bluuebunny/crossref_metadata_2025 huggingface dataset:
Effect of Temperature on Electrical Resonance in Leopard Frog Saccular Hair Cells
Authors: Smotherman M. S. , Narins P. M.
Published: December 2017

Smotherman, M. S. and P. M. Narins. Effect of temperature on electrical resonance in leopard frog saccular hair cells. J. Neurophysiol. 79: 312–321, 1998. Leopard frog saccular hair cells exhibit an electrical resonance in response to a depolarizing stimulus that has been proposed to contribute to the tuning properties of the frog sacculus by acting as an electrical band-pass filter. With the whole cell patch-clamp technique, we have investigated the effect of temperature on electrical resonances in isolated saccular hair cells, and we have described the effects of temperature on the currents and channel kinetics underlying electrical resonance. A hair cell's onset resonant frequency in response to a constant depolarizing current pulse increases linearly with temperature at a rate of 11 Hz/1°C, exhibiting a mean Q 10 of 1.7 between 15 and 35°C. However, offset resonant frequencies continue to double every 10°C, exhibiting a mean Q 10 of 2.1. If steady-state voltage during the stimulus is held constant, all oscillatory frequencies increase with a mean Q 10 of 2.1. The average level of steady-state depolarization during a +150-pA depolarizing current pulse decreases with increasing temperature (−6 mV from 15 to 25°C). This temperature-dependent reduction of the steady-state membrane potential causes a shift in the voltage-dependent channel kinetics to slower rates, thus reducing the apparent Q 10 for onset resonant frequencies. The peak outward tail current and net steady-state outward current, which is the sum of a voltage-dependent inward calcium current ( I Ca) and an outward calcium-dependent potassium current ( I K(Ca)), increase with temperature, exhibiting a mean Q 10 of 1.7 between 15 and 25°C. The activation rate ( T 1/2) of the outward current exhibits a mean Q 10 of 2.3 between 15 and 25°C, while the deactivation rate (τrel) exhibits a mean Q 10 of 2.9 over the same temperature range. These results support previous models of the molecular determination of resonant frequency, which have proposed that a combination of I K(Ca) channel kinetics and the overall magnitude of the outward current are primarily responsible for determining the resonant frequency of an isolated hair cell. The robust temperature sensitivity of the hair cell receptor potential contrasts sharply with the temperature-insensitive tuning properties of in vivo saccular nerve fiber recordings. Possible explanations for this discrepancy are discussed.
Postinhibitory Rebound During Locomotor-Like Activity in Neonatal Rat Motoneurons In Vitro
Authors: Bertrand Sandrine , Cazalets Jean-René
Published: December 2017

Bertrand, Sandrine and Jean-René Cazalets. Postinhibitory rebound during locomotor-like activity in neonatal rat motoneurons in vitro. J. Neurophysiol. 79: 342–351, 1998. The aim of this study was to establish how a membrane property contributes to the neuronal discharge during ongoing behavior. We therefore studied the role of the postinhibitory rebound (PIR) in the bursting discharge of lumbar motoneurons intracellularly recorded in newborn rat in vitro brain stem/spinal cord preparation. The PIR is a transient depolarization that occurs after a hyperpolarization. We first investigated how it was expressed during experimentally induced hyperpolarizations. Its amplitude increased with the inhibition and was voltage dependent. The Ca2+ channel blockers Mn2+ and Co2+ partly suppressed the PIR in a few of the motoneurons tested. When hyperpolarized, the motoneurons exhibited a sag that was associated with the PIR. Adding caesium to the bath abolished both sag and rebound, which suggested that the PIR in the lumbar motoneurons was mainly due to the activation of the inward rectifying current I Q. In the second part, we studied the physiological involvement of PIR during fictive locomotion induced by bath application of N-methyl-d-l-aspartate and serotonin. We established that experimentally induced PIR could initiate or modulate the bursting discharge of motoneurons during fictive locomotion. We then studied whether the firing patterns of the motoneurons were correlated in one way with the synaptic inhibition. When the monosynaptic inhibitory input to the motoneurons was abolished with the glycinergic blocker strychnine, these neurons stopped discharging (although they still were depolarized rhythmically). The firing of action potentials was restored by applying negative current pulses. This study provides evidence as to how one membrane property in mammals is involved in a complex type of behavior, namely locomotion.
Early Locomotor Training With Clonidine in Spinal Cats
Authors: Chau Connie , Barbeau Hugues , Rossignol Serge
Published: December 2017

Chau, Connie, Hugues Barbeau, and Serge Rossignol. Early locomotor training with clonidine in spinal cats. J. Neurophysiol. 79: 392–409, 1998. Clonidine, a noradrenergic alpha-2 agonist, can initiate locomotion early after spinalization in cats. Because this effect lasts 4–6 h, we have injected clonidine daily, intraperitoneally or intrathecally, and intensively trained five spinal cats to perform hindlimb walking on a treadmill starting at day 3 and continuing until 10 days posttransection. Each day, clonidine was injected to induce locomotor activity and cats were trained to walk with as much weight support as possible and at different speeds during multiple (1–5) locomotor training sessions, each lasting from 10 to 20 min, until the effects of clonidine wore off. Electromyographic (EMG) activity synchronized to video images of the hindlimbs were recorded before and after each clonidine injection. The results showed, first, a day-to-day change of the locomotor pattern induced by clonidine from the 3rd to the 11th day including an increase in the duration of the step cycle, an increase in the duration of extensor EMG activity, and an increase in total angular excursion of the hip, knee, and ankle joints. Second, after 6–11 days of this regimen, there was an emergence of a coordinated locomotor pattern with weight support of the hindquarters that was visible even before that day's clonidine injection. The results suggested that daily injection of clonidine followed by early and daily interactive locomotor training can enhance the recovery of locomotion in spinal cats.
Transmitter Regulation of Plateau Properties in Turtle Motoneurons
Authors: Svirskis Gytis , Hounsgaard Jørn
Published: December 2017

Svirskis, Gytis and Jørn Hounsgaard. Transmitter regulation of plateau properties in turtle motoneurons. J. Neurophysiol. 79: 45–50, 1998. In motoneurons, generation of plateau potentials is promoted by modulators that block potassium channels. In voltage-clamp experiments with triangular voltage ramp commands, we show that cis-(±)-1-aminocyclopentane-1,3-dicarboxylic acid ( cis-ACPD) and muscarine promote the generation of plateau potentials by increasing the dihydropyridine sensitive inward current, by increasing the input resistance, and by depolarizing the resting membrane potential. Type I metabotropic glutamate receptors (mGluR I) mediate the effects of cis-ACPD. Baclofen suppresses generation of plateau potentials by decreasing the dihydropyridine sensitive inward current, by decreasing the input resistance, and by hyperpolarizing the resting membrane potential. These results suggest that membrane properties of motoneurons are continuously modulated by synaptic activity in ways that may have profound effects on synaptic integration and pattern generation.
Parietal Cortex and Spatial-Postural Transformation During Arm Movements
Authors: Rushworth M.F.S. , Johansen-Berg H. , Young S. A.
Published: December 2017

Rushworth, M.F.S., H. Johansen-Berg, and S. A. Young. Parietal cortex and spatial-postural transformation during arm movements. J. Neurophysiol. 79: 478–482, 1998. Cells in the parietal motor areas 5, MIP, and 7b have spatially tuned activity during movements. Lesions, however, do not disrupt visual reaching or learned nonspatial movement selection. The role of such parietal cells in sensorimotor coordinate transformations is unclear. The present experiment investigates whether the parietal motor areas are concerned with the following: 1) the transformation between the desired position in space of the hand and the limb's postural configuration during movement and 2) interjoint coordination. Six macaque monkeys were trained to reach in the dark. Spatial-postural transformations assume a simple form in the absence of vision and so may be most easily studied when animals reach in the dark. A lesion was placed in the parietal cortex that included areas 5, MIP, and 7b of three macaques. The simple relation between hand position and limb postural configuration seen in controls was disrupted after the lesion. The intercoordination of movements of the hand with those of the rest of the arm was also affected. The lesion did not affect the range or velocity of joint movements or the curvature of the hand's trajectory. The cell activity in parietal areas 5, MIP, and 7b may not be essential for the transformation between retinocentric representation of the target and shoulder centered representations of the desired position of the hand, but it is essential for both the subsequent transformation between desired hand position and the postural configuration of the arm and for interjoint integration.
Differential Expression of Kv4 K+ Channel Subunits Mediating Subthreshold Transient K+ (A-Type) Currents in Rat Brain
Authors: Serôdio Paulo , Rudy Bernardo
Published: December 2017

Serôdio, Paulo and Bernardo Rudy. Differential expression of Kv4 K+ channel subunits mediating subthreshold transient K+(A-type) currents in rat brain. J. Neurophysiol. 79: 1081–1091, 1998. The mammalian Kv4 gene subfamily and its Drosophila Shal counterpart encode proteins that form fast inactivating K+ channels that activate and inactivate at subthreshold potentials and recover from inactivation at a faster rate than other inactivating Kv channels. Taken together, the properties of Kv4 channels compare best with those of low-voltage activating “A-currents” present in the neuronal somatodendritic compartment and widely reported across several types of central and peripheral neurons, as well as the (Ca2+-independent) transient outward potassium conductance of heart cells ( I to). Three distinct genes have been identified that encode mammalian Shal homologs (Kv4.1, Kv4.2, and Kv4.3), of which the latter two are abundant in rat adult brain and heart tissues. The distribution in the adult rat brain of the mRNA transcripts encoding the three known Kv4 subunits was studied by in situ hybridization histochemistry. Kv4.1 signals are very faint, suggesting that Kv4.1 mRNAs are expressed at very low levels, but Kv4.2 and Kv4.3 transcripts appear to be abundant and each produces a unique pattern of expression. Although there is overlap expression of Kv4.2 and Kv4.3 transcripts in several neuronal populations, the dominant feature is one of differential, and sometimes reciprocal expression. For example, Kv4.2 transcripts are the predominant form in the caudate-putamen, pontine nucleus and several nuclei in the medula, whereas the substantia nigra pars compacta, the restrosplenial cortex, the superior colliculus, the raphe, and the amygdala express mainly Kv4.3. Some brain structures contain both Kv4.2 and Kv4.3 mRNAs but each dominates in distinct neuronal subpopulations. For example, in the olfactory bulb Kv4.2 dominates in granule cells and Kv4.3 in periglomerular cells. In the hippocampus Kv4.2 is the most abundant isoform in CA1 pyramidal cells, whereas only Kv4.3 is expressed in interneurons. Both are abundant in CA2-CA3 pyramidal cells and in granule cells of the dentate gyrus, which also express Kv4.1. In the dorsal thalamus strong Kv4.3 signals are seen in several lateral nuclei, whereas medial nuclei express Kv4.2 and Kv4.3 at moderate to low levels. In the cerebellum Kv4.3, but not Kv4.2, is expressed in Purkinje cells and molecular layer interneurons. In the cerebellar granule cell layer, the reciprocity between Kv4.2 and Kv4.3 is observed in subregions of the same neuronal population. In fact, the distribution of Kv4 channel transcripts in the cerebellum defines a new pattern of compartmentation of the cerebellar cortex and the first one involving molecules directly involved in signal processing.
Dorsal Premotor Cortex and Conditional Movement Selection: A PET Functional Mapping Study
Authors: Grafton S. T. , Fagg A. H. , Arbib M. A.
Published: December 2017

Grafton, S. T., A. H. Fagg, and M. A. Arbib. Dorsal premotor cortex and conditional movement selection: a PET functional mapping study. J. Neurophysiol. 79: 1092–1097, 1998. Positron emission tomography (PET) brain mapping was used to investigate whether or not human dorsal premotor cortex is involved in selecting motor acts based on arbitrary visual stimuli. Normal subjects performed four movement selection tasks. A manipulandum with three graspable stations was used. An imperative visual cue (LEDs illuminated in random order) indicated which station to grasp next with no instructional delay period. In a power task, a large aperture power grip was used for all trials, irrespective of the LED color. In a precision task, a pincer grasp of thumb and index finger was used. In a conditional task, the type of grasp (power or precision) was randomly determined by LED color. Comparison of the conditional selection task versus the average of the power and precision tasks revealed increased blood flow in left dorsal premotor cortex and superior parietal lobule. The average rate of producing the different grasp types and transport to the manipulandum stations was equivalent across this comparison, minimizing the contribution of movement attributes such as planning the individual movements (as distinct from planning associated with use of instructional stimuli), kinematics, or direction of target or limb movement. A comparison of all three movement tasks versus a rest task identified movement related activity involving a large area of central, precentral and postcentral cortex. In the region of the precentral sulcus movement related activity was located immediately caudal to the area activated during selection. The results establish a role for human dorsal premotor cortex and superior parietal cortex in selecting stimulus guided movements and suggest functional segregation within dorsal premotor cortex.
Effects of Hyposmolar Solutions on Membrane Currents of Hippocampal Interneurons and Mossy Cells In Vitro
Authors: Baraban Scott C. , Schwartzkroin Philip A.
Published: December 2017

Baraban, Scott C. and Philip A. Schwartzkroin. Effects of hyposmolar solutions on membrane currents of hippocampal interneurons and mossy cells in vitro. J. Neurophysiol. 79: 1108–1112, 1998. Whole cell voltage-clamp recordings in rat hippocampal slices were used to investigate the effect of changes in extracellular osmolarity on voltage-activated potassium currents. Currents were evoked from oriens/alveus (O/A) interneurons, hilar interneurons, and mossy cells. Hyposmolar external solutions produced a significant potentiation of K+ current recorded from O/A and hilar interneurons, but not from mossy cells. Hyposmolar solutions also dramatically potentiated the spontaneous excitatory postsynaptic currents recorded from mossy cells. These results suggest that hippocampal excitability can be modulated by the complex actions exerted by changes in extracellular osmolarity.
Zn2+ Blocks the NMDA- and Ca2+-Triggered Postexposure Current I pe in Hippocampal Pyramidal Cells
Authors: Chen Qiang X. , Perkins Katherine L. , Wong Robert K. S.
Published: December 2017

Chen, Qiang X., Katherine L. Perkins, and Robert K. S. Wong. Zn2+ blocks the NMDA- and Ca2+-triggered postexposure current I pe in hippocampal pyramidal cells. J. Neurophysiol. 79: 1124–1126, 1998. Whole cell voltage-clamp recordings from acutely isolated hippocampal CA1 pyramidal cells from adult guinea pigs were used to evaluate divalent cations as possible blockers of the postexposure current ( I pe). I pe is a cation current that is triggered by the rise in intracellular Ca2+ concentration that occurs after the application of a toxic level of N-methyl-d-aspartate (NMDA). Once triggered, I pe continues to grow until death of the neuron occurs. I pe may be a critical link between transient NMDA exposure and cell death. I pe was blocked by micromolar concentrations of Zn2+. The Zn2+ effect had an IC50 of 64 μM and saturated at 500 μM. Prolonged Zn2+ block of I pe revealed that the maintenance of a steady I pe is not dependent on I pe-mediated Ca2+ influx but that the continuous growth in I pe is dependent on I pe-mediated Ca2+ influx. The availability of an effective blocker of I pe should facilitate the investigation of the intracellular activation pathway of I pe and the role of I pe in neuronal death.
Protein Kinase C Is Required for Long-Lasting Synaptic Enhancement by the Neuropeptide DRNFLRFamide in Crayfish
Authors: Friedrich Rainer W. , Molnar G. F. , Schiebe Michael , Mercier A. Joffre
Published: December 2017

Friedrich, Rainer W., G. F. Molnar, Michael Schiebe, and A. Joffre Mercier. Protein kinase C is required for long-lasting synaptic enhancement by the neuropeptide DRNFLRFamide in crayfish. J. Neurophysiol. 79: 1127–1131, 1998. The FMRFamide-related neuropeptide AspArgAsnPheLeuArgPhe-NH2(DRNFLRFamide, DF2) induces a long-lasting enhancement of synaptic transmission at neuromuscular junctions on the crayfish deep abdominal extensor muscles. Here we investigated the function of protein kinase C (PKC) in this effect because PKC has been implied in the control of long-term synaptic modulation in other systems. The general kinase antagonist staurosporine reduced both the initial increase in excitatory postsynaptic potential (EPSP) amplitude and the duration of synaptic enhancement. Unlike staurosporine, the selective PKC inhibitors, chelerythrine and bisindolylmaleimide, augmented the initial EPSP increase. However, like staurosporine, they also reduced the duration of synaptic enhancement. The PKC activator, phorbol-12-myristate 13-acetate, induced a long-lasting synaptic enhancement that was blocked by chelerythrine. These results show that synaptic enhancement by DF2is mediated by different intracellular signaling systems that act in temporal sequence. The initial increase in EPSP amplitudes is negatively regulated by PKC and involves another, staurosporine-sensitive, kinase; whereas, the maintenance of synaptic enhancement requires PKC.
Functional and Pharmacological Differences Between RecombinantN-Methyl-d-Aspartate Receptors
Authors: Vicini Stefano , Wang Jian Feng , Li Jin Hong , Zhu Wei Jian , Wang Yue Hua , Luo Jian Hong , Wolfe Barry B. , Grayson Dennis R.
Published: December 2017

Vicini, Stefano, Jian Feng Wang, Jin Hong Li, Wei Jian Zhu, Yue Hua Wang, Jian Hong Luo, Barry B. Wolfe, and Dennis R. Grayson. Functional and pharmacological differences between recombinant N-methyl-d-aspartate receptors. J. Neurophysiol. 79: 555–566, 1998. N-methyl-d-aspartic acid (NMDA) receptors transiently transfected into mammalian HEK-293 cells were characterized with subunit-specific antibodies and electrophysiological recordings. Deactivation time course recorded in response to fastl-glutamate pulses were studied in isolated and lifted cells, as well as in outside-out membrane patches excised from cells expressing recombinant NR1 subunits in combination with the NR2A, NR2B, NR2C, or NR2D NMDA receptor subunits. Transfected cells were preidentified by the fluorescence emitted from the coexpressed Aequorea victoria jellyfish Green Lantern protein. Currents generated by NR1/NR2A channels displayed double exponential deactivation time course being faster than that in NR1/NR2B or NR1/NR2C channels. However, a large decay variability was observed within each cotransfection, suggesting that mechanisms additional to subunit composition may also regulate deactivation time course. NR1/NR2D channels displayed slowly deactivating currents. Channel deactivation was fast and comparable among receptors obtained by cotransfecting five distinct spliced variants of the NR1 subunit, each with the NR2A subunit. Additionally, recovery from desensitization was slower for NR1/NR2B than for NR1/NR2A channels. The average deactivation time course of responses to brief l-glutamate applications in cells where NR1/NR2A/NR2B cDNAs were cotransfected at variable ratio was intermediate between those of the NR1/NR2A and NR1/NR2B channels. Although immunocytochemical evidence indicates that the majority of cells are cotransfected by all plasmids in triple transfection, our experimental condition did not allow for a tight control of the expression of NMDA receptor subunits. This produced the result that many cells were characterized by deactivation time course and haloperidol sensitivities of separate NR1/NR2A and NR1/NR2B subunit heteromers. We also speculate on the possible formation of channels resulting from the coassembly in the same receptor of NR1/NR2A/NR2B subunits from a minority of cells that gave responses to brief application of l-glutamate characterized by slow deactivation time course and decreased haloperidol sensitivity.
Functional Characterization of Ion Permeation Pathway in the N-Type Ca2+Channel
Authors: Wakamori Minoru , Strobeck Mark , Niidome Tetsuhiro , Teramoto Tetsuyuki , Imoto Keiji , Mori Yasuo
Published: December 2017

Wakamori, Minoru, Mark Strobeck, Tetsuhiro Niidome, Tetsuyuki Teramoto, Keiji Imoto, and Yasuo Mori. Functional characterization of ion permeation pathway in the N-type Ca2+channel. J. Neurophysiol. 79: 622–634, 1998. Multiple types of high-voltage-activated Ca2+channels, including L-, N-, P-, Q- and R-types have been distinguished from each other mainly employing pharmacological agents that selectively block particular types of Ca2+channels. Except for the dihydropyridine-sensitive L-type Ca2+channels, electrophysiological characterization has yet to be conducted thoroughly enough to biophysically distinguish the remaining Ca2+channel types. In particular, the ion permeation properties of N-type Ca2+channels have not been clarified, although the kinetic properties of both the L- and N-type Ca2+channels are relatively well described. To establish ion conducting properties of the N-type Ca2+channel, we examined a homogeneous population of recombinant N-type Ca2+channels expressed in baby hamster kidney cells, using a conventional whole cell patch-clamp technique. The recombinant N-type Ca2+channel, composed of the α1B, α2a, and β1asubunits, displayed high-voltage-activated Ba2+currents elicited by a test pulse more positive than −30 mV, and were strongly blocked by the N-type channel blocker ω-conotoxin-GVIA. In the presence of 110 mM Ba2+, the unitary current showed a slope conductance of 18.2 pS, characteristic of N-type channels. Ca2+and Sr2+resulted in smaller ion fluxes than Ba2+, with the ratio 1.0:0.72:0.75 of maximum conductance in current-voltage relationships of Ba2+, Ca2+, and Sr2+currents, respectively. In mixtures of Ba2+and Ca2+, where the Ca2+concentration was steadily increased in place of Ba2+, with the total concentration of Ba2+and Ca2+held constant at 3 mM, the current amplitude went through a clear minimum when 20% of the external Ba2+was replaced by Ca+2. This anomalous mole fraction effect suggests an ion-binding site where two or more permeant ions can sit simultaneously. By using an external solution containing 110 mM Na+without polyvalent cations, inward Na+currents were evoked by test potentials more positive than −50 mV. These currents were activated and inactivated in a kinetic manner similar to that of Ba2+currents. Application of inorganic Ca2+antagonists blocked Ba2+currents through N-type channels in a concentration-dependent manner. The rank order of inhibition was La3+≥ Cd2+≫ Zn2+> Ni2+≥ Co2+. When a short strong depolarization was applied before test pulses of moderate depolarizing potentials, relief from channel blockade by La3+and Cd2+and subsequent channel reblocking was observed. The measured rate (2 × 108M−1s−1) of reblocking approached the diffusion-controlled limit. These results suggest that N-type Ca2+channels share general features of a high affinity ion-binding site with the L-type Ca2+channel, and that this site is easily accessible from the outside of the channel pore.
Functional Changes in Potassium Conductances of the Human Neuroblastoma Cell Line SH-SY5Y During In Vitro Differentiation
Authors: Tosetti Patrizia , Taglietti Vanni , Toselli Mauro
Published: December 2017

Tosetti, Patrizia, Vanni Taglietti, and Mauro Toselli. Functional changes in potassium conductances of the human neuroblastoma cell line SH-SY5Y during in vitro differentiation. J. Neurophysiol. 79: 648–658, 1998. The electrophysiological properties of voltage-dependent outward currents were investigated under voltage-clamp conditions in the human neuroblastoma cell line SH-SY5Y before and after in vitro differentiation with retinoic acid, by using the whole cell variant of the patch-clamp technique. Voltage steps to depolarizing potentials from a holding level of −90 mV elicited, in both undifferentiated and differentiated cells, outward potassium currents that were blocked by tetraethylammonium, but were unaffected by 4-aminopyridine, cadmium, and by shifts of the holding potentials to −40 mV. These currents activated rapidly and inactivated slowly in a voltage-dependent manner. In undifferentiated cells the threshold for current activation was about −30 mV, with a steady-state half activation potential of 19.5 mV. Maximum conductance was 4.3 nS and mean conductance density was 0.34 mS/cm2. Steady-state half inactivation potential was −13.8 mV and ∼10% of the current was resistant to inactivation. Both activation and inactivation kinetics were voltage dependent. In differentiated cells the threshold for current activation was about −20 mV, with a half potential for steady-state activation of 37.0 mV. Maximum conductance was 15.2 nS and mean conductance density was 0.78 mS/cm2. Steady-state half inactivation potential was −9.7 mV and ∼37% of the current was resistant to inactivation. Both activation and inactivation kinetics were voltage dependent. This diversity in potassium channel properties observed between undifferentiated and differentiated cells was related to differences in cell excitability. Under current-clamp conditions, the action potential repolarization rate in differentiated cells was about threefold faster than that of the abortive action potentials elicitable in undifferentiated cells. Furthermore, during prolonged stimulation, trains of spikes could be generated in some differentiated cells but not in undifferentiated cells.
Opioid Receptor-Mediated Inhibition of ω-Conotoxin GVIA-Sensitive Calcium Channel Currents in Rat Intracardiac Neurons
Authors: Adams David J. , Trequattrini Carlo
Published: December 2017

Adams, David J. and Carlo Trequattrini. Opioid receptor-mediated inhibition of ω-conotoxin GVIA-sensitive calcium channel currents in rat intracardiac neurons. J. Neurophysiol. 79: 753–762, 1998. Modulation of depolarization-activated ionic conductances by opioid receptor agonists was investigated in isolated parasympathetic neurons from neonatal rat intracardiac ganglia by using the whole cell perforated patch clamp technique. Met-enkephalin (10 μM) altered the action potential waveform, reducing the maximum amplitude and slowing the rate of rise and repolarization but the afterhyperpolarization was not appreciably altered. Under voltage clamp, 10 μM Met-enkephalin selectively and reversibly inhibited the peak amplitude of high-voltage–activated Ca2+ channel currents elicited at 0 mV by ∼52% and increased three- to fourfold the time to peak. Met-enkephalin had no effect on the voltage dependence of steady-state inactivation but shifted the voltage dependence of activation to more positive membrane potentials whereby stronger depolarization was required to open Ca2+ channels. Half-maximal inhibition of Ba2+ current ( I Ba) amplitude was obtained with 270 nM Met-enkephalin or Leu-enkephalin. The opioid receptor subtype selective agonists, DAMGO and DADLE, but not DPDPE, inhibited I Ba and were antagonized by the opioid receptor antagonists, naloxone and naltrindole with IC50s of 84 nM and 1 μM, respectively. The κ-opioid receptor agonists, bremazocine and dynorphin A, did not affect Ca2+ channel current amplitude or kinetics. Taken together, these data suggest that enkephalin-induced inhibition of Ca2+ channels in rat intracardiac neurons is mediated primarily by the μ-opioid receptor type. Addition of Met-enkephalin after exposure to 300 nM ω-conotoxin GVIA, which blocked ∼75% of the total Ca2+ channel current, failed to cause a further decrease of the residual current. Met-enkephalin inhibited the ω-conotoxin GVIA-sensitive but not the ω-conotoxin-insensitive I Ba in rat intracardiac neurons. Dialysis of the cell with a GTP-free intracellular solution or preincubation of the neurons in Pertussis toxin (PTX) abolished the attenuation of I Ba by Met-enkephalin, suggesting the involvement of a PTX-sensitive Gprotein in the signal transduction pathway. The activation of μ-opioid receptors and subsequent inhibition of N-type Ca2+ channels in the soma and terminals of postganglionic intracardiac neurons is likely to inhibit the release of ACh and thereby regulate vagal transmission to the mammalian heart.
Forebrain Pathway for Auditory Space Processing in the Barn Owl
Authors: Cohen Yale E. , Miller Greg L. , Knudsen Eric I.
Published: December 2017

Cohen, Yale E., Greg L. Miller, and Eric I. Knudsen. Forebrain pathway for auditory space processing in the barn owl. J. Neurophysiol. 79: 891–902, 1998. The forebrain plays an important role in many aspects of sound localization behavior. Yet, the forebrain pathway that processes auditory spatial information is not known for any species. Using standard anatomic labeling techniques, we used a “top-down” approach to trace the flow of auditory spatial information from an output area of the forebrain sound localization pathway (the auditory archistriatum, AAr), back through the forebrain, and into the auditory midbrain. Previous work has demonstrated that AAr units are specialized for auditory space processing. The results presented here show that the AAr receives afferent input from Field L both directly and indirectly via the caudolateral neostriatum. Afferent input to Field L originates mainly in the auditory thalamus, nucleus ovoidalis, which, in turn, receives input from the central nucleus of the inferior colliculus. In addition, we confirmed previously reported projections of the AAr to the basal ganglia, the external nucleus of the inferior colliculus (ICX), the deep layers of the optic tectum, and various brain stem nuclei. A series of inactivation experiments demonstrated that the sharp tuning of AAr sites for binaural spatial cues depends on Field L input but not on input from the auditory space map in the midbrain ICX: pharmacological inactivation of Field L eliminated completelyauditory responses in the AAr, whereas bilateral ablation of the midbrain ICX had no appreciable effect on AAr responses. We conclude, therefore, that the forebrain sound localization pathway can process auditory spatial information independently of the midbrain localization pathway.
Self-Inhibition in Ca2+-Evoked Taste Responses: A Novel Tool for Functional Dissection of Salt Taste Transduction Mechanisms
Authors: Kloub Mamoun A. , Heck Gerard L. , Desimone John A.
Published: December 2017

Kloub, Mamoun A., Gerard L. Heck, and John A. DeSimone. Self-inhibition in Ca2+-evoked taste receptors: a novel tool for functional dissection of salt taste transduction mechanisms. J. Neurophysiol. 79: 911–921, 1998. Rat chorda tympani (CT) responses to CaCl2 were obtained during simultaneous current and voltage clamping of the lingual receptive field. Unlike most other salts, CaCl2 induced negatively directed transepithelial potentials and gave CT responses that were auto-inhibitory beyond a critical concentration. CT responses increased in a dose-dependent manner to ∼0.3 M, whereafter they decreased with increasing concentration. At concentrations where Ca2+ was self-inhibitory, it also inhibited responses to NaCl, KCl, and NH4Cl present in mixtures with CaCl2. Ca2+ completely blocked the amiloride-insensitive component of the NaCl CT response, the entire KCl-evoked CT response, and the high-concentration-domain CT responses of NH4Cl (≥0.3 M). The overlapping Ca2+-sensitivity between the responses of the three Cl− salts (Na+, K+, and NH+ 4) suggests a common, Ca2+-sensitive, transduction pathway. Extracellular Ca2+ has been shown to modulate the paracellular pathways in different epithelial cell lines by decreasing the water permeability and cation conductance of tight junctions. Ca2+-induced modulation of tight junctions is associated with Ca2+ binding to fixed negative sites. This results in a conversion of ion selectivity from cationic to anionic, which we also observed in our system through simultaneous monitoring of the transepithelial potential during CT recording. The data indicate the paracellular pathway as the stimulatory and modulatory site of CaCl2 taste responses. In addition, they indicate that important transduction sites for NaCl, KCl, and NH4Cl taste reception are accessible only through the paracellular pathways. More generally, they show that modulation of paracellular transport by Ca2+ in an intact epithelium has functional consequences at a systemic level.
Mechanisms Underlying the Synchronizing Action of Corticothalamic Feedback Through Inhibition of Thalamic Relay Cells
Authors: Destexhe Alain , Contreras Diego , Steriade Mircea
Published: December 2017

Destexhe, Alain, Diego Contreras, and Mircea Steriade. Mechanisms underlying the synchronizing action of corticothalamic feedback through inhibition of thalamic relay cells. J. Neurophysiol. 79: 999–1016, 1998. Early studies have shown that spindle oscillations are generated in the thalamus and are synchronized over wide cortical territories. More recent experiments have shown that this large-scale synchrony depends on the integrity of corticothalamic feedback. Previously proposed mechanisms emphasized exclusively intrathalamic mechanisms to generate the synchrony of these oscillations. In the present paper, we propose a cellular mechanism in which the synchrony is dependent of a mutual interaction between cortex and thalamus. This cellular mechanism is tested by computational models consisting of pyramidal cells, interneurons, thalamic reticular (RE) and thalamocortical (TC) relay cells, on the basis of voltage-clamp data on intrinsic currents and synaptic receptors present in the circuitry. The model suggests that corticothalamic feedback must operate on the thalamus mainly through excitation of GABAergic RE neurons, therefore recruiting relay cells essentially through inhibition and rebound. We provide experimental evidence for such dominant inhibition in the lateral posterior nucleus. In these conditions, the model shows that cortical discharges optimally evoked thalamic oscillations. This feature is essential to the present cellular mechanism and is also consistently observed experimentally. The model further shows that, with this type of corticothalamic feedback, cortical discharges recruited large areas of the thalamus because of the divergent cortex-to-RE and RE-to-TC axonal projections. Consequently, the thalamocortical network generated patterns of oscillations and synchrony similar to in vivo recordings. The model also emphasizes the important role of the modulation of the I h current by calcium in TC cells. This property conferred a relative refractoriness to the entire network, a feature also observed experimentally, as we show here. Further, the same property accounted for various spatiotemporal features of oscillations, such as systematic propagation after low-intensity cortical stimulation, local oscillations, and more generally, a high variability in the patterns of spontaneous oscillations, similar to in vivo recordings. We propose that the large-scale synchrony of spindle oscillations in vivo is the result of thalamocortical interactions in which the corticothalamic feedback acts predominantly through the RE nucleus. Several predictions are suggested to test the validity of this model.
Lateral Inhibitory Interactions in the Intermediate Layers of the Monkey Superior Colliculus
Authors: Munoz Douglas P. , Istvan Peter J.
Published: December 2017

Munoz, Douglas P. and Peter J. Istvan. Lateral inhibitory interactions in the intermediate layers of the monkey superior colliculus. J. Neurophysiol. 79: 1193–1209, 1998. The intermediate layers of the monkey superior colliculus (SC) contain neurons the discharges of which are modulated by visual fixation and saccadic eye movements. Fixation neurons, located in the rostral pole of the SC, discharge action potentials tonically during visual fixation and pause for most saccades. Saccade neurons, located throughout the remainder of the intermediate layers of the SC, discharge action potentials for saccades to a restricted region of the visual field. We defined the fixation zone as that region of the rostral SC containing fixation neurons and the saccade zone as the remainder of the SC. It recently has been hypothesized that a network of local inhibitory interneurons may help shape the reciprocal discharge pattern of fixation and saccade neurons. To test this hypothesis, we combined extracellular recording and microstimulation techniques in awake monkeys trained to perform oculomotor paradigms that enabled us to classify collicular fixation and saccade neurons. Microstimulation was used to electrically activate the fixation and saccade zones of the ipsilateral and contralateral SC to test for inhibitory and excitatory inputs onto fixation and saccade neurons. Saccade neurons were inhibited at short latencies following electrical stimulation of either the ipsilateral (1–5 ms) or contralateral (2–7 ms) fixation or saccade zones. Fixation neurons were inhibited 1–4 ms after electrical stimulation of the ipsilateral saccade zone. Stimulation of the contralateral saccade zone led to much weaker inhibition of fixation neurons. Stimulation of the contralateral fixation zone led to short-latency (1–2 ms) excitation of fixation neurons. Only a small percentage of saccade and fixation neurons were activated by the electrical stimulation (latency: 0.5–2.0 ms). These responses were confirmed as either orthodromic or antidromic responses using collision testing. The results suggest that a local network of inhibitory interneurons may help shape not only the reciprocal discharge pattern of fixation and saccade neurons but also permit lateral interactions between all regions of the ipsilateral and contralateral SC. These interactions therefore may be critical for maintaining stable visual fixation, suppressing unwanted saccades, and initiating saccadic eye movements to targets of interest.
Long-Term Changes in Excitability Induced by Protein Kinase C Activation inAplysiaSensory Neurons
Authors: Manseau Frédéric , Sossin Wayne S. , Castellucci Vincent F.
Published: December 2017

Manseau, Frédéric, Wayne S. Sossin, and Vincent F. Castellucci. Long-term changes in excitability induced by protein kinase C activation in Aplysia sensory neurons. J. Neurophysiol. 79: 1210–1218, 1998. Protein kinases A (PKA) and C (PKC) play a central role as intracellular transducers during simple forms of learning in Aplysia. These two proteins seem to cooperate in mediating the different forms of plasticity underlying behavioral modifications of defensive reflexes in a state- and time-dependent manner. Although short- and long-term changes in the synaptic efficacy of the connections between mechanosensory neurons and motoneurons of the reflex have been well characterized, there is also a distinct intermediate phase of plasticity that is not as well understood. Biochemical and physiological experiments have suggested a role for PKC in the induction and expression of this form of facilitation. In this report, we demonstrate that PKC activation can induce both intermediate- and long-term changes in the excitability of sensory neurons (SNs). Short application of 4β-phorbol ester 12,13-dibutyrate (PDBU), a potent activator of PKC, produced a long-lasting increase in the number of spikes fired by SNs in response to depolarizing current pulses. This effect was observed in isolated cell culture and in the intact ganglion; it was blocked by a selective PKC inhibitor (chelerythrine). Interestingly, the increase in excitability measured at an intermediate-term time point (3 h) after treatment was independent of protein synthesis, while it was disrupted at the long-term (24 h) time point by the general protein synthesis inhibitor, anisomycin. In addition to suggesting that PKC as well as PKA are involved in long-lasting excitability changes, these findings support the idea that memory formation involves multiple stages that are mechanistically distinct at the biochemical level.
Hemispheric Differences in Motor Cortex Excitability During a Simple Index Finger Abduction Task in Humans
Authors: Semmler John G. , Nordstrom Michael A.
Published: December 2017

Semmler, John G. and Michael A. Nordstrom. Hemispheric differences in motor cortex excitability during a simple index finger abduction task in humans. J. Neurophysiol. 79: 1246–1254, 1998.Transcranial magnetic (TMS) and electrical (TES) stimulation was used to assess the contribution of the corticospinal pathway to activation of the first dorsal interosseous muscle (FDI) in each hand of 16 right-handed subjects. TMS was applied at relaxed threshold intensity while the subject performed isometric index finger abduction at seven force levels [0.5 N to 50% maximal voluntary contraction (MVC)]. In a separate session, TES of equivalent intensity was applied to each hemisphere in 5 of these subjects while they performed the same force-matching protocol. In the resting state, mean threshold intensity for a muscle-evoked potential (MEP) in FDI using TMS was similar for the hemispheres controlling the dominant and nondominant hands. The size of the threshold MEPs in resting FDI after TMS and TES were also similar in each hand. With TMS, contraction-induced facilitation of the MEP in FDI was significantly larger when the nondominant hand was used for index finger abduction. In the pooled data, the nondominant/dominant ratio of MEP areas (normalized to the maximum M wave) ranged from 1.7 in the weakest contraction (0.5 N) to 1.1 in the strongest (50% MVC). Eight subjects had significant differences between hands in favour of the nondominant hand, whereas in two subjects contraction-induced facilitation of MEPs was larger in the dominant hand. In five subjects for whom detailed motor unit data were available from a previous study, lateral differences in MEP facilitation were positively correlated with differences in FDI motor unit synchronization between hands. With TES, contraction-induced facilitation of the MEP was similar in each hand, suggesting that spinal excitability was equivalent on both sides. For the group of five subjects tested with both stimulation techniques, contraction-induced facilitation of the MEP was significantly larger after TMS than that obtained with TES when the contraction was performed with the nondominant hand, but not when the dominant hand was used to perform the task. We conclude that the extent of corticospinal neuron involvement in the command for simple index finger abduction in right-handed subjects is generally greater when the nondominant hand is used, compared with the same task performed with the dominant hand.
(+)-MCPG Blocks Induction of LTP in CA1 of Rat Hippocampus via Agonist Action at an mGluR Group II Receptor
Authors: Breakwell N. A. , Rowan M. J. , Anwyl R.
Published: December 2017

Breakwell, N. A., M. J. Rowan, and R. Anwyl. (+)-MCPG blocks induction of LTP in CA1 of rat hippocampus via agonist action at an mGluR group II receptor. J. Neurophysiol. 79: 1270–1276, 1998. We investigated the effect of metabotropic glutamate receptor (mGluR) ligands on the induction of long-term potentiation (LTP) of field excitatory postsynaptic potentials (EPSPs) in CA1 of rat hippocampus, in particular the manner by which the nonsubtype selective mGluR ligand α-methyl-4-carboxyphenylglycine [(+)-MCPG] blocks LTP induction. Normalized control LTP was blocked by (+)-MCPG (250 μM), but not by the mGluRI selective antagonist (S)-4-carboxyphenylglycine (4-CPG), the mGluRII selective antagonist 1/(2S,3S,4S)-2-methyl-2-(carboxycyclopropyl) glycine (MCCG), or the mGluRIII antagonist (S)-2-amino-2-methyl-4-phosphonobutanoic acid/α-methyl (MAP4). In contrast the mGluRII agonist {(1S,3S)-1-aminocyclopentante-1,3-dicarboxylic acid [(1S,3S)-ACPD]; 10 or 25 μM} completely and consistently blocked LTP. The block of LTP by both (1S,3S)-ACPD and (+)-MCPG could be prevented by preincubation with the mGluRII antagonist MCCG. These studies demonstrate that (+)-MCPG blocks LTP induction through an agonist action at an mGluRII receptor and not through a nonselective antagonist action.
Changes in Intracellular Calcium Concentration Affect Desensitization of GABAA Receptors in Acutely Dissociated P2–P6 Rat Hippocampal Neurons
Authors: Mozrzymas Jerzy W. , Cherubini Enrico
Published: December 2017

Mozrzymas, Jerzy W. and Enrico Cherubini. Changes in intracellular calcium concentration affect desensitization of GABAA receptors in acutely dissociated P2–P6 rat hippocampal neurons. J. Neurophysiol. 79: 1321–1328, 1998. The whole cell configuration of the patch-clamp technique was used to study the effects of different cytosolic calcium concentrations [Ca2+]i on desensitization kinetics of γ-aminobutyric acid (GABA)-activated receptors in acutely dissociated rat hippocampal neurons. Two different intrapipette concentrations of the calcium chelator 1,2-bis(2-aminophenoxy)ethane- N, N, N′, N′-tetraacetic acid (BAPTA; 11 and 0.9 mM, respectively) were used to yield a low (1.2 × 10−8 M) or a high (2.2 × 10−6 M) [Ca2+]i. In low [Ca2+]i, peak values of GABA-evoked currents (20 μM) evoked at −30 mV, were significantly larger than those recorded in high calcium [2,970 ± 280 (SE) pA vs. 1,870 ± 150 pA]. The extent of desensitization, assessed from steady-state to peak ratio was significantly higher in high calcium conditions (0.14 ± 0.007 vs. 0.11 ± 0.008). Similar effects of [Ca2+]i on desensitization were observed with GABA (100 μM). Recovery from desensitization, measured at 30 s interval with double pulse protocol was significantly slower in high [Ca2+]i than in low [Ca2+]i (54 ± 3% vs. 68 ± 2%). The current-voltage relationship of GABA-evoked currents was linear in the potential range between −50 and 50 mV. The kinetics of desensitization process including the rate of onset, extent of desensitization, and recovery were voltage independent. The run down of GABA-evoked currents was faster with the higher intracellular calcium concentration. The run down process was accompanied by changes in desensitization kinetics: in both high and low [Ca2+]i desensitization rate was progressively increasing with time as the slow component of the desensitization onset was converted into the fast one. In excised patches, the desensitization kinetics was much faster and more profound than in the whole cell configuration, indicating the involvement of intracellular factors in regulation of this process. In conclusion, [Ca2+]i affects the desensitization of GABAA receptors possibly by activating calcium-dependent enzymes that regulate their phosphorylation state. This may lead to modifications in cell excitability because of changes in GABA-mediated synaptic currents.