visual references or to specific approximations in the sensorimotor transformation. Nevertheless, observed increases in variability with longer memory delays indicate that the short-term storage of the target position does not simply mirror the retinal and ocular sensory signals of the visually acquired target location. Thus spatial memory is carried out in an internal representation that is viewer-centered but that may be isotropic with respect to Cartesian space.
Differential Impact of Miniature Synaptic Potentials on the Soma and Dendrites of Pyramidal Neurons In Vivo
Authors: Paré Denis , Lebel Elen , Lang Eric J.
Published: December 2017

Paré, Denis, Elen LeBel, and Eric J. Lang. Differential impact of miniature synaptic potentials on the somata and dendrites of pyramidal neurons in vivo. J. Neurophysiol. 78: 1735–1739, 1997. We studied the impact of transmitter release resistant to tetrodotoxin (TTX) in morphologically identified neocortical pyramidal neurons recorded intracellularly in barbiturate-anesthetized cats. It was observed that TTX-resistant release occurs in pyramidal neurons in vivo and at much higher frequencies than was previously reported in vitro. Further, in agreement with previous findings indicating that GABAergic and glutamatergic synapses are differentially distributed in the somata and dendrites of pyramidal cells, we found that most miniature synaptic potentials were sensitive to γ-aminobutyric acid-A (GABAA) or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) antagonists in presumed somatic and dendritic impalements, respectively. Pharmacological blockage of spontaneous synaptic events produced large increases in input resistance that were more important in dendritic (≈50%) than somatic (≈10%) impalements. These findings imply that in the intact brain, pyramidal neurons are submitted to an intense spike-independent synaptic bombardment that decreases the space constant of the cells. These results should be taken into account when extrapolating in vitro findings to intact brains.
Cellular Mechanisms Underlying Spontaneous Firing in Rat Suprachiasmatic Nucleus: Involvement of a Slowly Inactivating Component of Sodium Current
Authors: Pennartz C.M.A. , Bierlaagh M. A. , Geurtsen A.M.S.
Published: December 2017

Pennartz, C.M.A., M. A. Bierlaagh, and A.M.S. Geurtsen. Cellular mechanisms underlying spontaneous firing in rat suprachiasmatic nucleus: involvement of a slowly inactivating component of sodium current. J. Neurophysiol. 78: 1811–1825, 1997. Neurons constituting the pacemaker of circadian rhythms, located in the suprachiasmatic nucleus, generate spontaneous firing patterns that change across the day-night cycle. Their average spontaneous firing rate is considered an important functional marker of clock activity because it is highest during daytime and low at night. In this study we investigate the ionic mechanisms underlying spontaneous firing in acutely prepared slices and dissociated neurons of the suprachiasmatic nucleus. In current-clamp mode, spontaneous action potentials were consistently preceded by depolarizing ramps. These ramps were Na+ dependent, were sensitive to tetrodotoxin (TTX), and disappeared on hyperpolarization. Ramps and associated spikes were not abolished by blockers of the H current (1 mM cesium) or calcium currents (50 μM nickel or 200 μM cadmium). In voltage-clamped neurons in slices or dissociated neurons, TTX-sensitive and Na+-dependent inward current was observed to activate well below firing threshold (−60 to −50 mV). The low-threshold component of Na+ current inactivated slowly as compared with the fast component that mediates action potentials. However, its inactivation proceeded more rapidly than has been reported for the persistent Na+ current in cortical structures. Persistent Na+ current was generally absent or small in amplitude. The voltage dependence and kinetics of the slowly inactivating component of Na+ current are consistent with the hypothesis that it is partially deinactivated during spike afterhyperpolarizations and contributes significantly to subsequent depolarizing ramps. These observations implicate the slowly inactivating component of Na+ current in ionic mechanisms governing spontaneous firing in suprachiasmatic nucleus neurons.
Excitatory Amino Acid Receptors at a Feedback Pathway in the Electrosensory System: Implications for the Searchlight Hypothesis
Authors: Berman Neil J. , Plant James , Turner Ray W. , Maler Leonard
Published: December 2017

Berman, Neil J., James Plant, Ray W. Turner, and Leonard Maler. Excitatory amino acid receptors at a feedback pathway in the electrosensory system: implications for the searchlight hypothesis. J. Neurophysiol. 78: 1869–1881, 1997. The electrosensory lateral line lobe (ELL) of the South American gymnotiform fish Apteronotus leptorhynchus has a laminar structure: electroreceptor afferents terminate ventrally whereas feedback input distributes to a superficial molecular layer containing the dendrites of the ELL principle (pyramidal) cells. There are two feedback pathways: a direct feedback projection that enters the ELL via a myelinated tract (stratum fibrosum, StF) and terminates in the ventral molecular layer (VML) and an indirect projection that enters as parallel fibers and terminates in the dorsal molecular layer. It has been proposed that the direct feedback pathway serves as a “searchlight” mechanism. This study characterizes StF synaptic transmission to determine whether the physiology of the direct feedback projection is consistent with this hypothesis. We used field and intracellular recordings from the ELL to investigate synaptic transmission of the StF in an in vitro slice preparation. Stimulation of the StF produced field potentials with a maximal negativity confined to a narrow band of tissue dorsal to the StF. Current source density analysis revealed two current sinks: an early sink within the StF and a later sink that corresponded to the anatomically defined VML. Field potential recordings from VML demonstrated that stimulation of the StF evoked an excitatory postsynaptic potential (EPSP) that peaked at a latency of 4–7 ms with a slow decay (∼50 ms) to baseline. Intracellular recordings from pyramidal cells revealed that StF-evoked EPSPs consisted of at least two components: a fast gap junction mediated EPSP (peak 1.2–1.8 ms) and a chemical synaptic potential (peak 4–7 ms) with a slow decay phase (∼50 ms). The amplitudes of the peak and decay phases of the chemical EPSP were increased by depolarizing current injection. Pharmacological studies demonstrated that the chemical EPSP was mainly due to ionotropic glutamate receptors with both N-methyl-d-aspartate (NMDA) and non-NMDA components. NMDA receptors contributed substantially to both the early and late phase of the EPSP, whereas non-NMDA receptors contributed mainly to the early phase. Stimulation of the StF at physiological rates (100–200 Hz, 100 ms) produced an augmenting depolarization of the membrane potential of pyramidal cells. Temporal summation and a voltage-dependent enhancement of later EPSPs in the stimulus train permitted the compound EPSP to reach spike threshold. The nonlinear behavior of StF synaptic potentials is appropriate for the putative role of the direct feedback pathway as part of a searchlight mechanism allowing these fish to increase the electrodetectability of scanned objects.
In Vitro Plasticity of the Direct Feedback Pathway in the Electrosensory System of Apteronotus leptorhynchus
Authors: Wang Daliang , Maler Leonard
Published: December 2017

Wang, Daliang and Leonard Maler. In vitro plasticity of the direct feedback pathway in the electrosensory system of Apteronotus leptorhynchus. J. Neurophysiol. 78: 1882–1889, 1997. We have used field and intracellular recording from pyramidal cells in an in vitro preparation of the electrosensory lateral line lobe (ELL) of Apteronotus leptorhynchus to investigate synaptic plasticity of a direct feedback pathway: the (StF). Tetanic stimulation of the StF enhanced the StF-evoked synaptic response by 145% in field and the excitatory postsynaptic potential (EPSP) 190% in intracellular recordings. Maximal enhancement occurred at 5 s and lasted for ∼120 s. Tetanic frequencies of 100–300 Hz produced enhancement; lower or higher frequencies failed to produce statistically significant changes in EPSP amplitude. Rates of 100–200 Hz occur in vivo in the cells of origin of the StF, suggesting that this form of plasticity may be operative under natural conditions. We could not elicit either long-term potentiation or depression by any stimulation protocol of the StF; in the case of long-term potentiation, this held even when excitatory transmission was enhanced by application of bicuculline, a γ-aminobutyric acid-A antagonist. When tetanic stimulation of the StF was paired with hyperpolarization of pyramidal cells, subsequent StF-evoked EPSPs were increased by 146% (5 min posttetanus); this anti-Hebbian synaptic enhancement lasted for ∼10 min. Neither tetanic stimulation alone, hyperpolarization alone, nor tetanic stimulation paired with pyramidal cell depolarization altered StF-evoked EPSP amplitudes on this time scale. Anti-Hebbian synaptic enhancement was not blocked by the N-methyl-d-aspartate–receptor antagonist D.L-aminophosphovalerate. The in vitro demonstration of anti-Hebbian plasticity at StF synapses replicates similar in vivo results. Anti-Hebbian synaptic plasticity of the StF may be responsible in part for the ability of gymnotiform fish to reject redundant electrosensory signals.
Ion Transport and Membrane Potential in CNS Myelinated Axons I. Normoxic Conditions
Authors: Leppanen Lisa , Stys Peter K.
Published: December 2017

Leppanen, Lisa and Peter K. Stys. Ion transport and membrane potential in CNS myelinated axons. I. Normoxic conditions. J. Neurophysiol. 78: 2086–2094, 1997. Compound resting membrane potential was recorded by the grease gap technique during normoxic conditions (37°C) in rat optic nerve, a representative CNS myelinated tract. Mean potential was −47 ± 3 (SD) mV and remained stable for 2–3 h. Input impedance of a single optic nerve axon was calculated to be ≈5 GΩ. Contribution of the Na+ pump to resting axonal potential is estimated at −7 mV. Ouabain (10 μM to 10 mM) evoked a dose-dependent depolarization that was maximal at ≥1 mM, depolarizing the nerves to ∼35–40% of control after 60 min. Inhibiting energy metabolism (CN− and iodoacetate) during high-dose ouabain (1–10 mM) exposure caused an additional depolarization, suggesting additional ATP-dependent, ouabain-insensitive ion transport systems. Perfusion with zero-Na+ (choline substituted) caused a transient hyperpolarization, that was greater than with tetrodotoxin (TTX; 1 μM) alone, indicating both TTX-sensitive and -insensitive Na+ influx pathways in resting rat optic nerve axons. Resting probability (P)K:PNa is calculated at 20:1. In contrast to choline-substituted solution, Li+-substituted zero-Na+ perfusate caused a rapid depolarization due to Na+ pump inhibition and the ability of Li+ to permeate the Na+ channel. TTX reduced, but did not prevent, ouabain- or zero-Na+/Li+–induced depolarization. We conclude that the primary Na+ influx path in resting rat optic nerve axons is the TTX-sensitive Na+ channel, with evidence for additional TTX-insensitive routes permeable to Na+ and Li+. In addition, maintenance of membrane potential is critically dependent on continuous Na+ pump activity due to the relatively high exchange of Na+ (via the above mentioned routes) and K+ across the membrane of resting optic axons.
Distribution and Activation of Intracellular Ca2+Stores in Cultured Olfactory Bulb Neurons
Authors: Carlson Greg C. , Slawecki Melissa L. , Lancaster Eric , Keller Asaf
Published: December 2017

Carlson, Greg C., Melissa L. Slawecki, Eric Lancaster, and Asaf Keller. Distribution and activation of intracellular Ca2+stores in cultured olfactory bulb neurons. J. Neurophysiol. 78: 2176–2185, 1997. The presence and distribution of intracellular Ca2+release pathways in olfactory bulb neurons were studied in dissociated cell cultures. Histochemical techniques and imaging of Ca2+fluxes were used to identify two major intracellular Ca2+release mechanisms: inositol 1,4,5-triphosphate receptor (IP3R)-mediated release, and ryanodine receptor-mediated release. Cultured neurons were identified by immunocytochemistry for the neuron-specificmarker β-tubulin III. Morphometric analyses and immunocytochemistry for glutamic acid-decarboxylase revealed a heterogeneous population of cultured neurons with phenotypes corresponding to both projection (mitral/tufted) and intrinsic (periglomerular/granule) neurons of the in vivo olfactory bulb. Immunocytochemistry for the IP3R, and labeling with fluorescent-tagged ryanodine, revealed that, irrespective of cell type, almost all cultured neurons express IP3R and ryanodine binding sites in both somata and dendrites. Functional imaging revealed that intracellular Ca2+fluxes can be generated in the absence of external Ca2+, using agonists specific to each of the intracellular release pathways. Local pressure application of glutamate or quisqualate evoked Ca2+fluxes in both somata and dendrites in nominally Ca2+free extracellular solutions, suggesting the presence of IP3-dependent Ca2+release. These fluxes were blocked by preincubation with thapsigargin and persisted in the presence of the glutamate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione. Local application of caffeine, a ryanodine receptor agonist, also evoked intracellular Ca2+fluxes in the absence of extracellular Ca2+. These Ca2+fluxes were suppressed by preincubation with ryanodine. In all neurons, both IP3- and ryanodine-dependent release pathways coexisted, suggesting that they interact to modulate intracellular Ca2+concentrations.
Kinematic Principles of Primate Rotational Vestibulo-Ocular Reflex II. Gravity-Dependent Modulation of Primary Eye Position
Authors: Hess Bernhard J. M. , Angelaki Dora E.
Published: December 2017

Hess, Bernhard J. M. and Dora E. Angelaki. Kinematic principles of primate rotational vestibulo-ocular reflex. II. Gravity-dependent modulation of primary eye position. J. Neurophysiol. 78: 2203–2216, 1997. The kinematic constraints of three-dimensional eye positions were investigated in rhesus monkeys during passive head and body rotations relative to gravity. We studied fast and slow phase components of the vestibulo-ocular reflex (VOR) elicited by constant-velocity yaw rotations and sinusoidal oscillations about an earth-horizontal axis. We found that the spatial orientation of both fast and slow phase eye positions could be described locally by a planar surface with torsional variation of <2.0 ± 0.4° (displacement planes) that systematically rotated and/or shifted relative to Listing's plane. In supine/prone positions, displacement planes pitched forward/backward; in left/right ear-down positions, displacement planes were parallel shifted along the positive/negative torsional axis. Dynamically changing primary eye positions were computed from displacement planes. Torsional and vertical components of primary eye position modulated as a sinusoidal function of head orientation in space. The torsional component was maximal in ear-down positions and approximately zero in supine/prone orientations. The opposite was observed for the vertical component. Modulation of the horizontal component of primary eye position exhibited a more complex dependence. In contrast to the torsional component, which was relatively independent of rotational speed, modulation of the vertical and horizontal components of primary position depended strongly on the speed of head rotation (i.e., on the frequency of oscillation of the gravity vector component): the faster the head rotated relative to gravity, the larger was the modulation. Corresponding results were obtained when a model based on a sinusoidal dependence of instantaneous displacement planes (and primary eye position) on head orientation relative to gravity was fitted to VOR fast phase positions. When VOR fast phase positions were expressed relative to primary eye position estimated from the model fits, they were confined approximately to a single plane with a small torsional standard deviation (∼1.4–2.6°). This reduced torsional variation was in contrast to the large torsional spread (well >10–15°) of fast phase positions when expressed relative to Listing's plane. We conclude that primary eye position depends dynamically on head orientation relative to space rather than being fixed to the head. It defines a gravity-dependent coordinate system relative to which the torsional variability of eye positions is minimized even when the head is moved passively and vestibulo-ocular reflexes are evoked. In this general sense, Listing's law is preserved with respect to an otolith-controlled reference system that is defined dynamically by gravity.
GABAA-Mediated Local Synaptic Pathways Connect Neurons in the Rat Suprachiasmatic Nucleus
Authors: Strecker George J. , Wuarin Jean-Pierre , Dudek F. Edward
Published: December 2017

Strecker, George J., Jean-Pierre Wuarin, and F. EdwardDudek. GABAA-mediated local synaptic pathways connect neurons in the rat suprachiasmatic nucleus. J. Neurophysiol. 78: 2217–2220, 1997. The suprachiasmatic nucleus (SCN) in mammals functions as the biological clock controlling circadian rhythms, but the synaptic circuitry of the SCN is largely unexplored. Most SCN neurons use the neurotransmitter γ-aminobutyric acid (GABA), and anatomic studies indicate many GABAergic synapses and local axon collaterals; however, physiological evidence for synaptic communication among SCN neurons is indirect. We have used three approaches to investigate local circuitry in the SCN in acute hypothalamic slices from rat. First, tetrodotoxin was used to block action-potential-dependent synaptic release, which resulted in a decrease in the frequency of spontaneous synaptic currents in SCN neurons, suggesting that spontaneously active neurons in the slice connect synaptically to SCN neurons. Postsynaptic currents in SCN neurons were also evoked by the selective stimulation of other SCN neurons with glutamate, which avoids direct activation of axons that might originate outside the SCN. Two different methods of glutamate microapplication (i.e., pressure ejection and ultraviolet photolysis of caged glutamate) indicated that SCN neurons receive GABAA-receptor-mediated synaptic input from other SCN neurons. In contrast, glutamate-receptor-mediated synaptic connections between SCN neurons were not detected. The GABAergic synapses that comprise the network described here could conceivably be a substrate for the synchronization and amplification of the circadian rhythm of SCN firing. Alternatively, this circuitry might mediate other aspects of clock function such as the integration of environmental and physiological information.
Hyperpolarization-Activated Inward Current in Neurons of the Rat's Dorsal Nucleus of the Lateral Lemniscus In Vitro
Authors: Fu Xiao Wen , Brezden Borys L. , Wu Shu Hui
Published: December 2017

Fu, Xiao Wen, Borys L. Brezden, and Shu Hui Wu. Hyperpolarization-activated inward current in neurons of the rat's dorsal nucleus of the lateral lemniscus in vitro. J. Neurophysiol. 78: 2235–2245, 1997. The hyperpolarization-activated current ( I h) underlying inward rectification in neurons of the rat's dorsal nucleus of the lateral lemniscus (DNLL) was investigated using whole cell patch-clamp techniques. Patch recordings were made from DNLL neurons of young rats (21–30 days old) in 400 μm tissue slices. Under current clamp, injection of negative current produced a graded hyperpolarization of the cell membrane, often with a gradual sag in the membrane potential toward the resting value. The rate and magnitude of the sag depended on the amount of hyperpolarizing current. Larger current resulted in a larger and faster decay of the voltage. Under voltage clamp, hyperpolarizing voltage steps elicited a slowly activating inward current that was presumably responsible for the sag observed in the voltage response to a steady hyperpolarizing current recorded under current clamp. Activation of the inward current ( I h) was voltage and time dependent. The current just was seen at a membrane potential of −70 mV and was activated fully at −140 mV. The voltage value of half-maximal activation of I h was −78.0 ± 6.0 (SE) mV. The rate of I h activation was best approximated by a single exponential function with a time constant that was voltage dependent, ranging from 276 ± 27 ms at −100 mV to 186 ± 11 ms at −140 mV. Reversal potential ( E h) of I h current was more positive than the resting potential. Raising the extracellular potassium concentration shifted E h to a more depolarized value, whereas lowering the extracellular sodium concentration shifted E h in a more negative direction. I h was sensitive to extracellular cesium but relatively insensitive to extracellular barium. The current amplitude near maximal-activation (about −140 mV) was reduced to 40% of control by 1 mM cesium but was reduced to only 71% of control by 2 mM barium. When the membrane potential was near the resting potential (about −60 mV), cesium had no effect on the membrane potential, current-evoked firing rate and input resistance but reduced the spontaneous firing. When the membrane potential was more negative than −70 mV, cesium hyperpolarized the cell, decreased current-evoked firing and increased the input resistance. I h in DNLL neurons does not contribute to the normal resting potential but may enhance the extent of excitation, thereby making the DNLL a consistently powerful inhibitory source to upper levels of the auditory system.
GABAA Receptor-Mediated Cl− Currents in Rat Thalamic Reticular and Relay Neurons
Authors: Zhang Shuanglin J. , Huguenard John R. , Prince David A.
Published: December 2017

Zhang, Shuanglin J., John R. Huguenard, and David A. Prince. GABAA receptor-mediated Cl− currents in rat thalamic reticular and relay neurons. J. Neurophysiol. 78: 2280–2286, 1997. Spontaneous and evoked inhibitory postsynaptic currents (sIPSCs and eIPSCs) and responses to exogenously applied γ-aminobutyric acid (GABA), mediated by GABA type A (GABAA) receptors, were recorded in inhibitory neurons of nucleus reticularis thalami (nRt) and their target relay cells in ventrobasal (VB) nuclei by using patch clamp techniques in rat thalamic slices. The decay of sIPSCs in both nRt and VB neurons was best fitted with two exponential components. The decay time constants of sIPSCs in nRt neurons were much slower (τ1 = 38 ms; τ2 = 186 ms) than those previously reported in a variety of preparations and two to three times slower than those in VB neurons (τ1 = 17 ms; τ2 = 39 ms). GABAA receptor-mediated Cl− currents directly evoked by local GABA application also had a much slower decay time constant in nRt (225 ms) than in VB neurons (115 ms). Slow decay of GABA responses enhances the efficacy of recurrent intranuclear inhibition in nRt. The results suggest a functional diversity of GABAA receptors that may relate to the known heterogeneity of GABAA receptor subunits in these two thalamic nuclei.
Metabotropic Glutamate Receptor Enhancement of Spontaneous IPSCs in Neocortical Interneurons
Authors: Zhou Fu-Ming , Hablitz John J.
Published: December 2017

Zhou, Fu-Ming and John J. Hablitz. Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons. J. Neurophysiol. 78: 2287–2295, 1997. Using neocortical layer I neurons as a model for GABAergic interneurons, we have studied γ-aminobutyric acid-A (GABAA) receptor-mediated spontaneous inhibitory postsynaptic currents (IPSCs) and modulation by metabotropic glutamate receptors (mGluRs). In the presence of 0.5 μM tetrodotoxin (TTX) and ionotropic glutamate receptor antagonists and under symmetrical Cl− conditions, the mean amplitude of miniature IPSCs (mIPSCs) was ∼50 pA at a holding potential of −70 mV with individual events ranging from 10 to 400 pA. Averaged mIPSCs had a 10–90% rise time of ∼0.6 ms. The decay was double exponential. The fast component had a time constant of ∼4 ms and comprised ∼40% of the total amplitude. The slow component had a time constant of ∼22 ms. The frequency of spontaneous IPSCs (sIPSCs), recorded in the absence of TTX, was increased by bath application of the mGluR agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD; 10–100 μM) or the group I mGluR selective agonist quisqualic acid (Quis; 0.5–1 μM). Under identical conditions, mIPSCs were not affected. The kinetics of sIPSCs and mIPSCs were not altered by ACPD or Quis. Quis (1 μM) induced an inward current of ∼70 pA at a holding potential of −70 mV, whereas ACPD (40–200 μM) induced a smaller inward current. This current was linear over the voltage range −70 to +30 mV and reversed polarity near 0 mV. In current-clamp recordings, both Quis and ACPD induced a depolarization and action potential firing in layer I and deeper layer interneurons. We conclude that neocortical layer I neurons receive GABAA receptor-mediated inhibitory synaptic inputs. Activation of mGluRs, possibly mGluR1 and/or mGluR5, causes an enhancement of inhibitory synaptic transmission by directly depolarizing corticalGABAergic interneurons through the opening of nonselective cation channels.
Role of Voltage-Gated K+ Currents in Mediating the Regular-Spiking Phenotype of Callosal-Projecting Rat Visual Cortical Neurons
Authors: Locke Rachel E. , Nerbonne Jeanne M.
Published: December 2017

Locke, Rachel E. and Jeanne M. Nerbonne. Role of voltage-gated K+ currents in mediating the regular-spiking phenotype of callosal-projecting rat visual cortical neurons. J. Neurophysiol. 78: 2321–2335, 1997. Whole cell current- and voltage-clamp recordings were combined to examine action potential waveforms, repetitive firing patterns, and the functional roles of voltage-gated K+ currents ( I A, I D, and I K) in identified callosal-projecting (CP) neurons from postnatal (day 7–13) rat primary visual cortex. Brief (1 ms) depolarizing current injections evoke single action potentials in CP neurons with mean ± SD ( n = 60) durations at 50 and 90% repolarization of 1.9 ± 0.5 and 5.5 ± 2.0 ms, respectively; action potential durations in individual cells are correlated inversely with peak outward current density. During prolonged threshold depolarizing current injections, CP neurons fire repetitively, and two distinct, noninterconverting “regular-spiking” firing patterns are evident: weakly adapting CP cells fire continuously, whereas strongly adapting CP cells cease firing during maintained depolarizing current injections. Action potential repolarization is faster and afterhyperpolarizations are more pronounced in strongly than in weakly adapting CP cells. In addition, input resistances are lower and plateau K+ current densities are higher in strongly than in weakly adapting CP cells. Functional studies reveal that blockade of I D reduces the latency to firing an action potential, and increases action potential durations at 50 and 90% repolarization. Blockade of I D also increases firing rates in weakly adapting cells and results in continuous firing of strongly adapting cells. After applications of millimolar concentrations of 4-aminopyridine to suppress I A (as well as block I D), action potential durations at 50 and 90% repolarization are further increased, and firing rates are accelerated over those observed when only I D is blocked. Using VClamp/CClamp and the voltage-clamp data in the preceding paper, mathematical descriptions of I A, I D, and I K are generated and a model of the electrophysiological properties of rat visual cortical CP neurons is developed. The model is used to simulate the firing properties of strongly adapting and weakly adapting CP cells and to explore the functional roles of I A, I D, and I K in shaping the waveforms of individual action potentials and controlling the repetitive firing properties of these cells.
Ion Currents and Mechanisms of Modulation in the Radula Opener Muscles ofAplysia
Authors: Scott Marsha L. , Brezina Vladimir , Weiss Klaudiusz R.
Published: December 2017

Scott, Marsha L., Vladimir Brezina, and Klaudiusz R. Weiss. Ion currents and mechanisms of modulation in the radula opener muscles of Aplysia. J. Neurophysiol. 78: 2372–2387, 1997. Numerous studies of plasticity in the feeding behavior of Aplysia have shown that substantial plasticity is due to peripheral neuromodulation of the feeding musculature. Extensive previous work focusing on the accessory radula closer (ARC) muscle has led to the realization that a major function of the modulation in that muscle may be to ensure efficient coordination between its contractions and those of its antagonist muscles. For a more complete understanding, therefore, we must study these muscles also. Here we have studied the radula opener muscles I7–I10. Using single isolated muscle fibers under voltage clamp, we have characterized ion currents gated by voltage and by the physiological contraction-inducing neurotransmitter acetylcholine (ACh) and the effects of the physiological modulators serotonin, myomodulins A and B, and FMRFamide. Our results explain significant aspects of the electrophysiological behavior of the whole opener muscles, as well as why the opener and ARC muscles behave similarly in many ways yet differently in some key respects. Opener muscles express four types of K currents: inward rectifier, A-type [ IK(A)], delayed rectifier [ IK(V)], and Ca2+-activated [ IK(Ca)]. They also express an L-type Ca current [ ICa] and a leakage current. ACh activates a positive-reversing cationic current [ IACh(cat)] and a negative-reversing Cl current [ IACh(Cl)]. The opener muscles differ from the ARC in that, in the openers, activation of IK(A)occurs ∼9 mV more positive and there is much less IACh(Cl). In both muscles, IACh(cat)most likely serves to depolarize the muscle until ICaactivates to supply Ca2+for contraction, but further depolarization and spiking is opposed by coactivation of IK(A), IK(V), IK(Ca), and IACh(Cl). Thus the differences in IK(A)and IACh(Cl)may well be key factors that prevent spikes in the ARC but often allow them in the opener muscles. As in the ARC, the modulators enhance ICaand so potentiate contractions. They also activate a modulator-specific K current, which causes hyperpolarization and depression of contractions. Finally, in the opener muscles but not in the ARC, the modulators activate a depolarizing cationic current that may help phase-advance the contractions. Each modulator exerts these effects to different degrees and thus has a distinct effect on voltage and contraction size and shape. The overall effect then will depend on the specific combinations of modulators released in different behaviors. By understanding the modulation in the opener muscles, as well as in the ARC, we are now in a position to understand how the behavior of the two muscles is coordinated under a variety of circumstances.
Acetylcholine Increases Intracellular Calcium of Arterial Chemoreceptor Cells of Adult Cats
Authors: Shirahata Machiko , Fitzgerald Robert S. , Sham James S. K.
Published: December 2017

Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham. Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]iwas measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]iin ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]iwas dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]iin response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]iof cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+influx via nicotinic channels. In addition, other pathways such as Ca2+influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+release from intracellular stores may participate in increasing [Ca2+]iin response to ACh. Muscarinic receptors appear to play only a small role, if any.
GABA Receptors of Bipolar Cells From the Skate Retina: Actions of Zinc on GABA-Mediated Membrane Currents
Authors: Qian Haohua , Li Lihong , Chappell Richard L. , Ripps Harris
Published: December 2017

Qian, Haohua, Lihong Li, Richard L. Chappell, and Harris Ripps. GABA receptors of bipolar cells from the skate retina: actions of zinc on GABA-mediated membrane currents. J. Neurophysiol. 78: 2402–2412, 1997. γ-Aminobutyric acid (GABA)–induced currents were recorded from isolated bipolar cells of the skate retina using perforated patch-clamp methodology. Pharmacological analysis of the responses, using selective agonists and antagonists of the major classes of GABA receptor, revealed the presence of both GABAA and GABAC receptors at both the dendrites and axon terminals of the bipolar cells. The two receptor types showed very different reactions to zinc, a divalent metallic cation that was detected in the synaptic terminal region of skate photoreceptors. Currents mediated by the activation of GABAC receptors were down-regulated by zinc, a feature that is typical of the action of zinc on GABAC receptors. On the other hand, the effects of zinc on GABAA receptor–mediated activity was highly dependent on zinc concentration. Unlike theGABAA receptors on other neurons, responses mediated by activation of the GABAA receptor of skate bipolar cells were significantly enhanced by zinc concentrations in the range of 0.1–100 μM; at higher concentrations of zinc (>100 μM), response amplitudes were suppressed below control levels. The enhancement of GABAA receptor activity on skate bipolar cells showed little voltage dependence, suggesting that zinc is acting on the extracellular domain of the GABAA receptor. In the presence of 10 μM zinc, the dose-response curve for 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP; a GABAA agonist that suppresses GABAC-activated currents) was shifted to the left of the curve obtained in the absence of zinc, but without a significant change in the response maximum. This finding indicates that the enhancing effect of zinc is due primarily to its ability to increase the sensitivity of the GABAA receptor. The novel enhancement of neuronal GABAA receptor activity by zinc, observed previously in the GABAA-mediated responses of skate Müller (glial) cells, may reflect the presence of a unique subtype of GABAA receptor on the bipolar and Müller cells of the skate retina.
Electrophysiological and Morphological Characteristics of Neurons in Perinuclear Zone of Supraoptic Nucleus
Authors: Armstrong William E. , Stern Javier E.
Published: December 2017

Armstrong, William E. and Javier E. Stern. Electrophysiological and morphological characteristics of neurons in perinuclear zone of supraoptic nucleus. J. Neurophysiol. 78: 2427–2437, 1997. Neurons in the perinuclear zone (PZ) of the supraoptic nucleus (SON) are thought to serve as interneurons and may mediate changes in neurohypophysial hormone release in response to physiological changes in blood pressure. However, the morphology and electrophysiological characteristics of PZ neurons are unknown. In the present study, PZ neurons from male and female rats were recorded intracellularly to determine some membrane properties, then filled with biocytin or biotinamide for morphological analysis. In general, PZ neurons had faster spikes than magnocellular SON neurons, and the great majority were characterized by a subthreshold depolarizing hump when depolarized from a hyperpolarized (less than −80 mV) membrane potential. In most neurons, this hump was similar to low-threshold spikes described in other CNS regions. Near-threshold, fast action potentials were clustered near the onset of these depolarizations. Conspicuously absent in all PZ neurons was the strong transient and subthreshold outward rectification characteristic of vasopressin and oxytocin neurons of the SON. These results suggest that PZ neurons are electrophysiologically distinct from neurosecretory neurons of the SON. No differences were found between male and female rats in any of the basic properties examined, including input resistance, membrane time constant, spike height, spike width, spike threshold, and the size of the spike afterhyperpolarization. Morphologically, PZ neurons were diverse but were divided into spiny and aspiny groups. Three spiny neurons and one aspiny neuron contributed an axonal projection to the SON characterized by varicosities suggestive of terminals. In the case of the three spiny neurons, the SON projection was clearly a minor collateral projection. The axon arborized in the PZ, but one or more branches were cut at the edge of the explant, indicating a longer projection. In the remaining neurons, no axonal projection to the SON was detected and several had axons leaving the explant. Some portion of the dendritic tree penetrated the SON in several neurons. The morphology of PZ neurons was thus heterogeneous and suggests that, for some cells at least, the projection to the SON may be a minor collateral component of a much wider axonal projection.