bluuebunny/crossref_metadata_2025 huggingface dataset:
Similar Propagation of SD and Hypoxic SD-Like Depolarization in Rat Hippocampus Recorded Optically and Electrically
Authors: Aitken P. G. , Tombaugh G. C. , Turner D. A. , Somjen G. G.
Published: December 2017

Aitken, P. G., G. C. Tombaugh, D. A. Turner, and G. G. Somjen. Similar propagation of SD and hypoxic SD-like depolarization in rat hippocampus recorded optically and electrically. J. Neurophysiol. 80: 1514–1521, 1998. Neuron membrane changes and ion redistribution during normoxic spreading depression (SD) induced, for example, by potassium injection, closely resemble those that occur during hypoxic SD-like depolarization (HSD) induced by oxygen withdrawal, but the degree to which the two phenomena are related is controversial. We used extracellular electrical recording and imaging of intrinsic optical signals in hippocampal tissue slices to compare 1) initiation and spread of these two phenomena and 2) the effects of putative gap junction blocking agents, heptanol and octanol. Both events arose focally, after which a clear advancing wave front of increased reflectance and DC shift spread along the CA1 stratum radiatum and s. oriens. The rate of spread was similar: conduction velocity of normoxic SD was 8.73 ± 0.92 mm/min (mean ± SE) measured electrically and 5.84 ± 0.63 mm/min measured optically, whereas HSD showed values of 7.22 ± 1.60 mm/min (electrical) and 6.79 ± 0.42 mm/min (optical). When initiated in CA1, normoxic SD consistently failed to enter the CA3 region (7/7 slices) and could not be initiated by direct KCl injection in the CA3 region ( n = 3). Likewise, the hypoxic SD-like optical signal showed onset in the CA1 region and halted at the CA1/CA3 boundary (9/9 slices), but in some (4/9) slices the dentate gyrus region showed a separate onset of signal changes. Microinjection into CA1 stratum radiatum of octanol (1 mM), which when bath applied arrests the spread of normoxic SD, created a small focus that appeared to be protected from hypoxic depolarization. However, bath application of heptanol (3 mM) or octanol (2 mM) did not prevent the spread of HSD, although the onset was delayed. This suggests that, although gap junctions may be essential for the spread of normoxic SD, they may play a less important role in the spread of HSD.
Activation of Protein Kinase C Increases Neuronal Excitability by Regulating Persistent Na+ Current in Mouse Neocortical Slices
Authors: Astman Nadav , Gutnick Michael J. , Fleidervish Ilya A.
Published: December 2017

Astman, Nadav, Michael J. Gutnick, and Ilya A. Fleidervish. Activation of protein kinase C increases neuronal excitability by regulating persistent Na+ current in mouse neocortical slices. J. Neurophysiol. 80: 1547–1551, 1998. Effects of the protein kinase C activating phorbol ester, phorbol 12-myristate 13-acetate (PMA), were studied in whole cell recordings from layer V neurons in slices of mouse somatosensory neocortex. PMA was applied intracellularly (100 nM to 1 μM) to restrict its action to the cell under study. In current-clamp recordings, it enhanced neuronal excitability by inducing a 10- to 20-mV decrease in voltage threshold for action-potential generation. Because spike threshold in neocortical neurons critically depends on the properties of persistent Na+ current ( I NaP), effects of PMA on this current were studied in voltage clamp. After blocking K+ and Ca2+ currents, I NaP was revealed by applying slow depolarizing voltage ramps from −70 to 0 mV. Intracellular PMA induced a decrease in I NaP at very depolarized membrane potentials. It also shifted activation of I NaP in the hyperpolarizing direction, however, such that there was a significant increase in persistent inward current at potentials more negative than −45 mV. When tetrodotoxin (TTX) was added to the bath, blocking I NaP and leaving only an outward nonspecific cationic current ( I cat), PMA had no apparent effect on responses to voltage ramps. Thus PMA did not affect I cat, and it did not induce any additional current. Intracellular application of the inactive PMA analogue, 4α-PMA, did not affect I NaP. The specific protein kinase C inhibitors, chelerythrine (20 μM) and calphostin C (10 μM), blocked the effect of PMA on I NaP. The data suggest that PMA enhances neuronal excitability via a protein kinase C–mediated increase in I NaP at functionally critical subthreshold voltages. This novel effect would modulate all neuronal functions that are influenced by I NaP, including synaptic integration and active backpropagation of action potential from the soma into the dendrites.
Amplification of Perforant-Path EPSPs in CA3 Pyramidal Cells by LVA Calcium and Sodium Channels
Authors: Urban Nathaniel N. , Henze Darrell A. , Barrionuevo German
Published: December 2017

Urban, Nathaniel N., Darrell A. Henze, and German Barrionuevo. Amplification of perforant-path EPSPs in CA3 pyramidal cells by LVA calcium and sodium channels. J. Neurophysiol. 80: 1558–1561, 1998. The perforant path forms a monosynaptic connection between the cells of layer II of the entorhinal cortex and the pyramidal cells in hippocampal area CA3. Although this projection is prominent anatomically, very little is known about the physiological properties of this input. The distal location of these synapses suggests that somatically recorded perforant-path excitatory postsynaptic potentials (EPSPs) may be influenced by the activation of voltage-dependent channels in CA3 cells. We observed that perforant-path EPSPs are reduced (by ∼25%) by blockade of postsynaptic low-voltage–activated calcium and sodium channels, indicating that perforant-path EPSPs are amplified by the activation of these channels. These data suggest that the perforant path may represent an important and highly modifiable direct connection between the entorhinal cortex and area CA3.
Changes in the Temporal Pattern of Primary Motor Cortex Activity in a Directional Isometric Force Versus Limb Movement Task
Authors: Sergio Lauren E. , Kalaska John F.
Published: December 2017

Sergio, Lauren E. and John F. Kalaska. Changes in the temporal pattern of primary motor cortex activity in a directional isometric force versus limb movement task. J. Neurophysiol. 80: 1577–1583, 1998. We recorded the activity of 75 proximal-arm-related cells in caudal primary motor cortex (MI) while a monkey generated either isometric forces or limb movements against an inertial load. The forces and movements were in eight directions in a horizontal plane. The isometric force generated at the hand increased monotonically in the direction of the target force level. The force exerted against the load in the movement task was more complex, including a transient decelerative phase during the movement as the hand approached the target. Electromyographic (EMG) activity of proximal-arm muscles reflected the task-dependent changes in dynamics, showing a ramp increase in activity during the isometric task and a reciprocal triphasic burst pattern in the movement task. A sliding 50-ms window analysis showed that the directionality of the EMG, when expressed in hand-centered spatial coordinates, remained stable throughout the isometric ramp but often showed a significant transient shift during the limb movements. Many cells in M1 showed corresponding significant changes in activity pattern and instantaneous directionality between the two tasks. This momentary dissociation of discharge from the directional kinematics of hand displacement is evidence that the activity of many single proximal-arm related M1 cells is not coupled only to the direction and velocity of hand motion.
Reflex Suppression in the Anti-Saccade Task Is Dependent on Prestimulus Neural Processes
Authors: Everling Stefan , Dorris Michael C. , Munoz Douglas P.
Published: December 2017

Everling, Stefan, Michael C. Dorris, and Douglas P. Munoz. Reflex suppression in the anti-saccade task is dependent on prestimulus neural processes. J. Neurophysiol. 80: 1584–1589, 1998. Reflexive responses often must be suppressed to correctly execute a voluntary behavior. It is largely unknown why this control sometimes fails. To examine the neural processes responsible for these failures, we recorded single-neuron activity in the superior colliculus (SC) in behaving monkeys during an anti-saccade task in which they had to suppress a saccade to a visual stimulus that suddenly appeared in the periphery and generate a saccade to the opposite side. We found that the level and distribution of prestimulus activity of buildup neurons in the SC was highly predictive of whether a correct response or an error occurred. A high level of prestimulus activity in buildup neurons at the location in the SC where the visual stimulus was represented was associated with the generation of a reflexive saccade to the stimulus. These findings suggest that the successful suppression of reflexive saccades is dependent on prestimulus neural processes in the SC.
Effect of a Serotonergic Extrinsic Modulatory Neuron (MCC) on Radula Mechanoafferent Function inAplysia
Authors: Alexeeva Vera , Borovikov Dmitry , Miller Mark W. , Rosen Steven C. , Cropper Elizabeth C.
Published: December 2017

Alexeeva, Vera, Dmitry Borovikov, Mark W. Miller, Steven C. Rosen, and Elizabeth C. Cropper. Effect of a serotonergic extrinsic modulatory neuron (MCC) on radula mechanoafferent function in Aplysia. J. Neurophysiol. 80: 1609–1622, 1998. The serotonergic metacerebral cells (MCCs) and homologous neurons in related mollusks have been extensively investigated within the context of feeding. Although previous work has indicated that the MCCs exert widespread actions, MCC modulation of sensory neurons has not been identified. We characterized interactions between the MCCs and a cell that is part of a recently described group of buccal radula mechanoafferents. The cell, B21, has a peripheral process in the tissue underlying the chitinous radula [the subradula tissue (SRT)]. Previous studies have shown that B21 can fire phasically during ingestive motor programs and provide excitatory drive to the circuitry active during radula closing/retraction. We now show that activity of B21 can be modulated by serotonin (5-HT) and the MCCs. Centrally, although a slow depolarization is typically recorded in B21 as a result of MCC stimulation, this depolarization does not cause B21 to spike. It can, however, increase B21 excitability enabling a pulse that was previously subthreshold to elicit an action potential in B21. B21 is in fact rhythmically depolarized during the radula closing/retraction phase of ingestive motor programs. Thus central effects of the MCCs on radula mechanoafferent activity are only likely to be apparent while B21 is receiving input from the feeding central pattern generator. Peripherally, radula mechanoafferent neurons can be activated 1) when a mechanical stimulus is applied to the biting surface of the SRT and 2) when the SRT contracts. MCC stimulation and 5-HT modulate B21 responses to both types of stimuli. For example, MCC stimulation and low concentrations of 5-HT cause subthreshold mechanical stimuli applied to the SRT to become suprathreshold. 5-HT and MCC stimulation also enhance SRT contractility. Peripheral effects of MCC activity are also likely to be phase dependent. For example, MCC stimulation does not cause B21 to respond to peripheral stimuli with an afterdischarge. Consequently, radula mechanoafferents are likely to be activated when food is present between the radula halves during radula closing/retraction but are not likely to continue to fire as opening/protraction is initiated. In a similar vein, MCC effects on the contractility of the SRT will only be apparent when contractions are elicited by motor neuron activity. SRT motor neurons are rhythmically activated during ingestive motor programs. Thus we have shown that radula mechanoafferent activity can be modulated by the MCCs and that this modulation is likely to occur in a phase-dependent manner.
Duration of NMDA-Dependent Synaptic Potentiation in Piriform Cortex In Vivo Is Increased After Epileptiform Bursting
Authors: Kapur A. , Haberly L. B.
Published: December 2017

Kapur, A. and L. B. Haberly. Duration of NMDA-dependent synaptic potentiation in piriform cortex in vivo is increased after epileptiform bursting. J. Neurophysiol. 80: 1623–1629, 1998. Stimulation of afferent fibers with current pulse trains has been reported to induce long-term potentiation (LTP) in piriform cortex in vitro but not in vivo. LTP has been observed in vivo only when trains are paired with behavioral reinforcement and as a consequence of kindled epileptogenesis. This study was undertaken in the urethan-anesthetized rat to determine if the reported failures to observe pulse-train evoked LTP in vivo may be related to a lesser persistence rather than lack of occurrence, if disinhibition might facilitate induction, and to examine the nature of the relationship between seizure activity and LTP. Stimulation of afferent fibers in the lateral olfactory tract with θ-burst trains under control conditions potentiated the monosynaptic field excitatory postsynaptic potential (EPSP) by approximately the same extent (20.3 ± 2%; n = 12) as reported for the slice. However, in contrast to the slice, potentiation in vivo decayed to a low level within 1–2 h after induction (70% loss in 1.5 h, on average). The N-methyl-d-aspartate (NMDA)-receptor antagonists d-APV and MK-801 blocked the induction of this decremental potentiation. Pharmacological reduction of γ-aminobutyric acid–mediated inhibition at the recording site did not increase the duration of potentiation. In contrast, θ-burst stimulation applied after recovery from a period of epileptiform bursting induced stable NMDA-dependent potentiation. Mean increase in the population EPSP was approximately the same as under control conditions (21 ± 2%; n = 6), but in five of six experiments there was little or no decay in potentiation for the duration of the monitoring period (≤6 h). It is concluded that seizure activity has an enabling action on the induction of persistent synaptic potentiation by stimulus trains that bypasses the need for behavioral reinforcement.
Zinc and Zolpidem Modulate mIPSCs in Rat Neocortical Pyramidal Neurons
Authors: Defazio Tony , Hablitz John J.
Published: December 2017

DeFazio, Tony and John J. Hablitz. Zinc and zolpidem modulate mIPSCs in rat neocortical pyramidal neurons. J. Neurophysiol. 80: 1670–1677, 1998. Pharmacological modulation of γ-aminobutyric acid-A (GABAA) receptors can provide important information on the types of subunits composing these receptors. In recombinant studies, zinc more potently inhibits αβ subunits compared with the αβγ combination, whereas modulation by nanomolar concentrations of the benzodiazepine type 1-selective agonist zolpidem is conferred by the α1βγ2 subunit combination. We examined four properties of miniature inhibitory postsynaptic currents (mIPSCs) from identified necortical pyramidal cells in rat brain slices: decay time constant, peak amplitude, rate of rise, and interevent interval. Exposure to 50 μM zinc reduced the decay time constant, peak amplitude, and rate of rise with no effect on interevent interval. Zolpidem enhanced mIPSCs in a concentration-dependent manner. Both 20 and 100 nM zolpidem increased the decay time constants of mIPSCs. In some cells, both peak amplitude and rate of rise were also enhanced. All cells treated with zinc were also responsive to zolpidem. These results show that neocortical pyramidal cells have a population of GABAA receptors sensitive to both zinc and zolpidem.
Reticulospinal Systems Mediate Atonia With Short and Long Latencies
Authors: Kohyama Jun , Lai Yuan-Yang , Siegel Jerome M.
Published: December 2017

Kohyama, Jun, Yuan-Yang Lai, and Jerome M. Siegel. Reticulospinal systems mediate atonia with short and long latencies. J. Neurophysiol. 80: 000–000, 1998. The pontomedullary region is responsible for both the tonic and phasic reduction of muscle activity in rapid-eye-movement sleep and contributes to the control of muscle tone in waking. This study focused on determining the time course of activity in the pontomedullary systems mediating atonia. Short-train stimulations (3 0.2-ms pulses at 330 Hz) of the pons and medulla suppressed neck and hindlimb muscle activity in decerebrate cats. We identified two distinct phases of suppression, early and late. The anatomic sites that produced each suppression were intermixed. We estimated the dividing value of the conduction velocity for reticulospinal projections responsible for early and late phases of hindlimb muscle tone suppression to be 22.8 m/s. In the medial medulla, 238 reticulospinal units, which send axons to the L1 level of the spinal cord, were identified. Pontine stimulation that suppressed hindlimb muscle tone increased the firing rate of 138 units (type I). Sixteen type I units showed a delayed response to the pontine stimulation with a latency of 10 ms or longer (type Id), whereas 122 type I units exhibited an earlier response (type Ie). Seven type Ie units had an axonal conduction velocity of <22.8 m/s, whereas the remaining 115 conducted at faster than 22.8 m/s. Early and late hindlimb muscle tone suppressions were hypothesized to be mediated through fast and slow conducting type Ie reticulospinal units. The activity of type Id neurons may contribute to the cessation of the early-phase suppression as well as to the induction, maintenance, or cessation of the late-phase suppression.
Coexpression of Multiple Metabotropic Glutamate Receptors in Axon Terminals of Single Suprachiasmatic Nucleus Neurons
Authors: Chen Gong , van den Pol Anthony N.
Published: December 2017

Chen, Gong and Anthony N. van den Pol. Coexpression of multiple metabotropic glutamate receptors in axon terminals of single suprachiasmatic nucleus neurons. J. Neurophysiol. 80: 1932–1938, 1998. Glutamate is the primary excitatory transmitter in axons innervating the hypothalamic suprachiasmatic nucleus (SCN) and is responsible for light-induced phase shifts of circadian rhythms generated by the SCN. By using self-innervating single neuron cultures and patch-clamp electrophysiology, we studied metabotropic glutamate receptors (mGluRs) expressed by SCN neurons. The selective agonists for group I (3,5-dihydroxy-phenylglycine), group II ((S)-4-carboxy-3-hydroxyphenylglycine), and group III (l(+)-2-amino-4-phosphonobutyric acid) mGluRs all depressed the evoked IPSC in a subset (33%) of single autaptic neurons, suggesting a coexpression of all three groups of mGluRs in the same axon terminals of a single neuron. Other neurons showed a variety of combinations of mGluRs, including an expression of only one group of mGluR (18%) or coexpression of two groups of mGluRs (27%). Some neurons had no response to any of the three agonists (22%). The three mGluR agonists had no effect on postsynaptic γ-aminobutyric acid (GABA) receptor responses, indicating a presynaptic modulation of GABA release by mGluRs. We conclude that multiple mGluRs that act through different second messenger pathways are coexpressed in single axon terminals of SCN neurons where they modulate the release of GABA presynaptically, usually inhibiting release.
Intracellular Sodium and Calcium Homeostasis During Hypoxia in Dopamine Neurons of Rat Substantia Nigra Pars Compacta
Authors: Guatteo Ezia , Mercuri Nicola B. , Bernardi Giorgio , Knöpfel Thomas
Published: December 2017

Guatteo, Ezia, Nicola B. Mercuri, Giorgio Bernardi, and Thomas Knöpfel. Intracellular sodium and calcium homeostasis during hypoxia in dopamine neurons of rat substantia nigra pars compacta. J. Neurophysiol. 80: 2237–2243, 1998. We investigated the hypoxia-induced disturbance of cytosolic sodium concentration ([Na+]i) and of cytosolic calcium concentration ([Ca2+]i) in dopamine neurons of the substantia nigra pars compacta in rat midbrain slices, by combining whole cell patch-clamp recordings and microfluorometry. Transient hypoxia (3–5 min) induced an outward current (118.7 ± 15.1 pA, mean ± SE; VH= −60 mV). The development of this outward current was associated with an elevation in [Na+]iand in [Ca2+]i. The hypoxia-induced outward current as well as the elevations in [Na+]iand [Ca2+]iwere not affected by the ionotropic and metabotropic glutamate receptor antagonists d-amino-phosphonovalerate (50 μM), 6nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3-dione (10 μM) and S-(α)-methyl-4-carboxyphenylglycine (500 μM). Tolbutamide, a blocker of ATP-dependent K+channels, depressed the hypoxia-induced outward current but did not affect the increases in [Na+]ior [Ca2+]i. Increasing the concentration of ATP in the internal solution from 2 to 10 mM strongly reduced the hypoxia-induced outward current but did not reduce the rise in [Na+]i. Decreasing the concentration of extracellular Na+to 19.2 mM depressed the hypoxia-induced outward current and resulted in a decrease in resting [Na+]i. Under this condition hypoxia still increased [Na+]i, albeit to levels not exceeding those of resting [Na+]iobserved under control conditions. We conclude that 1) a major component of the hypoxia-induced outward current of these cells is caused by a depletion of intracellular ATP in combination with an increase in [Na+]i, 2) that the [Na+]iand [Ca2+]iresponses are not mediated by glutamate receptors, 3) that the [Na+]iand [Ca2+]iresponses are not depressed by activation of sulfonylurea receptors, and 4) that the rise in [Na+]iinduced by short-lasting hypoxia is not due to a ATP depletion-induced failure of Na+extrusion.
Differential Effects of GABAAReceptor Antagonists in the Control of Respiratory Neuronal Discharge Patterns
Authors: Dogas Z. , Krolo M. , Stuth E. A. , Tonkovic-Capin M. , Hopp F. A. , McCrimmon D. R. , Zuperku E. J.
Published: December 2017

Dogas, Z., M. Krolo, E. A. Stuth, M. Tonkovic-Capin, F. A. Hopp, D. R. McCrimmon, and E. J. Zuperku. Differential effects of GABAAreceptor antagonists in the control of respiratory neuronal discharge patterns. J. Neurophysiol. 80: 2368–2377, 1998. To ascertain the role of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) in shaping and controlling the phasic discharge patterns of medullary respiratory premotor neurons, localized pressure applications of the competitive GABAAreceptor antagonist bicuculline (BIC) and the noncompetitive GABAAreceptor antagonist picrotoxin (PIC) were studied. Multibarrel micropipettes were used in halothane anesthetized, paralyzed, ventilated, vagotomized dogs to record single unit activity from inspiratory and expiratory neurons in the caudal ventral respiratory group and to picoeject GABAAreceptor antagonists. The moving time average of phrenic nerve activity was used to determine respiratory phase durations and to synchronize cycle-triggered histograms of discharge patterns. Picoejection of BIC and PIC had qualitatively different effects on the discharge patterns of respiratory neurons. BIC caused an increase in the discharge rate during the neuron's active phase without inducing activity during the neuron's normally silent phase. The resulting discharge patterns were amplified replicas (×2–3) of the underlying preejection phasic patterns. In contrast, picoejection of PIC did not increase the peak discharge rate during the neuron's active phase but induced a tonic level of activity during the neuron's normally silent phase. The maximum effective BIC dose (15 ± 1.8 pmol/min) was considerably smaller than that for PIC (280 ± 53 pmol/min). These findings suggest that GABAAreceptors with differential pharmacology mediate distinct functions within the same neuron, 1) gain modulation that is BIC sensitive but PIC insensitive and 2) silent-phase inhibition blocked by PIC. These studies also suggest that the choice of an antagonist is an important consideration in the determination of GABA receptor function within the respiratory motor control system.
Potassium Conductance Causing Hyperpolarization of CA1 Hippocampal Neurons During Hypoxia
Authors: Erdemli G. , Xu Y. Z. , Krnjevic K.
Published: December 2017

Erdemli, G., Y. Z. Xu, and K. Krnjević. Potassium conductance causing hyperpolarization of CA1 hippocampal neurons during hypoxia. J. Neurophysiol. 80: 2378–2390, 1998. In experiments on slices (from 100- to 150-g Sprague-Dawley rats) kept at 33°C, we studied the effects of brief hypoxia (2–3 min) on CA1 neurons. In whole cell recordings from submerged slices, with electrodes containing only KMeSO4and N-2-hydroxyethylpiperazine- N′-2-ethanesulfonic acid, and in the presence of kynurenate and bicuculline (to minimize transmitter actions), hypoxia produced the following changes: under current clamp, 36 cells were hyperpolarized by 2.7 ± 0.5 (SE) mV and their input resistance ( Rin) fell by 23 ± 2.7%; in 30 cells under voltage clamp, membrane current increased by 114 ± 22.3 pA and input conductance ( Gin) by 4.9 ± 0.9 nS. These effects are much greater than those seen previously with K gluconate whole cell electrodes, but only half those seen with “sharp” electrodes. The hypoxic hyperpolarizations (or outward currents) were not reduced by intracellular ATP (1–5 mM) or bath-applied glyburide (10 μM): therefore they are unlikely to be mediated by conventional ATP-sensitive K channels. On the other hand, their depression by internally applied ethylene glycol-bis-(β-aminoethyl ether)- N, N, N′, N′-tetraacetic acid (1.1 and 11 mM) and especially 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid (11–33 mM) indicated a significant involvement of Ca-dependent K (KCa) channels. The β-adrenergic agonist isoprenaline (10 μM) reduced hypoxic hyperpolarizations and decreases in Rin( n = 4) (and in another 11 cells corresponding changes in Gin); and comparable but more variable effects were produced by internally applied 3′:5′-adenosine cyclic monophosphate (cAMP, 1 mM, n = 6) and bath-applied 8-bromo-cAMP ( n = 8). Thus afterhyperpolarization-type KCachannels probably take part in the hypoxic response. A major involvement of G proteins is indicated by the near total suppression of the hypoxic response by guanosine 5′- O-(3-thiotriphosphate) (0.1–0.3 mM, n = 23) and especially guanosine 5′- O-(2-thiodiphosphate) (0.3 mM, n = 26), both applied internally. The adenosine antagonist 8-( p-sulfophenyl)theophylline (10–50 μM) significantly reduced hypoxic hyperpolarizations and outward currents in whole cell recordings (with KMeSO4electrodes) from submerged slices but not in intracellular recordings (with KCl electrodes) from slices kept at gas/saline interface. In further intracellular recordings, antagonists of γ-aminobutyric acid-B or serotonin receptors also had no clear effect. In conclusion, these G-protein-dependent hyperpolarizing changes produced in CA1 neurons by hypoxia are probably initiated by Ca2+release from internal stores stimulated by enhanced glycolysis and a variable synergistic action of adenosine.
Raised Object on a Planar Surface Stroked Across the Fingerpad: Responses of Cutaneous Mechanoreceptors to Shape and Orientation
Authors: Lamotte R. H. , Friedman R. M. , Lu C. , Khalsa P. S. , Srinivasan M. A.
Published: December 2017

LaMotte, R. H., R. M. Friedman, C. Lu, P. S. Khalsa, and M. A. Srinivasan. Raised object on a planar surface stroked across the fingerpad: responses of cutaneous mechanoreceptors to shape and orientation. J. Neurophysiol. 80: 2446–2466, 1998. The representations of orientation and shape were studied in the responses of cutaneous mechanoreceptors to an isolated, raised object on a planar surface stroked across the fingerpad. The objects were the top portions of a sphere with a 5-mm radius, and two toroids each with a radius of 5 mm along one axis and differing radii of 1 or 3 mm along the orthogonal axis. The velocity and direction of stroking were fixed while the orientation of the object in the horizontal plane was varied. Each object was stroked along a series of laterally shifted, parallel, linear trajectories over the receptive fields of slowly adapting, type I (SA), and rapidly adapting, type I (RA) mechanoreceptive afferents innervating the fingerpad of the monkey. “Spatial event plots” (SEPs) of the occurrence of action potentials, as a function of the location of each object on the receptive field, were interpreted as the responses of a spatially distributed population of fibers. That portion of the plot evoked by the curved object (the SEPc) provided a representation of the shape and orientation of the two-dimensional outline of the object in the horizontal plane in contact with the skin. For both SAs and RAs, the major vector of the SEPc, obtained by a principal components analysis, was linearly related to the physical orientation of the major axis of each toroid. The spatial distribution of discharge rates [spatial rate surface profiles (SRSs), after plotting mean instantaneous frequency versus spatial locus within the SEPc] represented object shape in a third dimension, normal to the skin surface. The shape of the SA SRSs, well fitted by Gaussian equations, better represented object shape than that of the RA SRSs. A cross-sectional profile along the minor axis [spatial rate profile (SRP)] was approximately triangular for SAs. After normalization for differences in peak height, the falling slopes of the SA SRPs increased, and the base widths decreased with curvature of the object's minor axis. These curvature-related differences in slopes and widths were invariant with changes in object orientation. It is hypothesized that circularity in object shape is coded by the constancy of slopes of SA SRPs between peak and base and that the constancy of differences in the widths and falling slopes evoked by different raised objects encodes, respectively, the differences in their sizes and shapes regardless of differences in their orientation on the skin.
Protein Kinase C Regulates a Vesicular Class of Calcium Channels in the Bag Cell Neurons of Aplysia
Authors: White Benjamin H. , Nick Teresa A. , Carew Thomas J. , Kaczmarek Leonard K.
Published: December 2017

White, Benjamin H., Teresa A. Nick, Thomas J. Carew, and Leonard K. Kaczmarek. Protein kinase C regulates a vesicular class of calcium channels in the bag cell neurons of Aplysia. J. Neurophysiol. 80: 2514–2520, 1998. Protein kinase C (PKC) acutely increases calcium currents in Aplysia bag cell neurons by recruiting calcium channels different from those constitutively active in the plasma membrane. To study the mechanism of PKC regulation we previously identified two calcium channel α1-subunits expressed in bag cell neurons. One of these, BC-α1A, is localized to vesicles concentrated primarily in somata and growth cones. We used antibodies to BC-α1A to analyze its expression in the bag cell neurons of juvenile Aplysia at a developmental stage at which PKC-sensitive calcium currents have previously been shown to be low. We find that vesicular BC-α1A staining is generally reduced in juvenile bag cell neurons but that its expression level can vary among juvenile animals. In 17 bag cell clusters examined, the percentage of neurons that displayed punctate αBC-α1A staining ranged from 0 to 85%. Sampling of calcium currents from cells of the same clusters by whole cell patch-clamp techniques revealed that the PKC-sensitive calcium current density is significantly correlated with the degree of vesicular staining. In contrast, no correlation of basal calcium current levels with aBC-α1A staining was found. These results strongly suggest that BC-α1A, a member of the ABE-subfamily of calcium channels, carries the PKC-sensitive calcium current in bag cell neurons. They are consistent with a model in which PKC recruits channels from the vesicular pool to the plasma membrane.
Inactivation of Macroscopic Late Na+ Current and Characteristics of Unitary Late Na+ Currents in Sensory Neurons
Authors: Baker Mark D. , Bostock Hugh
Published: December 2017

Baker, Mark D. and Hugh Bostock. Inactivation of macroscopic late Na+ current and characteristics of unitary late Na+ currents in sensory neurons. J. Neurophysiol. 80: 2538–2549, 1998. Na+ currents in adult rat large dorsal root ganglion neurons were recorded during long duration voltage-clamp steps by patch clamping whole cells and outside-out membrane patches. Na+ current present >60 ms after the onset of a depolarizing pulse (late Na+ current) underwent partial inactivation; it behaved as the sum of three kinetically distinct components, each of which was blocked by nanomolar concentrations of tetrodotoxin. Inactivation of one component (late-1) of the whole cell current reached equilibrium during the first 60 ms; repolarizing to −40 or −50 mV from potentials of −30 mV or more positive gave rise to a characteristic increase in current (τ ≥ 5 ms), attributed to removal of inactivation. A second component (late-2) underwent slower inactivation (τ > 80 ms) at potentials more positive than −80 mV, and steady-state inactivation appeared complete at −30 mV. In small membrane patches, bursts of brief openings (γ = 13–18 pS) were usually recorded. The distribution of burst durations indicated that two populations of channel were present with inactivation rates corresponding to late-1 and late-2 macroscopic currents. The persistent Na+ current in the whole cell that extended to potentials more positive than −30 mV appeared to correspond to sporadic, brief openings that were recorded in patches (mean open time ∼0.1 ms) over a wide potential range. None of the three types of gating described corresponded to activation/inactivation gating overlap of fast transient currents.
Modeling of Auditory Spatial Receptive Fields With Spherical Approximation Functions
Authors: Jenison Rick L. , Reale Richard A. , Hind Joseph E. , Brugge John F.
Published: December 2017

Jenison, Rick L., Richard A. Reale, Joseph E. Hind, and John F. Brugge. Modeling of auditory spatial receptive fields with spherical approximation functions. J. Neurophysiol. 80: 2645–2656, 1998. A spherical approximation technique is presented that affords a mathematical characterization of a virtual space receptive field (VSRF) based on first-spike latency in the auditory cortex of cat. Parameterizing directional sensitivity in this fashion is much akin to the use of difference-of-Gaussian (DOG) functions for modeling neural responses in visual cortex. Artificial neural networks and approximation techniques typically have been applied to problems conforming to a multidimensional Cartesian input space. The problem with using classical planar Gaussians is that radial symmetry and consistency on the plane actually translate into directionally dependent distortion on spherical surfaces. An alternative set of spherical basis functions, the von Mises basis function (VMBF), is used to eliminate spherical approximation distortion. Unlike the Fourier transform or spherical harmonic expansions, the VMBFs are nonorthogonal, and hence require some form of gradient-descent search for optimal estimation of parameters in the modeling of the VSRF. The optimization equations required to solve this problem are presented. Three descriptive classes of VSRF (contralateral, frontal, and ipsilateral) approximations are investigated, together with an examination of the residual error after parameter optimization. The use of the analytic receptive field model in computational models of population coding of sound direction is discussed, together with the importance of quantifying receptive field gradients. Because spatial hearing is by its very nature three dimensional or, more precisely, two dimensional (directional) on the sphere, we find that spatial receptive field models are best developed on the sphere.
Neuronal Activity in Medial Frontal Cortex During Learning of Sequential Procedures
Authors: Nakamura Kae , Sakai Katsuyuki , Hikosaka Okihide
Published: December 2017

Nakamura, Kae, Katsuyuki Sakai, and Okihide Hikosaka. Neuronal activity in medial frontal cortex during learning of sequential procedures. J. Neurophysiol. 80: 2671–2687, 1998. To study the role of medial frontal cortex in learning and memory of sequential procedures, we examined neuronal activity of the presupplementary motor area (pre-SMA) and supplementary motor area (SMA) while monkeys ( n = 2) performed a sequential button press task, “2 × 5 task.” In this paradigm, 2 of 16 (4 × 4 matrix) light-emitting diode buttons (called “set”) were illuminated simultaneously and the monkey had to press them in a predetermined order. A total of five sets (called “hyperset”) was presented in a fixed order for completion of a trial. We examined the neuronal activity of each cell using two kinds of hypersets: new hypersets that the monkey experienced for the first time for which he had to find the correct orders of button presses by trial-and-error and learned hypersets that the monkey had learned with extensive practice ( n = 16 and 10 for each monkey). To investigate whether cells in medial frontal cortex are involved in the acquisition of new sequences or execution of well-learned procedures, we examined three to five new hypersets and three to five learned hypersets for each cell. Among 345 task-related cells, we found 78 cells that were more active during performance of new hypersets than learned hypersets (new-preferring cells) and 18 cells that were more active for learned hypersets (learned-preferring cells). Among new-preferring cells, 33 cells showed a learning-dependent decrease of cell activity: their activity was highest at the beginning of learning and decreased as the animal acquired the correct response for each set with increasing reliability. In contrast, 11 learned-preferring cells showed a learning-dependent increase of neuronal activity. We found a difference in the anatomic distribution of new-preferring cells. The proportion of new-preferring cells was greater in the rostral part of the medial frontal cortex, corresponding to the pre-SMA, than the posterior part, the SMA. There was some trend that learned-preferring cells were more abundant in the SMA. These results suggest that the pre-SMA, rather than SMA, is more involved in the acquisition of new sequential procedures.
Voltage Imaging of Epileptiform Activity in Slices From Rat Piriform Cortex: Onset and Propagation
Authors: Demir Rezan , Haberly Lewis B. , Jackson Meyer B.
Published: December 2017

Demir, Rezan, Lewis B. Haberly, and Meyer B. Jackson. Voltage imaging of epileptiform activity in slices from rat piriform cortex: onset and propagation. J. Neurophysiol. 80: 2727–2742, 1998. The piriform cortex is a temporal lobe structure with a very high seizure susceptibility. To investigate the spatiotemporal characteristics of epileptiform activity, slices of piriform cortex were examined by imaging electrical activity with a voltage-sensitive fluorescent dye. Discharge activity was studied for different sites of stimulation and different planes of slicing along the anterior-posterior axis. Epileptiform behavior was elicited either by disinhibition with a γ-aminobutyric acid-A receptor antagonist or by induction with a transient period of spontaneous bursting in low-chloride medium. Control activity recorded with fluorescent dye had the same pharmacological and temporal characteristics as control activity reported previously with microelectrodes. Simultaneous optical and extracellular microelectrode recordings of epileptiform discharges showed the same duration, latency, and all-or-none character as described previously with microelectrodes. Under all conditions examined, threshold electrical stimulation applied throughout the piriform cortex evoked all-or-none epileptiform discharges originating in a site that included the endopiriform nucleus, a previously identified site of discharge onset. In induced slices, but not disinhibited slices, the site of onset also included layer VI of the adjoining agranular insular cortex and perirhinal cortex, in slices from anterior and posterior piriform cortex, respectively. These locations had not been identified previously as sites of discharge onset. Thus like the endopiriform nucleus, the deep agranular insular cortex and perirhinal cortex have a very low seizure threshold. Additional subtle differences were noted between the induced and disinhibited models of epileptogenesis. Velocity was determined for discharges after onset, as they propagated outward to the overlying piriform cortex. Propagation in other directions was examined as well. In most cases, velocities were below that for action potential conduction, suggesting that recurrent excitation and/or ephaptic interactions play a role in discharge propagation. Future investigations of the cellular and organizational properties of regions identified in this study should help clarify the neurobiological basis of high seizure susceptibility.
Intracortical Inhibition and Facilitation in Different Representations of the Human Motor Cortex
Authors: Chen Robert , Tam Alda , Bütefisch Cathrin , Corwell Brian , Ziemann Ulf , Rothwell JOHN C. , Cohen Leonardo G.
Published: December 2017

Chen, Robert, Alda Tam, Cathrin Bütefisch, Brian Corwell, Ulf Ziemann, John C. Rothwell, and Leonardo G. Cohen. Intracortical inhibition and facilitation in different representations of the human motor cortex. J. Neurophysiol. 80: 2870–2881, 1998. Intracortical inhibition (ICI) and intracortical facilitation (ICF) of the human motor cortex can be studied with paired transcranial magnetic stimulation (TMS). Plastic changes and some neurological disorders in humans are associated with changes in ICI and ICF. Although well characterized in the hand representation, it is not known if ICI and ICF vary across different body part representations. Therefore we studied ICI and ICF in different motor representations of the human motor cortex. The target muscles were rectus abdominus (RA), biceps brachii (BB), abductor pollicis brevis (APB), quadriceps femoris (QF), and abductor hallucis (AH). For each muscle, we measured the rest and active motor thresholds (MTs), the motor-evoked potential (MEP) stimulus-response curve (MEP recruitment), ICI, and ICF. The effects of different interstimulus intervals (ISIs) were studied with a conditioning stimulus (CS) intensity of 80% active MT. The effects of different CS intensities were studied at ISI of 2 ms for ICI and ISI of 15 ms for ICF. MT was lowest for APB, followed by BB, AH, and QF, and was highest for RA. Except for BB, MEP recruitment was generally steeper for muscles with lower MT. ICI and ICF were present in all the motor representations tested. The stimulus intensity necessary to elicit ICI was consistently lower than that required to elicit ICF, suggesting that they are mediated by separate mechanisms. Despite wide differences in MT and MEP recruitment, the absolute CS intensities (expressed as percentage of the stimulator's output) required to elicit ICI and ICF appear unrelated to MT and MEP recruitment in the different muscles tested. These findings suggest that the intracortical mechanisms for inhibition and facilitation in different motor representations are not related to the strength of corticospinal projections.
Spatio-Temporal Subthreshold Receptive Fields in the Vibrissa Representation of Rat Primary Somatosensory Cortex
Authors: Moore Christopher I. , Nelson Sacha B.
Published: December 2017

Moore, Christopher I. and Sacha B. Nelson. Spatio-temporal subthreshold receptive fields in the vibrissa representation of rat primary somatosensory cortex. J. Neurophysiol. 80: 2882–2892, 1998. Whole cell recordings of synaptic responses evoked by deflection of individual vibrissa were obtained from neurons within adult rat primary somatosensory cortex. To define the spatial and temporal properties of subthreshold receptive fields, the spread, amplitude, latency to onset, rise time to half peak amplitude, and the balance of excitation and inhibition of subthreshold input were quantified. The convergence of information onto single neurons was found to be extensive: inputs were consistently evoked by vibrissa one- and two-away from the vibrissa that evoked the largest response (the “primary vibrissa”). Latency to onset, rise time, and the incidence and strength of inhibitory postsynaptic potentials (IPSPs) varied as a function of position within the receptive field and the strength of evoked excitatory input. Nonprimary vibrissae evoked smaller amplitude subthreshold responses [primary vibrissa, 9.1 ± 0.84 (SE) mV, n = 14; 1-away, 5.1 ± 0.5 mV, n = 38; 2-away, 3.7 ± 0.59 mV, n = 22; 3-away, 1.3 ± 0.70 mV, n = 8] with longer latencies (primary vibrissa, 10.8 ± 0.80 ms; 1-away, 15.0 ± 1.2 ms; 2-away, 15.7 ± 2.0 ms). Rise times were significantly faster for inputs that could evoke action potential responses (suprathreshold, 4.1 ± 1.3 ms, n = 8; subthreshold, 12.4 ± 1.5 ms, n = 61). In a subset of cells, sensory evoked IPSPs were examined by deflecting vibrissa during injection of hyperpolarizing and depolarizing current. The strongest IPSPs were evoked by the primary vibrissa ( n = 5/5), but smaller IPSPs also were evoked by nonprimary vibrissae ( n = 8/13). Inhibition peaked by 10–20 ms after the onset of the fastest excitatory input to the cortex. This pattern of inhibitory activity led to a functional reversal of the center of the receptive field and to suppression of later-arriving and slower-rising nonprimary inputs. Together, these data demonstrate that subthreshold receptive fields are on average large, and the spatio-temporal dynamics of these receptive fields vary as a function of position within the receptive field and strength of excitatory input. These findings constrain models of suprathreshold receptive field generation, multivibrissa interactions, and cortical plasticity.
Inositol-1,4,5-Trisphosphate Receptor-Mediated Ca Mobilization Is Not Required for Cerebellar Long-Term Depression in Reduced Preparations
Authors: Narasimhan Kalyani , Pessah Isaac N. , Linden David J.
Published: December 2017

Narasimhan, Kalyani, Isaac N. Pessah, and David J. Linden. Inositol-1,4,5-trisphosphate receptor-mediated Ca mobilization is not required for cerebellar long-term depression in reduced preparations. J. Neurophysiol. 80: 2963–2974, 1998. Cerebellar long-term depression (LTD) is a cellular model system of information storage in which coincident parallel fiber and climbing fiber activation of a Purkinje neuron (PN) gives rise to a sustained attenuation of parallel fiber–PN synaptic strength. Climbing fiber and parallel fiber inputs may be replaced by direct depolarization of the PN and exogenous glutamate pulses, respectively. The parallel fiber–PN synapse has a high-density of mGluR1 receptors that are coupled to phosphoinositide turnover. Several lines of evidence indicated that activation of mGluR1 by parallel fiber stimulation is necessary for the induction of cerebellar LTD. Because phosphoinositide hydrolysis has two initial products, 1,2-diacylglycerol and inositol-1,4,5-trisphosphate (IP3), we wished to determine whether IP3 signaling via IP3 receptors and consequent Ca mobilization were necessary for the induction of cerebellar LTD. First, ratiometric imaging of free cytosolic Ca was performed on both acutely dissociated and cultured PNs. It was determined that the threshold for glutamate pulses to contribute to LTD induction was below the threshold for producing a Ca transient. Furthermore, the Ca transients produced by depolarization alone and glutamate plus depolarization were not significantly different. Second, the potent and selective IP3 receptor channel blocker xestospongin C was not found to affect the induction of LTD in either acutely dissociated or cultured PNs at a concentration that was sufficient to block mGluR1-evoked Ca mobilization. Third, replacement of mGluR activation by exogenous synthetic diacylglycerol in an LTD induction protocol was successful. Taken together, these results suggest that activation of an IP3 signaling cascade is not required for induction of cerebellar LTD in reduced preparations.