bluuebunny/crossref_metadata_2025 huggingface dataset:
Calcium Channels Involved in Synaptic Transmission From Reticulospinal Axons in Lamprey
Authors: Krieger P. , Büschges A. , el Manira A.
Published: December 2017

Calcium channels involved in synaptic transmission from reticulospinal axons in lamprey. The pharmacology of calcium channels involved in glutamatergic synaptic transmission from reticulospinal axons in the lamprey spinal cord was analyzed with specific agonists and antagonists of different high-voltage activated calcium channels. The N-type calcium channel blocker ω-conotoxin GVIA (ω-CgTx) induced a large decrease of the amplitude of reticulospinal-evoked excitatory postsynaptic potentials (EPSPs). The P/Q-type calcium channel blocker ω-agatoxin IVA (ω-Aga) also reduced the amplitude of the reticulospinal EPSPs, but to a lesser extent than ω-CgTx. The dihydropyridine agonist Bay K and antagonist nimodipine had no effect on the amplitude of the reticulospinal EPSP. Combined application of ω-CgTx and ω-Aga strongly decreased the amplitude the EPSPs but was never able to completely block them, indicating that calcium channels insensitive to these toxins (R-type) are also involved in synaptic transmission from reticulospinal axons. We have previously shown that the group III metabotropic glutamate receptor agonistl(+)-2-amino-4-phosphonobutyric acid (l-AP4) mediates presynaptic inhibition at the reticulospinal synapse. To test if this presynaptic effect is mediated through inhibition of calcium influx, the effect of l-AP4 on reticulospinal transmission was tested before and after blockade of N-type channels, which contribute predominantly to transmitter release at this synapse. Blocking the N-type channels with ω-CgTx did not prevent inhibition of reticulospinal synaptic transmission by l-AP4. In addition, l-AP4 had no affect on the calcium current recorded in the somata of reticulospinal neurons or on the calcium component of action potentials in reticulospinal axons. These results show that synaptic transmission from reticulospinal axons in the lamprey is mediated by calcium influx through N-, P/Q- and R-type channels, with N-type channels playing the major role. Furthermore, presynaptic inhibition of reticulospinal transmission byl-AP4 appears not to be mediated through inhibition of presynaptic calcium channels.
Force-Frequency and Fatigue Properties of Motor Units in Muscles That Control Digits of the Human Hand
Authors: Fuglevand Andrew J. , Macefield Vaughan G. , Bigland-Ritchie Brenda
Published: December 2017

Force-frequency and fatigue properties of motor units in muscles that control digits of the human hand. Modulation of motor unit activation rate is a fundamental process by which the mammalian nervous system encodes muscle force. To identify how rate coding of force may change as a consequence of fatigue, intraneural microstimulation of motor axons was used to elicit twitch and force-frequency responses before and after 2 min of intermittent stimulation (40-Hz train for 330 ms, 1 train/s) in single motor units of human long finger flexor muscles and intrinsic hand muscles. Before fatigue, two groups of units could be distinguished based on the stimulus frequency needed to elicit half-maximal force; group 1 ( n = 8) required 9.1 ± 0.5 Hz (means ± SD), and group 2 ( n = 5) required 15.5 ± 1.1 Hz. Twitch contraction times were significantly different between these two groups (group 1 = 66. 5 ms; group 2 = 45.9 ms). Overall 18% of the units were fatigue resistant [fatigue index (FI) > 0.75], 64% had intermediate fatigue sensitivity (0.25 ≤ FI ≤ 0.75), and 18% were fatigable (FI < 0.25). However, fatigability and tetanic force were not significantly different among groups. Therefore unlike findings in some other mammals, fast-contracting motor units were neither stronger nor more susceptible to fatigue than slowly contracting units. Fatigue, however, was found to be greatest in those units that initially exerted the largest forces. Despite significant slowing of contractile responses, fatigue caused the force-frequency relation to become displaced toward higher frequencies (44 ± 41% increase in frequency for half-maximal force). Moreover, the greatest shift in the force-frequency relation occurred among those units exhibiting the largest force loss. A selective deficit in force at low frequencies of stimulation persisted for several minutes after the fatigue task. Overall, these findings suggest that with fatigue higher activation rates must be delivered to motor units to maintain the same relative level of force. Questions regarding classification of motor units and possible mechanisms by which fatigue-related slowing might coexist with a shift in the force-frequency curve toward higher frequencies are discussed.
FMRFamide-Activated Ca2+Channels inLymnaeaHeart Cells Are Modulated by “SEEPLY,” a Neuropeptide Encoded on the Same Gene
Authors: Brezden B. L. , Yeoman M. S. , Gardner D. R. , Benjamin P. R.
Published: December 2017

FMRFamide-activated Ca2+channels in Lymnaeaheart cells are modulated by “SEEPLY,” a neuropeptide encoded on the same gene. The cell-attached, patch-clamp technique was used to investigate the modulatory role of the neuropeptide SEQPDVDDYLRDVVLQSEEPLY (“SEEPLY”) on FMRFamide-activated Ca2+channels in isolated Lymnaea heart ventricular cells. Both SEEPLY and FMRFamide are encoded on the same neuropeptide gene and are coexpressed in a pair of excitatory motor neurons that innervate the heart. FMRFamide applied alone was capable of significantly increasing the P(open)time of a Ca2+channel in isolated heart muscle cells. However, SEEPLY applied alone did not significantly alter the basal level of Ca2+channel activity in the same cells. Repeated applications of FMRFamide (15 s every min) resulted in a progressive reduction in the number of Ca2+channel openings and the overall P(open)time of the channel. The fifth successive 15-s application of FMRFamide failed to cause the Ca2+channels to open in the majority of cells tested. When FMRFamide and SEEPLY were repeatedly applied together (2-min applications every 4 min) the FMRFamide-activated Ca2+channels continued to respond after the fifth application of the two peptides. Indeed channel activity was seen to continue after repeated 2-min applications of FMRFamide and SEEPLY for as long as the patch lasted (≤60 min). As well as preventing the loss of response to FMRFamide, SEEPLY was also capable of both up- and down-regulating the response of the Ca2+channel to FMRFamide. The direction of the response depended on the P(open)time of the channel before the application of SEEPLY. When the P(open)time for the FMRFamide-activated channel was initially 0.004 ± 0.002 (means ± SE), subsequent perfusion with a mixture of FMRFamide and SEEPLY produced a statistically significant increase in Ca2+channel activity (13 cells). In two cells where no channel activity was observed in response to an initial application of FMRFamide, superfusing the heart cells with a mixture of FMRFamide and SEEPLY induced openings of the Ca2+channel. When the P(open)time of FMRFamide-induced Ca2+channel openings was 0.058 ± 0.017 the subsequent application of a mixture of SEEPLY and FMRFamide caused a statistically significant decrease in Ca2+channel activity (8 cells). As up- and down-regulation of FMRFamide-activated Ca2+channel openings by SEEPLY were observed in the same cells (8 cells), this suggested that corelease of the two peptides might act together to regulate the level of Ca2+channel activity within a defined range.
Membrane Dysfunction Induced by In Vitro Ischemia in Immature Rat Hippocampal CA1 Neurons
Authors: Isagai T. , Fujimura N. , Tanaka E. , Yamamoto S. , Higashi H.
Published: December 2017

Membrane dysfunction induced by in vitro ischemia in immature rat hippocampal CA1 neurons. We investigated differences between immature and mature hippocampal neurons in their response to deprivation of oxygen and glucose (in vitro ischemia), using intracellular recording techniques from CA1 pyramidal neurons in rat brain slices. The membrane was more depolarized in immature hippocampal CA1 neurons (postnatal day 7, P7) compared with the adult neurons (P140), and the apparent input resistance in immature neurons was higher than that in adult neurons. In immature neurons, the threshold for action potential generation was high, and the peak amplitude of the action potential was low in comparison with adult neurons. A time-dependent inward rectification, at potentials negative than the resting potential, was prominent in neurons of P14 and P21. After P21, the resting membrane potential, the apparent input resistance, and the threshold and the peak amplitude of the action potential did not significantly change with increasing age. In adult neurons, application of ischemia-simulating medium caused irreversible changes in membrane potential consisting of an initial hyperpolarization followed by a slow depolarization and a rapid depolarization. Once the rapid depolarization occurred, reintroduction of oxygen and glucose failed to restore the membrane potential, a state referred to as irreversible membrane dysfunction. In neurons of ages P7 or P14, the initial hyperpolarization was not apparent, whereas a slow depolarization followed by a rapid depolarization was observed. With development of the neurons, the latency for onset of the rapid depolarization became shorter and its maximal slope increased. Moreover, neurons of ages P14 or P21 showed a partial or complete recovery after reintroduction of oxygen and glucose, unlike mature neurons. In summary, the present study has demonstrated that the initial hyperpolarization and rapid depolarization induced by in vitro ischemia is age dependent. The rapid depolarization is not readily produced in the neurons in age less than P21 during ischemic exposure.
Optical Mapping of Neural Network Activity in Chick Spinal Cord at an Intermediate Stage of Embryonic Development
Authors: Arai Yoshiyasu , Momose-Sato Yoko , Sato Katsushige , Kamino Kohtaro
Published: December 2017

Optical mapping of neural network activity in chick spinal cord at an intermediate stage of embryonic development. We have applied multiple-site optical recording of transmembrane potential changes to recording of neuronal pathway/network activity from embryonic chick spinal cord slice preparations. Spinal cord preparations were dissected from 8-day-old chick embryos at Hamburger-Hamilton stage 33, and transverse slice preparations were prepared with the 13th cervical spinal nerve or with the 2nd or 5th lumbosacral spinal nerve intact. The slice preparations were stained with a voltage-sensitive merocyanine-rhodanine dye (NK2761). Transmembrane voltage-related optical (dye-absorbance) changes evoked by spinal nerve stimulation with positive square-current pulses using a suction electrode were recorded simultaneously from many loci in the preparation, using a 128- or 1,020-element photodiode array. Optical responses were detected from dorsal and ventral regions corresponding to the posterior (dorsal) and anterior (ventral) gray horns. The optical signals were composed of two components, fast spike-like and slow signals. In the dorsal region, the fast spike-like signal was identified as the presynaptic action potential in the sensory nerve and the slow signal as the postsynaptic potential. In the ventral region, the fast spike-like signal reflects the antidromic action potential in motoneurons, and the slow signal is related to the postsynaptic potential evoked in the motoneuron. In preparations in which the ventral root was cut microsurgically, the antidromic action potential-related optical signals were eliminated. The areas of the maximal amplitude of the evoked signals in the dorsal and ventral regions were located near the dorsal root entry zone and the ventral root outlet zone, respectively. Quasiconcentric contour-line maps were obtained in the dorsal and ventral regions, suggesting the functional arrangement of the dorsal and ventral synaptic connections. Synaptic fatigue induced by repetitive stimuli in the ventral synapses was more rapid than in the dorsal synapses. The distribution patterns of the signals were essentially similar among C13, LS2, and LS5 preparations, suggesting that there is no difference in the spatiotemporal pattern of the neural responses along the rostrocaudal axis of the spinal cord at this developmental stage. In the ventral root-cut preparations, comparing the delay times between the ventral slow optical signals, we have been able to demonstrate that neural network-related synaptic connections are generated functionally in the embryonic spinal cord at Hamburger-Hamilton stage 33.
Na+-K+-2Cl−Cotransporter in Immature Cortical Neurons: A Role in Intracellular Cl−Regulation
Authors: Sun Dandan , Murali Sangita G.
Published: December 2017

Na+-K+-2Cl−cotransporter in immature cortical neurons: a role in intracellular Cl−regulation. Na+-K+-2Cl−cotransporter has been suggested to contribute to active intracellular Cl−accumulation in neurons at both early developmental and adult stages. In this report, we extensively characterized the Na+-K+-2Cl−cotransporter in primary culture of cortical neurons that were dissected from cerebral cortex of rat fetus at embryonic day 17. The Na+-K+-2Cl−cotransporter was expressed abundantly in soma and dendritic processes of cortical neurons evaluated by immunocytochemical staining. Western blot analysis revealed that an ∼145-kDa cotransporter protein was present in cerebral cortex at the early postnatal (P0–P9) and adult stages. There was a time-dependent upregulation of the cotransporter activity in cortical neurons during the early postnatal development. A substantial level of bumetanide-sensitive K+influx was detected in neurons cultured for 4–8 days in vitro (DIV 4–8). The cotransporter activity was increased significantly at DIV 12 and maintained at a steady level throughout DIV 12–14. Bumetanide-sensitive K+influx was abolished completely in the absence of either extracellular Na+or Cl−. Opening of γ-aminobutyric acid (GABA)-activated Cl−channel or depletion of intracellular Cl−significantly stimulated the cotransporter activity. Moreover, the cotransporter activity was elevated significantly by activation of N-methyl-d-aspartate ionotropic glutamate receptor via a Ca2+-dependent mechanism. These results imply that the inwardly directed Na+-K+-2Cl−cotransporter is important in active accumulation of intracellular Cl−and may be responsible for GABA-mediated excitatory effect in immature cortical neurons.
Cerebellar Lesions and Prism Adaptation in Macaque Monkeys
Authors: Baizer Joan S. , Kralj-Hans Ines , Glickstein Mitchell
Published: December 2017

Cerebellar lesions and prism adaptation in Macaque monkeys. If a laterally displacing prism is placed in front of one eye of a person or monkey with the other eye occluded, they initially will point to one side of a target that is located directly in front of them. Normally, people and monkeys adapt easily to the displaced vision and correct their aim after a few trials. If the prism then is removed, there is a postadaptation shift in which the subject misses the target and points in the opposite direction for a few trials. We tested five Macaque monkeys for their ability to adapt to a laterally displacing prism and to show the expected postadaptation shift. When tested as normals, all five animals showed the typical pattern of adaptation and postadaptation shift. Like human subjects, the monkeys also showed complete interocular transfer of the adaptation but no transfer of the adaptation between the two arms. When preoperative training and testing was complete, we made lesions of various target areas on the cerebellar cortex. A cerebellar lesion that included the dorsal paraflocculus and uvula abolished completely the normal prism adaptation for the arm ipsilateral to the lesion in one of the five monkeys. The other four animals retained the ability to prism-adapt normally and showed the expected postadaptation shift. In the one case in which the lesion abolished prism adaptation, the damage included Crus I and II, paramedian lobule and the dorsal paraflocculus of the cerebellar hemispheres as well as lobule IX, of the vermis. Thus in this case, the lesion included virtually all the cerebellar cortex that receives mossy-fiber visual information relayed via the pontine nuclei from the cerebral cortex. The other four animals had damage to lobule V, the classical anterior lobe arm area and/or vermian lobules VI/VII, the oculomotor region. When tested postoperatively, some of these animals showed a degree of ataxia equivalent to that of the case in which prism adaptation was affected, but prism adaptation and the postadaptation shift remained normal. We conclude that in addition to its role in long-term motor learning and reflex adaptation, the region of the cerebellum that was ablated also may be a critical site for a short-term motor memory. Prism adaptation seems to involve a region of the cerebellum that receives a mossy-fiber visual error signal and probably a corollary discharge of the movement.
Correlation of Primate Superior Colliculus and Reticular Formation Discharge With Proximal Limb Muscle Activity
Authors: Stuphorn Veit , Hoffmann Klaus-Peter , Miller Lee E.
Published: December 2017

Correlation of primate superior colliculus and reticular formation discharge with proximal limb muscle activity. We studied the discharge of neurons from both the superior colliculus (SC) and the underlying mesencephalic reticular formation (MRF) and its relation to the simultaneously recorded activity of 11 arm muscles. The 242 neurons tested with a center-out reach task yielded 2,586 pairs of neuron/muscle cross-correlations (normalized, such that perfect correlations are ±1.0). Of these, 43% had peaks with magnitude as large as 0.15, a value that corresponds to the 5% level of significance, and 16% were as large as 0.25. The great majority of peaks in this latter group was positive. The median lag time within this group was 52 ms, indicating that the neuronal discharge tended to precede the correlated muscle activity. We found a small but significantly higher proportion of cells with these relatively strong correlations in the MRF than in the SC. For both areas, these occurred most frequently with muscles of the shoulder girdle and became less frequent for axial as well as for increasingly distal arm musculature. The results support a role for the SC and MRF in guiding the arm during reach movements via the control of proximal limb musculature.
Simultaneous Early Processing of Sensory Input in Human Primary (SI) and Secondary (SII) Somatosensory Cortices
Authors: Karhu J. , Tesche C. D.
Published: December 2017

Simultaneous early processing of sensory input in human primary (SI) and secondary (SII) somatosensory cortices. The anatomic connectivity of the somatosensory system supports the simultaneous participation of widely separated cortical areas in the early processing of sensory input. We recorded evoked neuromagnetic responses noninvasively from human primary (SI) and secondary (SII) somatosensory cortices to unilateral median nerve stimulation. Brief current pulses were applied repetitively to the median nerve at the wrist at 2 Hz for 800–1,500 trials. A single pulse was omitted from the train at random intervals (15% of omissions). We observed synchronized neuronal population activity in contralateral SII area 20–30 ms after stimulation, coincident in time with the first responses generated in SI. Both contra- and ipsilateral SII areas showed prominent activity at 50–60 ms with an average delay of 13 ms for ipsilateral compared with contralateral responses. The refractory behavior of the early SII responses to the omissions differed from those observed at ∼100 ms, indicative of distinct neuronal assemblies responding at each latency. These results indicate that SII and/or associated cortices in parietal operculum, often viewed as higher-order processing areas for somatosensory perception, are coactivated with SI during the early processing of intermittent somatosensory input.
Differential Effects of Metabotropic Glutamate Receptor Antagonists on Bursting Activity in the Amygdala
Authors: Keele N. Bradley , Neugebauer Volker , Shinnick-Gallagher Patricia
Published: December 2017

Differential effects of metabotropic glutamate receptor antagonists on bursting activity in the amygdala. Metabotropic glutamate receptors (mGluRs) are implicated in both the activation and inhibition of epileptiform bursting activity in seizure models. We examined the role of mGluR agonists and antagonists on bursting in vitro with whole cell recordings from neurons in the basolateral amygdala (BLA) of amygdala-kindled rats. The broad-spectrum mGluR agonist 1 S,3 R-1-aminocyclopentane dicarboxylate (1 S,3 R-ACPD, 100 μM) and the group I mGluR agonist ( S)-3,5-dihydroxyphenylglycine (DHPG, 20 μM) evoked bursting in BLA neurons from amygdala-kindled rats but not in control neurons. Neither the group II agonist (2 S,3 S,4 S)-α-(carboxycyclopropyl)-glycine (l-CCG-I, 10 μM) nor the group III agonistl-2-amino-4-phosphonobutyrate (l-AP4, 100 μM) evoked bursting. The agonist-induced bursting was inhibited by the mGluR1 antagonists (+)-α-methyl-4-carboxyphenylglycine [(+)-MCPG, 500 μM] and ( S)-4-carboxy-3-hydroxyphenylglycine [( S)-4C3HPG, 300 μM]. Kindling enhanced synaptic strength from the lateral amygdala (LA) to the BLA, resulting in synaptically driven bursts at low stimulus intensity. Bursting was abolished by (S)-4C3HPG. Further increasing stimulus intensity in the presence of ( S)-4C3HPG (300 μM) evoked action potential firing similar to control neurons but did not induce epileptiform bursting. In kindled rats, the same threshold stimulation that evoked epileptiform bursting in the absence of drugs elicited excitatory postsynaptic potentials in ( S)-4C3HPG. In contrast (+)-MCPG had no effect on afferent-evoked bursting in kindled neurons. Because (+)-MCPG is a mGluR2 antagonist, whereas ( S)-4C3HPG is a mGluR2 agonist, the different effects of these compounds suggest that mGluR2 activation decreases excitability. Together these data suggest that group I mGluRs may facilitate and group II mGluRs may attenuate epileptiform bursting observed in kindled rats. The mixed agonist–antagonist ( S)-4C3HPG restored synaptic transmission to control levels at the LA-BLA synapse in kindled animals. The different actions of ( S)-4C3HPG and (+)-MCPG on LA-evoked bursting suggests that the mGluR1 antagonist–mGluR2 agonist properties may be the distinctive pharmacology necessary for future anticonvulsant compounds.
Enhancement of Bistability in Spinal Motoneurons In Vivo by the Noradrenergic α1 Agonist Methoxamine
Authors: Lee R. H. , Heckman C. J.
Published: December 2017

Enhancement of bistability in spinal motoneurons in vivo by the noradrenergic α1 agonist methoxamine. Like many types of motoneurons, spinal motoneurons in the adult mammal can exhibit bistable behavior. This means that short periods of excitatory input can initiate long periods of self-sustained firing and that equally short periods of inhibition can return the cell to the quiescent state. Usually, the presence of one of the monoamines (either serotonin or norepinephrine) is required for spinal motoneurons to express bistable behaviors. Because the decerebrate cat preparation has tonic activity in monoaminergic fibers that originate in the brain stem and project to spinal motoneurons, these cells sometimes exhibit bistable behavior. However, exogenous application of the noradrenergic α1 agonist methoxamine greatly enhances bistable behavior in the decerebrate. The goal of this study was to identify the mechanisms of this action of methoxamine. The total persistent inward current ( I PIC) in spinal motoneurons in the decerebrate cat was measured from I-V functions generated by triangular voltage commands applied using discontinuous single electrode voltage clamp. The effect of methoxamine on I PIC was assessed by comparing its properties in a control cell sample without methoxamine to its properties in a sample of cells obtained after application of methoxamine. In most experiments, at least one cell was obtained from each sample. Our results showed that methoxamine approximately doubled the amplitude of I PIC without changing its onset voltage, its offset voltage, or its persistence. The reduced amplitude was a consistent finding within experiments and so was unlikely to be caused by interanimal variability. In addition, methoxamine depolarized motoneurons without altering their input conductances, so that a smaller amount of current was required to reach the onset voltage of I PIC. These effects of methoxamine were approximately equal in all cells. As a result of these changes, methoxamine greatly enhanced the tendency for motoneurons to become bistable. It is proposed that the methoxamine-induced increase in the amplitude of I PIC is effective in enhancing the duration of bistable firing because this increase makes I PIC more resistant to the deactivating effects of the afterhyperpolarizations between spikes.
Muscimol-Induced Inactivation of Monkey Frontal Eye Field: Effects on Visually and Memory-Guided Saccades
Authors: Dias Elisa C. , Segraves Mark A.
Published: December 2017

Muscimol-induced inactivation of the monkey frontal eye field: effects on visually and memory-guided saccades. Although neurophysiological, anatomic, and imaging evidence suggest that the frontal eye field (FEF) participates in the generation of eye movements, chronic lesions of the FEF in both humans and monkeys appear to cause only minor deficits in visually guided saccade generation. Stronger effects are observed when subjects are tested in tasks with more cognitive requirements. We tested oculomotor function after acutely inactivating regions of the FEF to minimize the effects of plasticity and reallocation of function after the loss of the FEF and gain more insight into the FEF contribution to the guidance of eye movements in the intact brain. Inactivation was induced by microinjecting muscimol directly into physiologically defined sites in the FEF of three monkeys. FEF inactivation severely impaired the monkeys’ performance of both visually guided and memory-guided saccades. The monkeys initiated fewer saccades to the retinotopic representation of the inactivated FEF site than to any other location in the visual field. The saccades that were initiated had longer latencies, slower velocities, and larger targeting errors than controls. These effects were present both for visually guided and for memory-guided saccades, although the memory-guided saccades were more disrupted. Initially, the effects were restricted spatially, concentrating around the retinotopic representation at the center of the inactivated site, but, during the course of several hours, these effects spread to flanking representations. Predictability of target location and motivation of the monkey also affected saccadic performance. For memory-guided saccades, increases in the time during which the monkey had to remember the spatial location of a target resulted in further decreases in the accuracy of the saccades and in smaller peak velocities, suggesting a progressive loss of the capacity to maintain a representation of target location in relation to the fovea after FEF inactivation. In addition, the monkeys frequently made premature saccades to targets in the hemifield ipsilateral to the injection site when performing the memory task, indicating a deficit in the control of fixation that could be a consequence of an imbalance between ipsilateral and contralateral FEF activity after the injection. There was also a progressive loss of fixation accuracy, and the monkeys tended to restrict spontaneous visual scanning to the ipsilateral hemifield. These results emphasize the strong role of the FEF in the intact monkey in the generation of all voluntary saccadic eye movements, as well as in the control of fixation.
Asynchrony of Quantal Events in Evoked Multiquantal Responses Indicates Presynaptic Quantal Interaction
Authors: Bykhovskaia Maria , Hackett John T. , Worden Mary Kate
Published: December 2017

Asynchrony of quantal events in evoked multiquantal responses indicates presynaptic quantal interaction. We have analyzed the possibility of quantal interactions by inspecting action potential-evoked postsynaptic multiquantal responses recorded extracellularly from the lobster neuromuscular junction. These recorded responses were compared with simulated multiquantal responses constructed from statistically independent quantal events. The simulated multiquantal responses were generated by random superposition of single quantal responses aligned according to the timing of the action potential. The methods of analysis consisted of 1) the comparison of quantal contents obtained from direct counting or by measuring of the size of the responses and 2) the analysis of distributions of quantal latencies. This analysis revealed a large error in the detection of quantal events for responses simulated with no quantal interaction. In contrast, very few errors in quantal detection were made in the analysis of experimental recordings. Latency histograms of recorded responses demonstrate that the proportion of late quantal events (those with latencies of ≥5 ms) increased as a function of quantal content. This shift in latency histograms was not observed for simulated responses. Our interpretation is that quanta interact presynaptically to cause asynchrony of quantal events in evoked responses.
Organization of Somatosensory Areas I and II in Marsupial Cerebral Cortex: Parallel Processing in the Possum Sensory Cortex
Authors: Coleman G. T. , Zhang H. Q. , Murray G. M. , Zachariah M. K. , Rowe M. J.
Published: December 2017

Organization of somatosensory areas I and II in marsupial cerebral cortex: parallel processing in the possum sensory cortex. Controversy exists over the organization of mammalian thalamocortical somatosensory networks. An issue of particular contention is whether the primary and secondary somatosensory areas of cortex (SI and SII) are organized in a parallel or serial scheme for processing tactile information. The current experiments were conducted in the anesthetized brush-tail possum ( Trichosurus vulpecula) to determine which organizational scheme operates in marsupials, which have taken a quite different evolutionary path from the placental species studied in this respect. The effect of rapid reversible inactivation of SI, achieved by localized cortical cooling, was examined on both evoked potential and single neuron responses in SII. SI inactivation was without effect on the amplitude, latency, and time course of SII-evoked potentials, indicating that the transient inputs responsible for the SII-evoked potential reach SII directly from the thalamus rather than traversing an indirect serial route via SI. Tactile responsiveness was examined quantitatively before, during, and after SI inactivation in 16 SII neurons. Fourteen were unchanged in their responsiveness, and two showed some reduction, an effect probably attributable to the loss of a facilitatory influence exerted by SI on a small proportion of SII neurons. The temporal precision and pattern of SII responses to dynamic forms of mechanical stimuli were unaffected, and temporal dispersion in the SII response bursts was unchanged in association with SI inactivation. In conclusion, the results establish that, within this marsupial species, tactile inputs can reach SII directly from the thalamus and are not dependent on a serially organized path through SI. A predominantly parallel organizational scheme for SI and SII operates in this representative of the marsupial order, as it does in a range of placental mammals including the cat and rabbit, the tree shrew and prosimian galago, and at least one primate representative, the marmoset monkey.
Emergence of Postural Patterns as a Function of Vision and Translation Frequency
Authors: Buchanan John J. , Horak Fay B.
Published: December 2017

Emergence of postural patterns as a function of vision and translation frequency. We examined the frequency characteristics of human postural coordination and the role of visual information in this coordination. Eight healthy adults maintained balance in stance during sinusoidal support surface translations (12 cm peak to peak) in the anterior–posterior direction at six different frequencies. Changes in kinematic and dynamic measures revealed that both sensory and biomechanical constraints limit postural coordination patterns as a function of translation frequency. At slow frequencies (0.1 and 0.25 Hz), subjects ride the platform (with the eyes open or closed). For fast frequencies (1.0 and 1.25 Hz) with the eyes open, subjects fix their head and upper trunk in space. With the eyes closed, large-amplitude, slow-sway motion of the head and trunk occurred for fast frequencies above 0.5 Hz. Visual information stabilized posture by reducing the variability of the head’s position in space and the position of the center of mass (CoM) within the support surface defined by the feet for all but the slowest translation frequencies. When subjects rode the platform, there was little oscillatory joint motion, with muscle activity limited mostly to the ankles. To support the head fixed in space and slow-sway postural patterns, subjects produced stable interjoint hip and ankle joint coordination patterns. This increase in joint motion of the lower body dissipated the energy input by fast translation frequencies and facilitated the control of upper body motion. CoM amplitude decreased with increasing translation frequency, whereas the center of pressure amplitude increased with increasing translation frequency. Our results suggest that visual information was important to maintaining a fixed position of the head and trunk in space, whereas proprioceptive information was sufficient to produce stable coordinative patterns between the support surface and legs. The CNS organizes postural patterns in this balance task as a function of available sensory information, biomechanical constraints, and translation frequency.
Intracellular Responses of Onset Chopper Neurons in the Ventral Cochlear Nucleus to Tones: Evidence for Dual-Component Processing
Authors: Paolini Antonio G. , Clark Graeme M.
Published: December 2017

Intracellular responses of onset chopper neurons in the ventral cochlear nucleus to tones: evidence for dual-component processing. The ventral cochlear nucleus (VCN) contains a heterogeneous collection of cell types reflecting the multiple processing tasks undertaken by this nucleus. This in vivo study in the rat used intracellular recordings and dye filling to examine membrane potential changes and firing characteristics of onset chopper (OC) neurons to acoustic stimulation (50 ms pure tones, 5 ms r/f time). Stable impalements were made from 15 OCneurons, 7 identified as multipolar cells. Neurons responded to characteristic frequency (CF) tones with sustained depolarization below spike threshold. With increasing stimulus intensity, the depolarization during the initial 10 ms of the response became peaked, and with further increases in intensity the peak became narrower. Onset spikes were generated during this initial depolarization. Tones presented below CF resulted in a broadening of this initial depolarizing component with high stimulus intensities required to initiate onset spikes. This initial component was followed by a sustained depolarizing component lasting until stimulus cessation. The amplitude of the sustained depolarizing component was greatest when frequencies were presented at high intensities below CF resulting in increased action potential firing during this period when compared with comparable high intensities at CF. During the presentation of tones at or above the high-frequency edge of a cell’s response area, hyperpolarization was evident during the sustained component. The presence of hyperpolarization and the differences seen in the level of sustained depolarization during CF and off CF tones suggests that changes in membrane responsiveness between the initial and sustained components may be attributed to polysynaptic inhibitory mechanisms. The dual-component processing resulting from convergent auditory nerve excitation and polysynaptic inhibition enables OCneurons to respond in a unique fashion to intensity and frequency features contained within an acoustic stimulus.
Physiological Properties of GABAA Receptors From Acutely Dissociated Rat Dentate Granule Cells
Authors: Kapur Jaideep , Haas Kevin F. , Macdonald Robert L.
Published: December 2017

Physiological properties of GABAA receptors from acutely dissociated rat dentate granule cells. Study of fast, GABAA receptor-mediated, inhibitory postsynaptic currents (IPSCs) in hippocampal dentate granule cells has suggested that properties of GABAA receptors influence the amplitude and time course of the IPSCs. This study describes the physiological properties of GABAA receptors present on hippocampal dentate granule cells acutely isolated from 18- to 35-day-old rats. Rapid application of 1 mM GABA to outside-out macropatches excised from granule cells produced GABAA receptor currents with rapid rise time and biexponential decay of current after removal of GABA. After activation, granule cell GABAA receptor currents desensitized incompletely. During a 400-ms application of 1 mM GABA, peak current only desensitized ∼40%. In symmetrical chloride solutions there was no outward rectification of whole cell current. Activation rates and peak currents elicited by rapid application of GABA to macropatches were also similar at positive and negative holding potentials. However, deactivation of GABAA receptor currents was slower at positive holding potentials. When whole cell currents were recorded without ATP in the pipette, current run-down was not apparent for 30 min in 50% of neurons, but run-down appeared to start soon after access was established in the remaining neurons. When 2 mM ATP was included in the recording pipette no run-down was apparent in 30 min of recording. The efficacy and potency of GABA were lower in cells recorded with no ATP in the pipette and during run-down compared with those recorded with 2 mM ATP and no run-down.
AuxiliaryHyperkineticβ Subunit of K+Channels: Regulation of Firing Properties and K+Currents inDrosophilaNeurons
Authors: Yao Wei-Dong , Wu Chun-Fang
Published: December 2017

Auxiliary Hyperkinetic β subunit of K+channels: regulation of firing properties and K+currents in Drosophila neurons. Molecular analysis and heterologous expression have shown that K+channel β subunits regulate the properties of the pore-forming α subunits, although how they influence neuronal K+currents and excitability remains to be explored. We studied cultured Drosophila “giant” neurons derived from mutants of the Hyperkinetic ( Hk) gene, which codes for a K+channel β subunit. Whole cell patch-clamp recording revealed broadened action potentials and, more strikingly, persistent rhythmic spontaneous activities in a portion of mutant neurons. Voltage-clamp analysis demonstrated extensive alterations in the kinetics and voltage dependence of K+current activation and inactivation, especially at subthreshold membrane potentials, suggesting a role in regulating the quiescent state of neurons that are capable of tonic firing. Altered sensitivity of Hk currents to classical K+channel blockers (4-aminopyridine, α-dendrotoxin, and TEA) indicated that Hk mutations modify interactions between voltage-activated K+channels and these pharmacological probes, apparently by changing both the intra- and extracellular regions of the channel pore. Correlation of voltage- and current-clamp data from the same cells indicated that Hkmutations affect not only the persistently active neurons, but also other neuronal categories. Shaker ( Sh) mutations, which alter K+channel α subunits, increased neuronal excitability but did not cause the robust spontaneous activity characteristic of some Hk neurons. Significantly, Hk Sh double mutants were indistinguishable from Sh single mutants, implying that the rhythmic Hk firing pattern is conferred by intact Shα subunits in a distinct neuronal subpopulation. Our results suggest that alterations in β subunit regulation, rather than elimination or addition of α subunits, may cause striking modifications in the excitability state of neurons, which may be important for complex neuronal function and plasticity.
Receptor Potentials and Electrical Properties of Nonspiking Stretch-Receptive Neurons in the Sand CrabEmerita analoga(Anomura, Hippidae)
Authors: Paul Dorothy H. , Bruner Jan
Published: December 2017

Receptor potentials and electrical properties of nonspiking stretch-receptive neurons in the sand crab Emerita analoga (Anomura, Hippidae). Four nonspiking, monopolar neurons with central somata and large peripheral dendrites constitute the sole innervation of the telson-uropod elastic strand stretch receptor in Emerita analoga. We characterized their responses to stretch and current injection, using two-electrode current clamp, in intact cells and in two types of isolated peripheral dendritic segments, one that included and one that excluded the dendritic termini (mechanosensory membrane). The membrane potentials of intact cells at rest (mean ± SD: −57 ± 4.4 mV, n = 30), recorded in peripheral or neuropil processes, are similar to the membrane potentials of isolated dendritic segments and always less negative than membrane potentials of motoneurons and interneurons recorded in the same preparations. Ion substitution experiments indicate that the membrane potential is influenced strongly by Na+conductance, probably localized in the mechanotransducing terminals within the elastic strand. The form of the receptor potential in response to ramp-hold-release stretch remains the same as stretch amplitude is varied and is not dependent on initial membrane potential (−70 to −30 mV) or recording site: initial depolarization (slope follows ramp of applied stretch), terminated by rapid, partial repolarization to a plateau (delayed depolarization) that is intermediate between the peak depolarization and the initial potential and sustained for the duration of the stretch. Responses to depolarizing current pulses are similar to stretch-evoked receptor potentials, except for small amplitude stimuli: an initial peak occurs only in response to stretch and probably reflects elastic recoil of the extracellular matrix surrounding the dendritic terminals. The rapid, partial repolarization depends on holding potential and is abolished by 4-aminopyridine (4-AP; 10 mM), implicating a fast-activating, fast-inactivating K+conductance; TEA (60 mM) abolishes the remaining slow repolarization to the plateau. In intact cells, but not dendritic segments, regenerative depolarizations can arise in response to stretch or depolarizing current pulses; they are reduced by CdCl2(10 μM) in the saline containing TEA and 4-AP and probably reflect current spread from Ca2+influx at presynaptic terminals in the ganglion. We found no evidence for other voltage-activated conductances. Unlike morphologically similar “nonspiking” thoracic receptors of other species, E. analoga’s nonspiking neurons are electrically compact and do not boost the analogue afferent signal by voltage-activated inward currents. The most prominent (only?) voltage-activated extra-ganglionic conductances are for potassium; by reducing the slope of the stretch-plateau depolarization curve, they extend each neuron’s functional range to the full range of sensitivity of the receptor.
Effects of Viewing Distance on the Responses of Horizontal Canal–Related Secondary Vestibular Neurons During Angular Head Rotation
Authors: Chen-Huang Chiju , McCrea Robert A.
Published: December 2017

Effects of viewing distance on the responses of horizontal canal–related secondary vestibular neurons during angular head rotation. The eye movements generated by the horizontal canal–related angular vestibuloocular reflex (AVOR) depend on the distance of the image from the head and the axis of head rotation. The effects of viewing distance on the responses of 105 horizontal canal–related central vestibular neurons were examined in two squirrel monkeys that were trained to fixate small, earth-stationary targets at different distances (10 and 150 cm) from their eyes. The majority of these cells (77/105) were identified as secondary vestibular neurons by synaptic activation following electrical stimulation of the vestibular nerve. All of the viewing distance–sensitive units were also sensitive to eye movements in the absence of head movements. Some classes of eye movement–related vestibular units were more sensitive to viewing distance than others. For example, the average increase in rotational gain (discharge rate/head velocity) of position-vestibular-pause units was 20%, whereas the gain increase of eye-head-velocity units was 44%. The concomitant change in gain of the AVOR was 11%. Near viewing responses of units phase lagged the responses they generated during far target viewing by 6–25°. A similar phase lag was not observed in either the near AVOR eye movements or in the firing behavior of burst-position units in the vestibular nuclei whose firing behavior was only related to eye movements. The viewing distance–related increase in the evoked eye movements and in the rotational gain of all unit classes declined progressively as stimulus frequency increased from 0.7 to 4.0 Hz. When monkeys canceled their VOR by fixating head-stationary targets, the responses recorded during near and far target viewing were comparable. However, the viewing distance–related response changes exhibited by central units were not directly attributable to the eye movement signals they generated. Subtraction of static eye position signals reduced, but did not abolish viewing distance gain changes in most units. Smooth pursuit eye velocity sensitivity and viewing distance sensitivity were not well correlated. We conclude that the central premotor pathways that mediate the AVOR also mediate viewing distance–related changes in the reflex. Because irregular vestibular nerve afferents are necessary for viewing distance–related gain changes in the AVOR, we suggest that a central estimate of viewing distance is used to parametrically modify vestibular afferent inputs to secondary vestibuloocular reflex pathways.