bluuebunny/crossref_metadata_2025 huggingface dataset:
Temporal Modulation of Spatial Borders in Rat Barrel Cortex
Authors: Sheth Bhavin R. , Moore Christopher I. , Sur Mriganka
Published: December 2017

Sheth, Bhavin R., Christopher I. Moore, and Mriganka Sur. Temporal modulation of spatial borders in rat barrel cortex. J. Neurophysiol. 79: 464–470, 1998. We examined the effects of varying vibrissa stimulation frequency on intrinsic signal and neuronal responses in rat barrel cortex. Optical imaging of intrinsic signals demonstrated that the region of cortex activated by deflection of a single vibrissa at 1 Hz is more diffuse and more widespread than the territory activated at 5 or 10 Hz. With the use of two different paradigms, constant time of stimulation and constant number of vibrissa deflections, we showed that the optically imaged spread of activity is more discrete at higher stimulation frequencies. We combined optical imaging with multiple electrode recording and confirmed that the neuronal response to individual vibrissa stimulation at the optically imaged center of activity is greater than the response away from the imaged center. Consistent with the imaging data, these recordings also showed no response to a second vibrissa deflection at 5 Hz at a peripheral recording site, though there was a significant response to a second vibrissa deflection at 1 Hz at the same peripheral site. These findings demonstrate that vibrissa stimulation at higher frequencies leads to more focused physiological responses in cortex. Thus the spread of activation in rat barrel cortex is modulated in a dynamic fashion by the frequency of vibrissa stimulation.
Acute Intrahippocampal Infusion of BDNF Induces Lasting Potentiation of Synaptic Transmission in the Rat Dentate Gyrus
Authors: Messaoudi Elhoucine , Bårdsen Kjetil , Srebro Bolek , Bramham Clive R.
Published: December 2017

Messaoudi, Elhoucine, Kjetil Bårdsen, Bolek Srebro, and Clive R. Bramham. Acute intrahippocampal infusion of BDNF induces lasting potentiation of synaptic transmission in the rat dentategyrus. J. Neurophysiol. 79: 496–499, 1998. The effect of acuteintrahippocampal infusion of brain-derived neurotrophic factor (BDNF) on synaptic transmission in the dentate gyrus was investigated in urethan-anesthetized rats. Medial perforant path-evoked field potentials were recorded in the dentate hilus and BDNF-containing buffer was infused (4 μl, 25 min) immediately above the dentate molecular layer. BDNF led to a slowly developing increase of the field excitatory postsynaptic potential (fEPSP) slope and population spike amplitude. The potentiation either reached a plateau level at ∼2 h after BDNF infusion or continued to increase for the duration of experiment; the longest time point recorded was 10 h. Mean increases at 4 h after BDNF infusion were 62.2 and 224% for the fEPSP slope and population spike, respectively. No changes in responses were observed in controls receiving buffer medium only or buffer containing cytochrome C. BDNF-induced potentiation developed in the absence of epileptiform activity in the hippocampal electroencephalogram or changes in recurrent inhibition on granule cells as assessed by paired-pulse inhibition of the population spike. We conclude that exogenous BDNF induces a lasting potentiation of synaptic efficacy in the dentate gyrus of anesthetized adult rats.
Interaction of the Two Frontal Eye Fields Before Saccade Onset
Authors: Schlag J. , Dassonville P. , Schlag-Rey M.
Published: December 2017

Schlag, J., P. Dassonville, and M. Schlag-Rey. Interaction of the two frontal eye fields before saccade onset. J. Neurophysiol. 79: 64–72, 1998. A normal environment often contains many objects of interest that compete to attract our gaze. Nevertheless, instead of initiating a flurry of conflicting signals, central populations of oculomotor neurons always seem to agree on the destination of the next saccade. How is such a consensus achieved? In a unit recording and microstimulation study on trained monkeys, we sought to elucidate the mechanism through which saccade-related cells in the frontal eye fields (FEF) avoid issuing competing commands. Presaccadic neuronal activity was recorded in one FEF while stimulating the contralateral FEF with low-intensity currents that evoked saccades. When an eye-movement cell was isolated, we determined: the movement field of the cell, the cell's response to contralateral FEF microstimulation, the cell's response when the evoked saccade was in the preferred direction of the cell (using the collision technique to deviate appropriately the evoked saccade vector), and the cell's response to a stimulation applied during a saccade in the cell's preferred direction, to reveal a possible inhibitory effect. Complete results were obtained for 71 stimulation-recording pairs of FEF sites. The unit responses observed were distributed as follows: 35% of the cells were unaffected, 37% were inhibited, and 20% excited by contralateral stimulation. These response types depended on the site of contralateral stimulation and did not vary when saccades were redirected by collision. This invariant excitation or inhibition of cells, seemingly due to hardwired connections, depended on the angular difference between their preferred vector and the vector represented by the cells stimulated. By contrast, 8% of the cells were either activated or inhibited depending on the vector of the saccade actually evoked by collision. These results suggest that the consensus between cells of oculomotor structures at the time of saccade initiation is implemented by functional connections such that the cells that command similar movements mutually excite each other while silencing those that would produce conflicting movements. Such a rule would be an effective implementation of a winner-take-all mechanism well suited to prevent conflicts.
Acute and Chronic Increases in Excitability in Rat Hippocampal Slices After Perinatal Hypoxia In Vivo
Authors: Jensen F. E. , Wang C. , Stafstrom C. E. , Liu Z. , Geary C. , Stevens M. C.
Published: December 2017

Jensen, F. E., C. Wang, C. E. Stafstrom, Z. Liu, C. Geary, and M. C. Stevens. Acute and chronic increases in excitability in rat hippocampal slices after perinatal hypoxia in vivo. J. Neurophysiol. 79: 73–81, 1998. We have previously shown that hypoxia induces both acute and chronic epileptogenic effects that are age dependent. Global hypoxia (3–4% O2) induces seizure activity in the developing brain [postnatal day (P)10–12] but not at younger or older ages. Adult rats with prior seizures induced by hypoxia at P10 show increased seizure susceptibility to chemical convulsants compared with controls. In the present study, we tested the hypothesis that acute and chronic epileptogenic effects of hypoxia are demonstrable in hippocampus both in vivo and in vitro. Depth electrode recordings confirmed the presence of ictal activity within hippocampus in P10 rats during global hypoxia. Hippocampal slices prepared from P10 pups killed at 10 min after recovery from hypoxia showed evidence of increased excitability. Extracellular field recordings revealed that the amplitude and duration of long-term potentiation (LTP) was increased significantly in area CA1 of hippocampal slices removed from hypoxic pups. In addition, extracellular recordings within areas CA1 and CA3 showed significantly longer afterdischarge durations in response to kindling stimuli in slices from hypoxic pups compared with controls. To evaluate whether there were also long-term changes in hippocampal excitability, hippocampal slices were prepared from adult rats that had underwent hypoxia at P10 and compared with slices from adult litter-mate controls. A Mg2+-free medium was superfused to induce epileptiform activity within the slices. Extracellular recordings from stratum pyramidale of area CA1 showed that Mg2+-free media induced significantly more frequent ictal discharges in slices from previously hypoxic rats compared with controls. These results provide evidence that the naturally occurring stimulus of hypoxia can result in both acute and chronic changes in the excitability of the CA1 neuronal network. These results parallel our previous in vivo studies demonstrating that global hypoxia acutely increases excitability in the immature brain and that hypoxia during the age window ∼P10 results in long-lasting increases in seizure susceptibility within hippocampus. Our results suggest that the age-dependent epileptogenic effects of hypoxia are in part mediated by a direct and permanent effect on neuronal excitability within hippocampal neuronal networks.
Dopaminergic Modulation of NMDA-Induced Whole Cell Currents in Neostriatal Neurons in Slices: Contribution of Calcium Conductances
Authors: Cepeda Carlos , Colwell Christopher S. , Itri Jason N. , Chandler Scott H. , Levine Michael S.
Published: December 2017

Cepeda, Carlos, Christopher S. Colwell, Jason N. Itri, Scott H. Chandler, and Michael S. Levine. Dopaminergic modulation of NMDA-induced whole cell currents in neostriatal neurons in slices: contribution of calcium conductances. J. Neurophysiol. 79: 82–94, 1998. The present experiments were designed to examine dopamine (DA) modulation of whole cell currents mediated by activation of N-methyl-d-aspartate (NMDA) receptors in visualized neostriatal neurons in slices. First, we assessed the ability of DA, D1 and D2 receptor agonists to modulate membrane currents induced by activation of NMDA receptors. The results of these experiments demonstrated that DA potentiated NMDA-induced currents in medium-sized neostriatal neurons. Potentiation of NMDA currents occurred at three different holding potentials, although it was more pronounced at −30 mV. It was mediated by D1 receptors, because it was mimicked by D1 agonists and blocked by exposure to a D1 antagonist. Activation of D2 receptors produced inconsistent effects on NMDA-induced membrane currents. Either decreases, increases, or no effects on NMDA currents occurred. Second, we examined the contributions of intrinsic, voltage-dependent conductances to DA potentiation of NMDA currents. Blockade of K+ conductances did not prevent DA enhancement of NMDA currents. However, voltage-activated Ca2+ conductances provided a major contribution to DA modulation. The dihydropyridine L-type Ca2+ channel blockers, nifedipine, and methoxyverapamil (D−600), markedly reduced but did not totally eliminate the ability of DA to modulate NMDA currents. The D1 receptor agonist SKF 38393 also enhanced Ba2+ currents in neostriatal neurons. Together, these findings provide evidence for a complex interplay between DA, NMDA receptor activation and dihydropyridine-sensitive Ca2+ conductances in controlling responsiveness of neostriatal medium-sized neurons.
Axon Conduction and Survival in CNS White Matter During Energy Deprivation: A Developmental Study
Authors: Fern Robert , Davis Peter , Waxman Stephen G. , Ransom Bruce R.
Published: December 2017

Fern, Robert, Peter Davis, Stephen G. Waxman, and Bruce R. Ransom. Axon conduction and survival in CNS white matter during energy deprivation: a developmental study. J. Neurophysiol. 79: 95–105, 1998. We investigated the postnatal development of axon sensitivity to the withdrawal of oxygen, glucose, or the combined withdrawal of oxygen + glucose in the isolated rat optic nerve (a CNS white matter tract). Removal of either oxygen or glucose for 60 min resulted in irreversible injury in optic nerves from adult rats, assessed by loss of the evoked compound action potential (CAP). Optic nerves at ages <P10 showed no permanent loss of function. CAP sensitivity to the withdrawal of oxygen or glucose emerged during a critical period in development between postnatal days 10–20 (P10–P20). The CAP was unchanged in adult optic nerve for 45 min after the withdrawal of glucose, demonstrating the presence of a significant energy reserve. Periods of glucose withdrawal >45 min caused the selective loss of late CAP components; this was not seen with oxygen deprivation. The amplitude of the early component recovered to 94.8% of control after 60 min of glucose withdrawal, although total CAP area recovered to only 42.3%. Combined oxygen + glucose withdrawal for 60 min produced a greater degree of permanent CAP loss than 60 min of glucose or oxygen withdrawal individually in optic nerves from rats older than P4. Younger than P4 optic nerves showed no permanent loss of function from 60 min of combined oxygen + glucose withdrawal. Unexpectedly, optic nerves from P21–P49 rats recovered significantly less after all three conditions than adult opticnerves (>P50). It is probable that this period of final myelination corresponds to a time of heightened metabolic activity in white matter. The tolerance of CNS white matter to energy deprivation can be categorized into four stages that are correlated with specific developmental features: premyelination (P0–P4), highly tolerant to anoxia, aglycemia and combined anoxia/aglycemia; early myelination (P5–P20), partially tolerant of anoxia and aglycemia but not to combined anoxia/aglycemia; late myelination (P21–P49), very low tolerance of anoxia, aglycemia and combined anoxia/aglycemia; and mature (>P50), low tolerance of anoxia, aglycemia and combined anoxia/aglycemia. The relative resistance of optic nerve function to glucose withdrawal in the presence of oxygen, compared with glucose withdrawal in the absence of oxygen, is presumably due to the presence of oxygen-dependent energy reserves such as astrocytic glycogen, amino acids. and phospholipids.
Spiral Intercellular Calcium Waves in Hippocampal Slice Cultures
Authors: Harris-White Marni E. , Zanotti Stephen A. , Frautschy Sally A. , Charles Andrew C.
Published: December 2017

Harris-White, Marni E., Stephen A. Zanotti, Sally A. Frautschy, and Andrew C. Charles. Spiral intercellular calcium waves in hippocampal slice cultures. J. Neurophysiol. 79: 1045–1052, 1998. Complex patterns of intercellular calcium signaling occur in the CA1 and CA2 regions of hippocampal slice organotypic cultures from neonatal mice. Spontaneous localized intercellular Ca2+ waves involving 5–15 cells propagate concentrically from multiple foci in the stratum oriens and s. radiatum. In these same regions, extensive Ca2+ waves involving hundreds of cells propagate as curvilinear and spiral wavefronts across broad areas of CA1 and CA2. Ca2+ waves travel at rates of 5–10 μm/s, are abolished by thapsigargin, and do not require extracellular Ca2+. Staining for astrocytes and neurons indicates that these intercellular waves occur primarily in astrocytes. The frequency and amplitude of Ca2+ waves increase in response to bath application of N-methyl-d-aspartate (NMDA) and decrease in response to removal of extracellular Ca2+ or application of tetrodotoxin. This novel pattern of intercellular Ca2+ signaling is characteristic of the behavior of an excitable medium. Networks of glial cells in the hippocampus may behave as an excitable medium whose spatial and temporal signaling properties are modulated by neuronal activity.
Role of the Human Rostral Supplementary Motor Area and the Basal Ganglia in Motor Sequence Control: Investigations With H2 15O PET
Authors: Boecker H. , Dagher A. , Ceballos-Baumann A. O. , Passingham R. E. , Samuel M. , Friston K. J. , Poline J.-B. , Dettmers C. , Conrad B. , Brooks D. J.
Published: December 2017

Boecker, H., A. Dagher, A. O. Ceballos-Baumann, R. E. Passingham, M. Samuel, K. J. Friston, J.-B. Poline, C. Dettmers, B. Conrad, and D. J. Brooks. Role of the human rostral supplementary motor area and the basal ganglia in motor sequence control: investigations with H2 15O PET. J. Neurophysiol. 79: 1070–1080, 1998. The aim of this study was to investigate the functional anatomy of distributed cortical and subcortical motor areas in the human brain that participate in the central control of overlearned complex sequential unimanual finger movements. On the basis of previous research in nonhuman primates, a principal involvement of basal ganglia (medial premotor loops) was predicted for central control of finger sequences performed automatically. In pertinent areas, a correlation of activation levels with the complexity of a motor sequence was hypothesized. H2 15O positron emission tomography (PET) was used in a group of seven healthy male volunteers [mean age 32.0 ± 10.4 yr] to determine brain regions where levels of regional cerebral blood flow (rCBF) correlated with graded complexity levels of five different key-press sequences. All sequences were overlearned before PET and involved key-presses of fingers II–V of the right hand. Movements of individual fingers were kept constant throughout all five conditions by external pacing at 1-Hz intervals. Positive correlations of rCBF with increasing sequence complexity were identified in the contralateral rostral supplementary motor area (pre-SMA) and the associated pallido-thalamic loop, as well as in right parietal area 7 and ipsilateral primary motor cortex (M1). In contrast, while rCBF in contralateral M1 and and extensive parts of caudal SMA was increased compared with rest during task performance, significant correlated increases of rCBF with sequence complexity were not observed. Inverse correlations of rCBF with increasing sequence complexity were identified in mesial prefrontal-, medial temporal-, and anterior cingulate areas. The findings provide further evidence in humans supporting the notion of a segregation of SMA into functionally distinct subcomponents: although pre-SMA was differentially activated depending on the complexity of a sequence of learned finger movements, such modulation was not detectable in caudal SMA (except the most antero-superior part), implicating a motor executive role. Our observations of complexity-correlated rCBF increases in anterior globus palllidus suggest a specific role for the basal ganglia in the process of sequence facilitation and control. They may act to filter and focus input from motor cortical areas as patterns of action become increasingly complex.
Adenosine A1 Receptors Mediate Retinotectal Presynaptic Inhibition: Uncoupling by C-Kinase and Role in LTP During Regeneration
Authors: Zhang Chunyi , Schmidt John T.
Published: December 2017

Zhang, Chunyi and John T. Schmidt. Adenosine A1 receptors mediate retinotectal presynaptic inhibition: uncoupling by C-kinase and role in LTP during regeneration. J. Neurophysiol. 79: 501–510, 1998. Presynaptic adenosine receptors inhibit transmitter release at many synapses and are known to exist on retinotectal terminals. In this paper we show that adenosine decreases retinotectal field potentials by ∼30% and investigate the mechanism. First, as judged by the effects of specific calcium channel blockers, retinotectal transmission was mediated almost exclusively by N-type calcium channels, which are known to be modulated by adenosine A1 receptors. Transmission was completely blocked by either ω-Conotoxin GVIA (−100%, N-type blocker) or ω-Conotoxin MVIIC (−99%, N-, P- and Q-type blocker) and was not significantly affected by ω-Agatoxin IVA [+1.7 ± 9.3% (SE), P-,Q-type blocker], but was augmented slightly by nifedipine(+9.3 ± 2.1%, L-type blocker). Second, the adenosine inhibition was presynaptic, as indicated by a 43% increase in paired-pulse facilitation. Third, the selective A1 agonist cyclohexyl adenosine (CHA) at 50 nM caused a 21% decrease in amplitude and the selective A2 agonist N 6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)-ethyl]adenosine (DPMA) at 100 nM caused a 24% increase. Fourth, the selective A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) alone produced an increase in the field potential, suggesting a tonic inhibition mediated by endogenous adenosine. Fifth, pertussis toxin eliminated adenosine inhibition implicating Gi or Go protein coupling. Sixth, C-kinase activation eliminated the A1-mediated inhibition. In regenerating projections, adenosine also caused a decrease in transmission (−30 ± 12%), but after induction of long-term potentiation (LTP) via trains of stimuli or via treatment with the phosphatase inhibitor okadaic acid, the adenosine response was converted to an augmentation. Because LTP is associated with C-kinase activation, this is consistent with C-kinase uncoupling the A1 receptor from inhibiting N-type Ca2+ channels. This uncovers the A2-mediated augmentation as demonstrated in normals with DPMA. Such an effect could account in part for the LTP of immature synapses and the change from rapidly fatiguing to robust synaptic transmission.
Nerve Conduction Block by Nitric Oxide That Is Mediated by the Axonal Environment
Authors: Shrager Peter , Custer Andrew W. , Kazarinova Katia , Rasband Matthew N. , Mattson David
Published: December 2017

Shrager, Peter, Andrew W. Custer, Katia Kazarinova, Matthew N. Rasband, and David Mattson. Nerve conduction block by nitric oxide that is mediated by the axonal environment. J. Neurophysiol. 79: 529–536, 1998. Conduction in rat peripheral nerve has been monitored following the stimulated release of nitric oxide (NO) from diethylamine-NONOate (DEA-NONOate). Branches of the sciatic nerve were dissected, but left otherwise intact, and propagating signals recorded externally. At levels consistent with inflammation, NO exposure resulted in a complete loss of the compound action potential. Conduction was fully restored on removal of the drug. Most notably, this loss of excitability was dependent on the axonal environment. Removal of the connective tissue sheaths surrounding the nerve bundle, a process that normally enhances drug action, prevented block of signal propagation by nitric oxide. The epineurium seemed not to be required, and the decreased susceptibility to NO appeared to be correlated with a gradual loss of a component of the endoneurium that surrounds individual fibers. Tested on the rat vagus nerve, NO eliminated action potentials in both myelinated and unmyelinated fibers. One chemical mechanism that is consistent with the reversibility of block and the observed lack of effect of 8-Br-cGMP on conduction is the formation of a nitrosothiol through reaction of NO with a sulfhydryl group. In contrast to DEA-NONOate, S-nitrosocysteine, which can both transfer nitrosonium cation (NO+) to another thiol and also release nitric oxide, was effective on both intact and desheathed preparations. It has previously been demonstrated that chemical modification of invertebrate axons by sulfhydryl-reactive compounds induces a slow inactivation of Na+channels. Nitric oxide block of axonal conduction may contribute to clinical deficits in inflammatory diseases of the nervous system.
Endogenous Opioid Peptides Acting at μ-Opioid Receptors in the Dorsal Horn Contribute to Midbrain Modulation of Spinal Nociceptive Neurons
Authors: Budai Dénes , Fields Howard L.
Published: December 2017

Budai, Dénes and Howard L. Fields. Endogenous opioid peptides acting at μ-opioid receptors in the dorsal horn contribute to midbrain modulation of spinal nociceptive neurons. J. Neurophysiol. 79: 677–687, 1998. Activation of neurons in the midbrain periaqueductal gray (PAG) inhibits spinal dorsal horn neurons and produces behavioral antinociception in animals and analgesia in humans. Although dorsal horn regions modulated by PAG activation contain all three opioid receptor classes (μ, δ, and κ), as well as enkephalinergic interneurons and terminal fields, descending opioid-mediated inhibition of dorsal horn neurons has not been demonstrated. We examined the contribution of dorsal hornμ-opioid receptors to the PAG-elicited descending modulation of nociceptive transmission. Single-unit extracellular recordings were made from rat sacral dorsal horn neurons activated by noxious heating of the tail. Microinjections of bicuculline (BIC) in the ventrolateral PAG led to a 60–80% decrease in the neuronal responses to heat. At the same time, the responses of the same neurons to iontophoretically applied NMDA or kainic acid were not consistently inhibited. The inhibition of heat-evoked responses by PAG BIC was reversed by iontophoretic application of the selective μ-opioid receptor antagonists, d-Phe-Cys-Tyr-d-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP) and d-Phe-Cys-Tyr-d-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP). A similar effect was produced by naloxone; however, naloxone had an excitatory influence on dorsal horn neurons in the absence of PAG-evoked descending inhibition. This is the first demonstration that endogenous opioids acting via spinal μ-opioid receptors contribute to brain stem control of nociceptive spinal dorsal horn neurons. The inhibition appears to result in part from presynaptic inhibition of afferents to dorsal horn neurons.
Characterization of an Intracellular Alkaline Shift in Rat Astrocytes Triggered by Metabotropic Glutamate Receptors
Authors: Amos Brian J. , Chesler Mitchell
Published: December 2017

Amos, Brian J. and Mitchell Chesler. Characterization of an intracellular alkaline shift in rat astrocytes triggered by metabotropic glutamate receptors. J. Neurophysiol. 79: 695–703, 1998. The modulation of intracellular pH by activation of metabotropic glutamate receptors was investigated in cultured and acutely dissociated rat astrocytes. One minute superfusion of 100 μM (1S,3R)-1-aminocyclopentane-1,3-dicarboxcylic acid (ACPD) evoked an alkaline shift of 0.13 ± 0.013 (mean ± SE) and 0.16 ± 0.03 pH units in cultured (cortical or cerebellar) and acutely dissociated cortical astrocytes, respectively. Alkalinizations were elicited by concentrations of ACPD as low as 1 μM. The ACPD response was mimicked by S-3-hydroxyphenylglycine (3-HPG) and by (s)-4-carboxy-3-hydroxyphenylglycine (4C-3HPG) but was not blocked by α-methyl-4-carboxyphenylglycine (MCPG) or (RS)-1-aminoindan-1,5-dicarboxcylic acid (AIDA), features consistent with an mGluR5 receptor–mediated mechanism. The ACPD-evoked alkaline shift was insensitive to amiloride, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (DIDS), and the v-type ATPase inhibitors 7-chloro-4-nitrobenz-2-oxa-1,3-diazol (NBD-Cl), bafilomycin, and concanamycin. The alkaline response persisted in Na+- or Cl−-free saline, but was reversibly blocked in bicarbonate-free, N-2-hydroxyethylpiperazine- N′-2-ethanesulfonic acid (HEPES)-buffered solutions. A bicarbonate-dependent and Na+-independent alkaline shift could also be elicited by either 3 mM caffeine or 1 μM ionomycin. These data suggest that a rise in cytosolic Ca2+activity is instrumental in triggering the alkalinizing mechanism and that this response is independent of the classic depolarization-induced alkalinization mediated by electrogenic sodium-bicarbonate cotransport.
Whole Cell Recordings of Lumbar Motoneurons During Locomotor-Like Activity in the In Vitro Neonatal Rat Spinal Cord
Authors: Hochman S. , Schmidt B. J.
Published: December 2017

Hochman, S. and B. J. Schmidt. Whole cell recordings of lumbar motoneurons during locomotor-like activity in the in vitro neonatal rat spinal cord. J. Neurophysiol. 79: 743–752, 1998. Whole cell current- and voltage-clamp recordings were obtained from lumbar motoneurons in the isolated neonatal rat spinal cord to characterize the behavior of motoneurons during neurochemically induced locomotor-like activity. Bath application of serotonin (10–100 μM) in combination with N-methyl-d-aspartate (1–12 μM) initially produced tonic membrane depolarization (mean = 26 mV), increased input resistance, decreased rheobase, and increased spike inactivation in response to depolarizing current pulse injections. After the initial tonic depolarization, rhythmic fluctuations of the motoneuron membrane potential (locomotor drive potentials; LDPs) developed that were modulated phasically in association with ventral root discharge. The peak and trough voltage levels of the LDP fluctuated above and below the membrane potential recorded immediately before the onset of rhythmic activity. Similarly, firing frequency was modulated above and below prelocomotion firing rates (in those motoneurons that displayed neurochemically induced tonic firing immediately before the onset of rhythmic activity). These observations are consistent with an alternation between phasic excitatory and inhibitory synaptic drives. The amplitude of LDPs and rhythmic excitatory drive current increased with membrane depolarization from −80 to −40 mV and then decreased with further depolarization, thus displaying nonlinear voltage-dependence. Faster frequency, small amplitude voltage fluctuations were observed superimposed on the depolarized phase of LDPs. In some motoneurons, the trajectory of these superimposed fluctuations was consistent with a synaptic origin, whereas in other cells, the regular sinusoidal appearance of the fluctuations and the occurrence of superimposed plateau potentials were more compatible with the activation of an intrinsic membrane property. One motoneuron displayed exclusively excitatory phasic drive, and another motoneuron was characterized by inhibitory phasic drive alone, during rhythmic activity. These findings are compatible with the concept of a central pattern generator that is capable of delivering both excitatory and inhibitory drive to motoneurons during locomotion. The data also suggest that the rhythmic excitatory and inhibitory outputs of the hypothetical half-center model can be dissociated and operate in isolation.
Substance P Regulates I h via a NK-1 Receptor in Vagal Sensory Neurons of the Ferret
Authors: Jafri M. Samir , Weinreich Daniel
Published: December 2017

Jafri, M. Samir and Daniel Weinreich. Substance P regulates I h via a NK-1 receptor in vagal sensory neurons of the ferret. J. Neurophysiol. 79: 769–777, 1998. Substance P (SP) hyperpolarizes ∼80% of ferret vagal sensory neurons (nodose ganglion neurons) via NK-1 receptor-mediated activation of a potassium current ( I K). A depolarizing current activated by membrane hyperpolarization could minimize the SP-induced hyperpolarization. Such a current exists in 65% of the nodose neurons ( n = 264). In this study, we examine this current and how it can interact with SP-induced membrane hyperpolarizations. This slowly developing, noninactivating inward current, designated I h, was activated maximally at about −120 mV and had a reversal potential value of −23 ± 4.4 mV ( n = 4). The time course of activation followed voltage-dependent, monoexponential kinetics. Steady-state activation curves derived from tail current analysis were well fit by a Boltzmann equation yielding a half-activation potential ( V 1/2) of−77 ± 1.5 mV and a k s value of 18 ± 0.5 ( n = 8). In the presence of 1 mM cesium, the current was completely abolished. These parameters are consistent with those derived for I h in other neurons. Substance P (200 nM) reduced the magnitude of I h elicited by membrane hyperpolarizations to about −110 mV but did not affect the magnitude of I h elicited by hyperpolarizations to more negative potentials. Tail current analysis revealed that this effect was the result of a SP-induced shift of the I h activation curve to more negative membrane potentials. The V 1/2 value for I h was shifted by −20 ± 1.4 mV in the presence of SP with no change in k s (18 ± 0.7; n = 5). The SP effect on I h, like its effect on I K, was blocked reversibly by 10 nM CP99,994, a NK-1 antagonist, and was mimicked by the NK-1 agonist Ac-[Arg6, Sar9, Met(O2)11]SP(6-11) (ASMSP; 200 nM). I h was not affected by NK-2 or NK-3 selective agonists ( n = 4 for each) nor was the effect of SP on I h reduced by an NK-2 antagonist ( n = 4). These results show that SP activates a NK-1 receptor coupled to the I h channel. Thus NK-1 receptor activation in ferret vagal afferents not only leads to membrane hyperpolarization but it also can enhance synergistically this inhibitory effect by decreasing I h.
Effects of Saccades on the Activity of Neurons in the Cat Lateral Geniculate Nucleus
Authors: Lee Daeyeol , Malpeli Joseph G.
Published: December 2017

Lee, Daeyeol and Joseph G. Malpeli. Effects of saccades on the activity of neurons in the cat lateral geniculate nucleus. J. Neurophysiol. 79: 922–936, 1998. Effects of saccades on individual neurons in the cat lateral geniculate nucleus (LGN) were examined under two conditions: during spontaneous saccades in the dark and during stimulation by large, uniform flashes delivered at various times during and after rewarded saccades made to small visual targets. In the dark condition, a suppression of activity began 200–300 ms before saccade start, peaked ∼100 ms before saccade start, and smoothly reversed to a facilitation of activity by saccade end. The facilitation peaked 70–130 ms after saccade end and decayed during the next several hundred milliseconds. The latency of the facilitation was related inversely to saccade velocity, reaching a minimum for saccades with peak velocity >70–80°/s. Effects of saccades on visually evoked activity were remarkably similar: a facilitation began at saccade end and peaked 50–100 ms later. When matched for saccade velocity, the time courses and magnitudes of postsaccadic facilitation for activity in the dark and during visual stimulation were identical. The presaccadic suppression observed in the dark condition was similar for X and Y cells, whereas the postsaccadic facilitation was substantially stronger for X cells, both in the dark and for visually evoked responses. This saccade-related regulation of geniculate transmission appears to be independent of the conditions under which the saccade is evoked or the state of retinal input to the LGN. The change in activity from presaccadic suppression to postsaccadic facilitation amounted to an increase in gain of geniculate transmission of ∼30%. This may promote rapid central registration of visual inputs by increasing the temporal contrast between activity evoked by an image near the end of a fixation and that evoked by the image immediately after a saccade.
Coding Strategies in Monkey V1 and Inferior Temporal Cortices
Authors: Gershon Ethan D. , Wiener Matthew C. , Latham Peter E. , Richmond Barry J.
Published: December 2017

Gershon, Ethan D., Matthew C. Wiener, Peter E. Latham, and Barry J. Richmond. Coding strategies in monkey V1 and inferior temporal cortices. J. Neurophysiol. 79: 1135–1144, 1998. We would like to know whether the statistics of neuronal responses vary across cortical areas. We examined stimulus-elicited spike count response distributions in V1 and inferior temporal (IT) cortices of awake monkeys. In both areas, the distribution of spike counts for each stimulus was well described by a Gaussian distribution, with the log of the variance in the spike count linearly related to the log of the mean spike count. Two significant differences in response characteristics were found: both the range of spike counts and the slope of the log(variance) versus log(mean) regression were larger in V1 than in IT. However, neurons in the two areas transmitted approximately the same amount of information about the stimuli and had about the same channel capacity (the maximum possible transmitted information given noise in the responses). These results suggest that neurons in V1 use more variable signals over a larger dynamic range than IT neurons, which use less variable signals over a smaller dynamic range. The two coding strategies are approximately as effective in transmitting information.
Evidence for Postsynaptic Induction and Expression of NMDA Receptor Independent LTP
Authors: Grover Lawrence M.
Published: December 2017

Grover, Lawrence M. Evidence for postsynaptic induction and expression of NMDA receptor independent LTP. J. Neurophysiol. 79: 1167–1182, 1998. Whole cell/patch-clamp and extracellular field potential recordings were used to study the induction and expression of N-methyl-d-aspartate (NMDA) receptor independent long-term potentiation (LTP) in area CA1 of the in vitro rat hippocampus. Induction of NMDA receptor independent LTP was prevented by manipulations that inhibited postsynaptic depolarization during tetanic stimulation: direct hyperpolarization of postsynaptic neurons and bath application of an α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) and kainate receptor antagonist. NMDA receptor independent LTP also was blocked by intracellular application of the lidocaine derivative, N-(2,6-dimethylphenylcarbamoylmethyl)triethylammonium bromide (QX-314), to CA1 pyramidal neurons. These results complement the previous findings that NMDA receptor independent LTP was inhibited by postsynaptic injections of the calcium chelator 1,2-bis(2-aminophenoxy)ethane- N,N,N′,N′-tetraacetic acid and also was inhibited by a L-type voltage-dependent calcium channel antagonist (nifedipine). Collectively, these data make a strong case for the postsynaptic induction of this form of LTP. This paper also provides evidence for postsynaptic expression of NMDA receptor independent LTP. In an experiment where AMPA- and NMDA-receptor–mediated excitatory postsynaptic potentials (EPSPs) were isolated pharmacologically, LTP was found for only the AMPA-receptor–mediated EPSPs. In a separate experiment, paired-pulse facilitation (PPF) was measured during NMDA receptor independent LTP. Although there was an initial decrease in PPF, suggesting a posttetanic increase in the probability of glutamate release, the change in PPF decayed within 30–40 min of the tetanic stimulation, whereas the magnitude of the LTP was constant over this same time period. In addition, the LTP, but not the corresponding change in PPF, was blocked by the metabotropic glutamate receptor antagonist (±)-α-methyl-4-carboxyphenylglycine. These results are accounted for most easily by a selective increase in postsynaptic AMPA receptor function, but one type of presynaptic modification—an increase in the number of release sites without an overall change in the probability of release—also could account for these results (assuming that the level of glutamate release before LTP induction fully saturated NMDA, but not AMPA, receptors). One possible presynaptic modification, an increase in axon excitability, was ruled out by analysis of the presynaptic fiber volley, which was not increased at any time after LTP induction.
Regulation of Synaptic Depression Rates in the Cricket Cercal Sensory System
Authors: Hill Andrew A. V. , Jin Ping
Published: December 2017

Hill, Andrew A. V. and Ping Jin. Regulation of synaptic depression rates in the cricket cercal sensory system. J. Neurophysiol. 79: 1277–1285, 1998. To assess the roles of pre- and postsynaptic mechanisms in the regulation of depression, short-term synaptic depression was characterized at the synapses between sensory neurons and two interneurons in the cricket cercal sensory system. Changes in excitatory postsynaptic potential (EPSP) amplitude with repetitive stimulation at 5 and 20 Hz were quantified and fitted to the depletion model of transmitter release. The depression rates of different sensory neuron synapses on a single interneuron varied with the age of the sensory neurons such that old sensory neuron synapses depressed faster than young synapses. Although all synapses showed depression, short-term facilitation was selectively expressed only at sensory neuron synapses on one interneuron, the medial giant interneuron (MGI). These synapses showed concurrent facilitation and depression with high-frequency stimulation (100 Hz), whereas the synapses on another interneuron, 10-3, showed only depression at all stimulus frequencies. A previous study showed that the ability of a synapse to facilitate is correlated with the identity of the postsynaptic neuron. The present results indicate that depression and facilitation are regulated independently. Depression is regulated presynaptically in a manner related to sensory neuron age; whereas, facilitation is regulated by the postsynaptic target.
Developmental Changes in the Electrophysiological Properties of Brain Stem Trigeminal Neurons During Pattern (Barrelette) Formation
Authors: Guido William , Günhan-Agar Emine , Erzurumlu Reha S.
Published: December 2017

Guido, William, Emine Günhan-Agar, and Reha S. Erzurumlu. Developmental changes in the electrophysiological properties of brain stem trigeminal neurons during pattern (barrelette) formation. J. Neurophysiol. 79: 1295–1306, 1998. In the brain stem trigeminal nuclei of rodents there is a patterned representation of whiskers and sinus hairs. The subnucleus interpolaris (SPI) contains the largest and the most conspicuous whisker patterns (barrelettes). Although neural activity plays a role in pattern formation, little is known about the electrophysiological properties of developing barrelette neurons. Here we examined the functional state of early postnatal SPI neurons during and after the consolidation of patterns by using in vitro intracellular recording techniques. After the consolidation of barrelettes [≥ postnatal day (P)4], responses to intracellular current injection consistently reflected the activation of a number voltage-dependent conductances. Most notable was a mixed cation conductance ( I H) that prevented strong hyperpolarization and a large low-threshold Ca2+ conductance, which led to Ca2+ spikes and burst firing. At the oldest ages tested (P11–P14) some cells also exhibited an outward K+ conductance ( I A), which led to significant delays in action-potential firing. Between P0–3, a time when the formation of barrelettes in the brain stem is still susceptible to damage of the sensory periphery, cells responded linearly to intracellular current injection, indicating they either lacked such voltage-gated properties or weakly expressed them. At all ages tested (P0–14), SPI cells were capable of generating trains of action potentials in response to intracellular injection of depolarizing current pulses. However, during the first few days of postnatal life, spikes were shorter and longer. Additionally, spike trains rose more linearly with stimulus intensity and showed frequency accommodation at early ages. Taken together, these results indicate that the electrophysiological properties of SPI neurons change markedly during the period of barrelette consolidation. Moreover, the properties of developing SPI neurons may play a significant role in pattern formation by minimizing signal distortion and ensuring that excitatory responses from sensory periphery are accurately received and transmitted according to stimulus strength.
GABABReceptor-Mediated Inhibition of GABAAReceptor Calcium Elevations in Developing Hypothalamic Neurons
Authors: Obrietan Karl , van den Pol Anthony N.
Published: December 2017

Obrietan, K. and Anthony N. van den Pol. GABABreceptor-mediated inhibition of GABAAreceptor calcium elevations in developing hypothalamic neurons. J. Neurophysiol. 79: 1360–1370, 1998. In the CNS, γ-aminobutyric acid (GABA) affects neuronal activity through both the ligand-gated GABAAreceptor channel and the G protein-coupled GABABreceptor. In the mature nervous system, both receptor subtypes decrease neural excitability, whereas in most neurons during development, the GABAAreceptor increases neural excitability and raises cytosolic Ca2+levels. We used Ca2+digital imaging to test the hypothesis that GABAAreceptor-mediated Ca2+rises were regulated by GABABreceptor activation. In young, embryonic day 18, hypothalamic neurons cultured for 5 ± 2 days in vitro, we found that cytosolic Ca2+rises triggered by synaptically activated GABAAreceptors were dramatically depressed (>80%) in a dose-dependent manner by application of the GABABreceptor agonist baclofen (100 nM–100 μM). Coadministration of the GABABreceptor antagonist 2-hydroxy-saclofen or CGP 35348 reduced the inhibitory action of baclofen. Administration of the GABABantagonist alone elicited a reproducible Ca2+rise in >25% of all synaptically active neurons, suggesting that synaptic GABA release exerts a tonic inhibitory tone on GABAAreceptor-mediated Ca2+rises via GABABreceptor activation. In the presence of tetrodotoxin the GABAAreceptor agonist muscimol elicited robust postsynaptic Ca2+rises that were depressed by baclofen coadministration. Baclofen-mediated depression of muscimol-evoked Ca2+rises were observed in both the cell bodies and neurites of hypothalamic neurons taken at embryonic day 15 and cultured for three days, suggesting that GABABreceptors are functionally active at an early stage of neuronal development. Ca2+rises elicited by electrically induced synaptic release of GABA were largely inhibited (>86%) by baclofen. These results indicate that GABABreceptor activation depresses GABAAreceptor-mediated Ca2+rises by both reducing the synaptic release of GABA and decreasing the postsynaptic Ca2+responsiveness. Collectively, these data suggest that GABABreceptors play an important inhibitory role regulating Ca2+rises elicited by GABAAreceptor activation. Changes in cytosolic Ca2+during early neural development would, in turn, profoundly affect a wide array of physiological processes, such as gene expression, neurite outgrowth, transmitter release, and synaptogenesis.
Are Complex Control Signals Required for Human Arm Movement?
Authors: Gribble Paul L. , Ostry David J. , Sanguineti Vittorio , Laboissière Rafael
Published: December 2017

Gribble, Paul L., David J. Ostry, Vittorio Sanguineti, and Rafael Laboissière. Are complex control signals required for human arm movement? J. Neurophysiol. 79: 1409–1424, 1998. It has been proposed that the control signals underlying voluntary human arm movement have a “complex” nonmonotonic time-varying form, and a number of empirical findings have been offered in support of this idea. In this paper, we address three such findings using a model of two-joint arm motion based on the λ version of the equilibrium-point hypothesis. The model includes six one- and two-joint muscles, reflexes, modeled control signals, muscle properties, and limb dynamics. First, we address the claim that “complex” equilibrium trajectories are required to account for nonmonotonic joint impedance patterns observed during multijoint movement. Using constant-rate shifts in the neurally specified equilibrium of the limb and constant cocontraction commands, we obtain patterns of predicted joint stiffness during simulated multijoint movements that match the nonmonotonic patterns reported empirically. We then use the algorithm proposed by Gomi and Kawato to compute a hypothetical equilibrium trajectory from simulated stiffness, viscosity, and limb kinematics. Like that reported by Gomi and Kawato, the resulting trajectory was nonmonotonic, first leading then lagging the position of the limb. Second, we address the claim that high levels of stiffness are required to generate rapid single-joint movements when simple equilibrium shifts are used. We compare empirical measurements of stiffness during rapid single-joint movements with the predicted stiffness of movements generated using constant-rate equilibrium shifts and constant cocontraction commands. Single-joint movements are simulated at a number of speeds, and the procedure used by Bennett to estimate stiffness is followed. We show that when the magnitude of the cocontraction command is scaled in proportion to movement speed, simulated joint stiffness varies with movement speed in a manner comparable with that reported by Bennett. Third, we address the related claim that nonmonotonic equilibrium shifts are required to generate rapid single-joint movements. Using constant-rate equilibrium shifts and constant cocontraction commands, rapid single-joint movements are simulated in the presence of external torques. We use the procedure reported by Latash and Gottlieb to compute hypothetical equilibrium trajectories from simulated torque and angle measurements during movement. As in Latash and Gottlieb, a nonmonotonic function is obtained even though the control signals used in the simulations are constant-rate changes in the equilibrium position of the limb. Differences between the “simple” equilibrium trajectory proposed in the present paper and those that are derived from the procedures used by Gomi and Kawato and Latash and Gottlieb arise from their use of simplified models of force generation.