bluuebunny/crossref_metadata_2025 huggingface dataset:
Comparison of evoked potentials and high-frequency (gamma-band) oscillating potentials in rat auditory cortex
Authors: Franowicz M. N. , Barth D. S.
Published: December 2017

1. Transient and steady-state (40 Hz) evoked potentials, as well as spontaneous and click-evoked gamma-band oscillations, were recorded from 15 lightly anesthetized rats using an 8 x 8 electrode epipial array covering auditory cortex and adjacent areas to determine and compare the spatiotemporal distributions of these four phenomena. 2. The transient evoked response replicated earlier findings in our laboratory, consisting of an initial biphasic sharp wave in area 41, a similar but delayed biphasic sharp wave in area 36, and more widely distributed slow-wave components. Spatiotemporal analysis supported a model of parallel and asynchronous activation of distinct groups of thalamocortical projections underlying the neurogenesis of these temporal components of the middle-latency auditory evoked potential (MAEP) complex. 3. The 40-Hz response to click trains was superimposed on a steady potential shift (SP), both of which were localized within primary auditory cortex. Epipial distributions of the SP were similar to those of the shortest-latency negative peak in area 41 recorded in the same animals, suggesting similar neural generators. The 40-Hz response was more focal and dissimilar from the SP and any other temporal components of the MAEP complex, suggesting that a unique subpopulation of cells underlies its neurogenesis. 4. Spontaneous gamma-band activity, as assessed by power spectrum analysis, was localized to primary and secondary auditory cortex but had a variable distribution between rats that did not conform to the cytoarchitectonic boundaries within subdivisions of this region. Digital movies computed for individual bursts of gamma-activity indicated a high degree of spatiotemporal variability within and between bursts. 5. Single-trial spectral analysis of click responses indicated an inhibition of gamma-band oscillations during most of the MAEP complex, with subsequent enhanced gamma-activity during the 300- to 350-ms slow-wave component that outlasted the MAEP by approximately 500 ms. The epipial distributions of prestimulus and enhanced poststimulus gamma-oscillations were the same. In contrast to the 40-Hz response to click trains, phase-locking of gamma-oscillations by the single click stimulus was not observed. 6. These results suggest that both the MAEP complex and the steady-state 40-Hz response with its associated SP are highly stereotyped in lightly anesthetized rodent cortex. Their spatiotemporal distributions are probably determined in large part by asynchronous activation of parallel thalamocortical projection systems. Our data suggest no direct link between either the MAEP or the steady-state 40-Hz response to spontaneous or evoked gamma-band oscillations in auditory cortex.(ABSTRACT TRUNCATED AT 400 WORDS)
Decreased monosynaptic GABAB-mediated inhibitory postsynaptic potentials in hippocampal CA1 pyramidal cells in the aged rat: pharmacological characterization and possible mechanisms
Authors: Billard J. M. , Lamour Y. , Dutar P.
Published: December 2017

1. gamma-Aminobutyric acid (GABA)-mediated inhibitory postsynaptic potentials (IPSPs) were compared in young and aged rats in CA1 area of the rat hippocampus, with the use of the in vitro intracellular recording technique. D-2-Amino-5-phosphonovaleric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were used to suppress synaptic potentials mediated by the excitatory amino acids. 2. Under these conditions, stimulation of the stratum radiatum elicited a monosynaptic fast GABAA (fIPSP) and a slow GABAB (sIPSP)-mediated IPSP. The fIPSP and the sIPSP were further isolated in the presence of the GABAB antagonist CGP 35348 or the GABAA antagonists bicuculline or picrotoxin. No age-related changes were observed in the amplitude and the duration of the fIPSP. In contrast, the amplitude (but not the duration) of the sIPSP was significantly reduced in the aged rat. 3. The postsynaptic hyperpolarization and increase in membrane conductance induced in pyramidal cells by bath application of the GABAB agonist baclofen were comparable in both groups of animals, indicating that the postsynaptic GABAB receptors are not altered in the aged rats. 4. Paired-pulse depression of IPSPs was used in young and aged rats to study possible alterations in GABA release or in presynaptic GABAB receptors that control GABA release. When fIPSPs were isolated by bath application of tetrahydro-9-aminoacridine (THA), no significant difference in the magnitude of the paired-pulse depression was observed between young and aged rats. A similar result was found with the paired-pulse depression of isolated sIPSPs in the presence of bicuculline or picrotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)
Responses of cells in the tail of the caudate nucleus during visual discrimination learning
Authors: Brown V. J. , Desimone R. , Mishkin M.
Published: December 2017

1. The tail of the caudate nucleus and adjacent ventral putamen (ventrocaudal neostriatum) are major projection sites of the extrastriate visual cortex. Visual information is then relayed, directly or indirectly, to a variety of structures with motor functions. To test for a role of the ventrocaudal neostriatum in stimulus-response association learning, or habit formation, neuronal responses were recorded while monkeys performed a visual discrimination task. Additional data were collected from cells in cortical area TF, which serve as a comparison and control for the caudate data. 2. Two monkeys were trained to perform an asymmetrically reinforced go-no go visual discrimination. The stimuli were complex colored patterns, randomly assigned to be either positive or negative. The monkey was rewarded with juice for releasing a bar when a positive stimulus was presented, whereas a negative stimulus signaled that no reward was available and that the monkey should withhold its response. Neuronal responses were recorded both while the monkey performed the task with previously learned stimuli and while it learned the task with new stimuli. In some cases, responses were recorded during reversal learning. 3. There was no evidence that cells in the ventrocaudal neostriatum were influenced by the reward contingencies of the task. Cells did not fire preferentially to the onset of either positive or negative stimuli; neither did cells fire in response to the reward itself or in association with the motor response of the monkey. Only visual responses were apparent. 4. The visual properties of cells in these structures resembled those of cells in some of the cortical areas projecting to them. Most cells responded selectively to different visual stimuli. The degree of stimulus selectivity was assessed with discriminant analysis and was found to be quantitatively similar to that of inferior temporal cells tested with similar stimuli. Likewise, like inferior temporal cells, many cells in the ventrocaudal neostriatum had large, bilateral receptive fields. Some cells had "doughnut"-shaped receptive fields, with stronger responses in the periphery of both visual fields than at the fovea, similar to the fields of some cells in the superior temporal polysensory area. Although the absence of task-specific responses argues that ventrocaudal neostriatal cells are not themselves the mediators of visual learning in the task employed, their cortical-like visual properties suggest that they might relay visual information important for visuomotor plasticity in other structures. (ABSTRACT TRUNCATED AT 400 WORDS)
Differences in the brain stem terminations of large- and small-diameter vestibular primary afferents
Authors: Huwe J. A. , Peterson E. H.
Published: December 2017

1. We visualized the central axons of 32 vestibular afferents from the posterior canal by extracellular application of horseradish peroxidase, reconstructed them in three dimensions, and quantified their morphology. Here we compare the descending limbs of central axons that differ in parent axon diameter. 2. The brain stem distribution of descending limb terminals (collaterals and associated varicosities) varies systematically with parent axon diameter. Large-diameter afferents concentrate their terminals in rostral regions of the medial/descending nuclei. As axon diameter decreases, there is a significant shift of terminal concentration toward the caudal vestibular complex and adjacent brain stem. 3. Rostral and caudal regions of the medial/descending nuclei have different labyrinthine, cerebellar, intrinsic, commissural, and spinal connections; they are believed to play different roles in head movement control. Our data help clarify the functions of large- and small-diameter afferents by showing that they contribute differentially to rostral and caudal vestibular complex.
Adenosine facilitates in vivo neurotransmission in the superior colliculus of the rat
Authors: Hirai H. , Okada Y.
Published: December 2017

1. Electrical responses to volleys in afferent fibers in the optic tract were recorded in the superficial gray layer of anesthetized rat superior colliculus. A prominent negative wave with 4- to 6-ms peak latency in the upper part of the superficial gray layer and a sharp negative wave with 1.5- to 2-ms peak latency in the lower part of the superficial gray layer were elicited, corresponding to the C2 (upper part of the superficial gray layer) and the C1 (lower part of the superficial gray layer) postsynaptic potentials reported by Sefton. 2. These C1 and C2 waves were depressed by kynurenic acid or quinoxaline dione (DNQX) applied just beside the recording electrode, suggesting that neurotransmission in these pathways is mediated by glutamate. 3. Adenosine (10 microM) injected in the superficial gray layer enhanced both C1 and C2 potentials up to 170 and 140%, respectively. 4. Administration of a potent inhibitor of adenosine deaminase, erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA; 5 mg/kg sc) increased the amplitudes of both C1 and C2 potentials to 125 and 130% of the initial levels, respectively. 5. The extracellular application of adenosine uptake inhibitors, dipyridamole (100 microM) and nitrobenzylthioinosine (NBI; 10 microM) also enhanced postsynaptic potentials. 6. Prior application of L-homocysteine thiolactone (10 microM), a compound that facilitates the incorporation of adenosine into S-adenosylhomocystein and reduces the extracellular concentration of adenosine, attenuated the excitatory action of exogenously applied adenosine. 7. Excitatory effects were also observed upon application of a selective adenosine A1 receptor agonist, N6-cyclohexyladenosine (CHA) or a selective A2 receptor agonist, 2-[4-(2-carboxylethyl)- phenethylamino]-5'N-ethylcarboxamide adenosine hydrochloride (CGS21680). Selective A1 and A2 receptor antagonists, 8-cyclopentyl-1,3-dimethylxanthine (CPT) and 3,7-dimethyl-1-propargylxanthine (DMPX), respectively, failed to suppress the excitatory action by adenosine. However, combined application of these two agents blocked the facilitatory action by adenosine on the excitatory synapses. 8. The application of adenosine (10 microM) to the superficial gray layer via a microdialysis probe increased the glutamate release by approximately 230% of the basal level. Similarly, the administration of EHNA (5 mg/kg sc) enhanced the extracellular glutamate level up to approximately 170%. However, prior application of L-homocysteine thiolactone (10 microM) failed to potentiate the glutamate release by adenosine. 9. This is the first in vivo study to demonstrate an excitatory action of adenosine on synaptic transmission.(ABSTRACT TRUNCATED AT 250 WORDS)
Regulation of cyclic nucleotide-gated channels and membrane excitability in olfactory receptor cells by carbon monoxide
Authors: Leinders-Zufall T. , Shepherd G. M. , Zufall F.
Published: December 2017

1. The effect of the putative neural messenger carbon monoxide (CO) and the role of the cGMP second-messenger system for olfactory signal generation was examined in isolated olfactory receptor neurons (ORNs) of the tiger salamander. 2. With the use of whole cell voltage-clamp recordings in combination with a series of ionic and pharmological tests, it is demonstrated that exogenously applied CO is a potent activator (K1/2 = 2.9 microM) of cyclic nucleotide-gated (CNG) channels previously described to mediate odor transduction. 3. Several lines of evidence suggest that CO mediates its effect through stimulation of a soluble guanylyl cyclase (sGC) leading to formation of the second-messenger cGMP. This conclusion is based on the findings that CO responses show an absolute requirement for guanosine 5'-triphosphate (GTP) in the internal solution, that no direct effect of CO on CNG currents in the absence of GTP is detectable, and that a blocker of sGC activation, LY85383 (10 microM), completely inhibits the CO response. 4. The dose-response curve for cGMP at CNG channels is used as a calibration to provide a quantitative estimate of the CO-stimulated cGMP formation. This analysis implies that CO is a potent activator of olfactory sGC. 5. Perforated patch recordings using amphotericin B demonstrate that low micromolar doses of CO effectively depolarize the membrane potential of ORNs through tonic activation of CNG channels. This effect in turn regulates excitable and adaptive properties of ORNs and modulates neuronal responsiveness. 6. These data argue for an important role of the cGMP pathway in olfactory signaling and support the idea that CO may function as a diffusible messenger in the olfactory system.
Whole cell calcium currents in acutely isolated olfactory bulb output neurons of the rat
Authors: Wang X. , McKenzie J. S. , Kemm R. E.
Published: December 2017

1. Voltage-gated whole cell Ca2+ currents have been investigated in olfactory bulb (OB) output neurons acutely isolated from neonatal rats. 2. Identification of OB output neurons, mitral or tufted cells, was based on morphology and size and validated by their retrograde labeling with rhodamine or Fast Blue. Of labeled neurons, 45% exhibited either phasic or nonphasic spontaneous firing that was blocked by 10(-7) M tetrodotoxin, 0.5 mM Cd2+, or 1 mM Co2+ in the bathing solution. 3. Whole cell Ca2+ currents displayed holding potential sensitivity indicative of low voltage-activated (LVA) and high voltage-activated (HVA) currents, which exhibited similar dependence on extracellular Ca2+ concentration and could be completely abolished by bathing in 500 microM Cd2+ or in Ca(2+)-free solution. 4. A T-type LVA Ca2+ current, detected in 65% of OB output neurons tested, was activated by depolarizing to -57 mV from holding potential -86 mV and fully inactivated at holding potentials more positive than -60 mV. It was permeated equally by 2.6 mM Ca2+, Sr2+ and Ba2+. The half-activation potential was -35 mV with a slope factor of 7 mV. Depolarizing to -26 mV from different holding potentials in a 2.6-mM Ca2+ solution gave a steady-state half-inactivation potential of -82 mV with a slope factor of 10.7 mV. This LVA current was not sensitive to 5 microM omega-conotoxin (omega-CgTx) or 5 microM Bay K 8644 and was resistant to block by 30 microM Cd2+, by 50 microM verapamil or by 5 microM nifedipine. 5. HVA Ca2+ currents, detected in 97% of OB output cells, activated at around -30 to -20 mV, with maximum peak current at approximately 4 mV in 2.6 mM Ca2+ external solution. They showed similar permeability to 2.6 mM Ca2+ and Sr2+, but the maximum peak current was increased 40% in 2.6 mM Ba2+. Depolarizing to 4 mV from different holding potentials yielded a half-inactivation potential of -67 mV with a slope factor of 13.2 mV. Two components, as suggested by their sensitivities to 5 microM Bay K 8644, nifedipine. omega-CgTx and to voltage, may resemble the L-type and N-type currents described in other neural preparations. However, 5 microM omega-CgTx seemed to block both components, being more effective at more positive potentials. There was a residual component of Cd(2+)-sensitive current not affected by cumulative addition of nifedipine and omega-CgTx. 6. omega-Agatoxin IVA (omega-Aga), a selective P-type Ca2+ channel blocker, had no detectable effect at 50 or 200 nM and 1 microM doses on whole cell Ca2+ currents elicited by 200-ms voltage steps to 4 mV from holding potential -86 mV. 7. We conclude that both LVA and HVA Ca2+ currents exist in neonatal rat OB output neurons, showing distinct kinetic and pharmacological characteristics. The HVA Ca2+ currents contain at least two components, probably resembling L- and N-type currents. Another fast-inactivating HVA component, insensitive to nifedipine, omega-CgTx and omega-Aga, could represent the newly established R-type Ca2+ current.
Projection neurons of the lateral amygdaloid nucleus are virtually silent throughout the sleep--waking cycle
Authors: Gaudreau H. , Pare D.
Published: December 2017

1. Amygdala neurons were recorded extracellularly during the sleep-waking cycle in chronically implanted cats. Neurons were identified as projection cells when they could be antidromically invaded from the perirhinal and/or entorhinal cortices. 2. In contrast with other nuclei of the amygdala, few spontaneously active neurons were encountered in the lateral nucleus. However, when hunting stimuli were applied to the parahippocampal cortices, we noticed the presence of numerous projection cells that would have otherwise remained undetected because they had little or no spontaneous activity. 3. In the states of waking, slow-wave sleep, and paradoxical sleep, the discharge rate of antidromically invaded neurons averaged 0.09 +/- 0.07 Hz (mean +/- SE) with 82% of cells firing at < 0.01 Hz in all states. However, they transiently increased their firing rate when cats were presented complex sensory stimuli, which apparently were specific to each cell. In contrast to projection cells, spontaneously active neurons of the lateral nucleus that could not be backfired from the parahippocampal cortices had an average firing rate of 4.34 +/- 1.15 Hz with 38% of cells firing at > or = 6 Hz in at least one state. 4. These results on the extremely low firing rates of identified projection cells suggest that previous extracellular studies of lateral amygdaloid neurons were biased toward a class of spontaneously active cells which probably includes local-circuit cells.
Intraaxonal injection of neurobiotin reveals the long-ranging projections of A beta-hair follicle afferent fibers to the cat dorsal horn
Authors: Wilson P. , Kitchener P. D. , Snow P. J.
Published: December 2017

1. The morphology and somatotopic organization of the spinal arborizations of identified A beta-hair follicle afferent fibers (HFAs) with receptive fields (RFs) on the digits have been investigated in the cat by the use of intraaxonal injection of the tracer n-(2 aminoethyl) biotinamide. 2. In three cats, the long-ranging projections of six HFAs were examined by selectively injecting afferents with RFs on digit 2, 4, or 5, directly over the digit 3 representation, and examining their collateral morphology in transverse sections of the spinal cord. The rostral and caudal boundaries of the digit 3 representation were determined by mapping the RFs of identified spinocervical tract (SCT) neurons. 3. In two more cats, three HFAs were injected at random rostrocaudal positions and their morphology was examined in parasagittal sections. In one animal (2 HFAs), the somatotopy of the digit representation was again determined by mapping the RFs of SCT neurons. In the remaining cat (1 HFA), the somatotopy of the dorsal horn was mapped from the RFs of unidentified dorsal horn neurons. 4. Hair follicle afferents emitted many more collaterals, over much greater rostrocaudal distances, than indicated by previous horseradish peroxidase studies, and all collaterals gave rise to synaptic boutons. 5. HFAs that have RFs confined to a small part of a digit give rise to bouton-bearing axonal branches throughout the entire rostrocaudal extent of the hindpaw representation.
Glutamate-mediated release of Ca2+ in mitral cells of the olfactory bulb
Authors: Geiling H. , Schild D.
Published: December 2017

1. Effects of glutamate on intracellular Ca2+ concentration ([Ca2+]i) were investigated in cultured olfactory bulb neurons of Xenopus laevis tadpoles. We imaged [Ca2+]i in these cells with the use of a confocal laser scanning microscope and the calcium indicator dyes Fluo3 and FuraRed. 2. In the standard bath solution, application of glutamate through a pipette resulted in an increase of [Ca2+]i in both mitral/ tufted (M/T) cells and interneurons. The increase occurred in all compartments of the cells, although in a nonhomogenous way. 3. In an ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid-buffered bath solution (Ca(2+)-free Ringer solution), glutamate reproducibly induced an increase of [Ca2+]i in M/T cells but not in interneurons. This increase in [Ca2+]i had the following properties: 1) it was delayed with respect to the combined ionotropic and metabotropic response to glutamate, 2) in some cases it stopped before the end of the glutamate application, and 3) it was not affected by D,L-2-amino-5-phosphonopentanoic acid and 6-cyano-7-nitroquinoxaline-2,3-dione added to the bath. It was interpreted as a release of Ca2+ from intracellular calcium stores. 4. Of 47 M/T cells that showed a glutamate-mediated release of [Ca2+]i, 46 also showed Ca2+ influx through ionotropic glutamate receptors, so that intracellular release of [Ca2+]i appeared to be associated with the presence of glutamate-gated ion channels. However, of 110 M/T cells showing an ionotropic response to glutamate, only 46 showed a glutamate-mediated release of [Ca2+]i. 5. The glutamate-mediated release of [Ca2+]i in the dendrites was higher than that in the soma. No indications for calcium waves were found. 6. Quisqualate and (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) mimicked the effect of glutamate on the release of [Ca2+]i, with potencies quisqualate > glutamate > > ACPD. N-acetyl-aspartyl-glutamate did not induce release of [Ca2+]i. The release was partly blocked by (+)-alpha-methyl-4-carboxyphenylglycine. 7. In conclusion, some but not all M/T cells of the olfactory bulb of X. laevis show a glutamate-mediated and predominantly dendritic increase of [Ca2+]i that is associated with glutamategated channels. The pharmacological properties of the corresponding metabotropic glutamate receptor (mGluR) resemble those of the mGluR1/5 receptors in rat.
Similarities and differences in the currents activated by capsaicin, piperine, and zingerone in rat trigeminal ganglion cells
Authors: Liu L. , Simon S. A.
Published: December 2017

1. Capsaicin, piperine, and zingerone are natural pungent-tasting compounds found in chili pepper, black pepper, and ginger, respectively. These structurally related compounds evoke many of the same physiological responses, but at comparable concentrations capsaicin produces complete tachyphylaxis, piperine produces partial tachyphylaxis, and zingerone can either induce or not induce tachyphylaxis. Whole cell patch-clamp studies were performed on rat trigeminal ganglion cells to determine the similarities and differences between these three pungent compounds. 2. Capsaicin (1 microM) activated a variety of inward currents having peak times ranging from 2 to 46 s that desensitized to various extents ranging from 0 to 100%. The inward currents activated by zingerone (30 mM) had peak times of approximately 2 s and all currents exhibited marked desensitization. The inward currents activated by piperine (100 microM) had peak times of approximately 25 s and all exhibited a small desensitization. 3. Piperine- and zingerone-induced currents were found only in cells that could be activated by capsaicin. 4. Capsazepine (10 microM), an established antagonist of capsaicin-induced currents, inhibited the currents evoked by piperine and zingerone, suggesting that all three compounds activate vanilloid receptors. 5. Dose-response relationships for capsaicin, piperine, and zingerone obtained at a holding potential of -60 mV had threshold and apparent dissociation constants of 0.1 and 0.68 microM, 3 and 35 microM, and 1 and 15 mM, respectively. These values were consistent with those previously obtained in behavioral studies. 6. After seven 30-s applications of 1 microM capsaicin or 100 microM piperine (in a buffer with 2 mM Ca2+), each interspersed with 2-min, 50-s washes, the peak currents were inhibited by approximately 60 and 40%, respectively. In contrast, 30 mM zingerone failed to evoke a current after six applications. After complete tachyphylaxis produced by 30 mM zingerone, 1 microM capsaicin failed to evoke a current, suggesting that these two compounds cross desensitize. 7. The similar physiological responses produced by these three compounds can be rationalized by their binding to receptors and activating currents that can all be inhibited by capsazepine. Their different physiological responses evoked by these compounds can be rationalized, in part, by their very different activation and desensitization kinetics, and perhaps by the existence of different subtypes of vanilloid receptors.
Increased calcium current in carotid body glomus cells following in vivo acclimatization to chronic hypoxia
Authors: Hempleman S. C.
Published: December 2017

1. Rat pups were gestated and born in normoxia (inspired O2 pressure 149 mmHg) or chronic hypoxia (insured O2 pressure 80 mmHg) to test whether chronic hypoxia alters carotid body glomus cell calcium currents. Carotid bodies were removed from 5- to 8-day-old-pups under halothane anesthesia, at which time blood hematocrits averaged 52 +/- 1% (mean +/- SE) in the chronically hypoxic pups and 36 +/- 1% in the normoxic pups (P < 0.05). Glomus cells were then enzymatically isolated from the carotid bodies, and calcium currents were recorded with whole cell patch clamp. 2. Compared with normoxic glomus cells (n = 29), chronically hypoxic glomus cells (n = 32) superfused with 10 mM CaCl2 had larger peak calcium current (146 +/- 16 pA vs. 49 +/- 7 pA, P < 0.05), larger peak calcium current density (12.0 +/- 1.1 pA/pF vs. 7.3 +/- 1.0 pA/pF, P < 0.05), and larger membrane capacitance (12.1 +/- 0.9 pF vs. 7.5 +/- 0.6 pF, P < 0.05). 3. Threshold for calcium current activation was approximately -40 mV. Currents showed little inactivation during 45-ms test pulses and were half-inactivated by a steady holding voltage of -11 +/- 2 mV (n = 15). Currents were reduced 43 +/- 13% by 50 microM nifedipine (n = 6, P < 0.05), and were augmented with barium as the charge carrier. These properties suggest that glomus cell calcium current is carried in part through L-type channels, and that is is relatively resistant to steady-state inactivation. 4. Augmented calcium influx through voltage-gated channels in glomus cells from chronically hypoxic neonatal rats may increase carotid body excitability through increased stimulus-secretion coupling. Overall, acclimatization to chronic hypoxia is known to depress acute hypoxic ventilatory reflex responses in neonates. The observations reported here suggest that inhibition of ventilatory reflexes by chronic hypoxia in neonates occurs centrally rather than peripherally.
Amino acid-mediated regulation of spontaneous synaptic activity patterns in the rat basolateral amygdala
Authors: Smith B. N. , Dudek F. E.
Published: December 2017

1. Spontaneous postsynaptic currents (PSCs) were examined in the basolateral amygdala using whole cell patch-clamp recordings in coronal slices (400 microns) from young rats (postnatal day 6-25). In most cells, Cs+ was used in the electrode to block putative voltage-activated K(+)-currents. Both inward and outward spontaneous PSCs were examined. 2. The alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist, 6,7-nitroquinoxaline-2,3-dione (DNQX) blocked all inward PSCs, which reversed near 0 mV. They therefore were considered to be glutamate-mediated excitatory postsynaptic currents (EPSCs). Averaged EPSCs had a rapid 10-90% rise time (1.0 +/- 0.04 ms; mean +/- SD) and monoexponential decay (tau = 3.6 +/- 0.18 ms) at potentials negative to about -50 mV. Above this potential, a second, slower time constant (tau 1 = 41 +/- 4.5 ms at -30 mV), accounting for 10-30% of the total EPSC amplitude was resolved in 8 of 10 cells examined. The slower decay time constant was sensitive to the N-methyl-D-aspartate (NMDA)-receptor antagonist, DL-2-amino-5-phosphonovaleric acid (AP5) and therefore probably was due to activation of NMDA receptors. 3. The gamma-aminobutyric acid-A (GABAA) antagonist, bicuculline, blocked all outward PSCs, which reversed near -70 mV. They therefore were considered to be GABA-mediated inhibitory postsynaptic currents (IPSCs). Averaged IPSCs displayed rapid 10-90% rise times (1.0 +/- 0.03 ms) and monoexponential decay time constants (tau = 5.16 +/- 0.14 ms). 4. Tetrodotoxin (TTX) reduced the frequency of synaptic activity and eliminated the largest PSCs, thus reducing slightly the mean EPSC and IPSC amplitude. Most cells received bursts of spontaneous IPSCs and/or EPSCs (30-68 Hz lasting 0.5-6 s), which were also TTX sensitive. The TTX data suggest that the somata of the cells responsible for the largest PSCs and the PSC bursts were contained within the slice. 5. In addition to blocking EPSCs, DNQX blocked the bursts of IPSCs, but not all individual IPSCs. DNQX had similar effects as TTX on the bursts and frequency of the IPSCs. 6. Bicuculline enhanced spontaneous EPSC frequency (231 +/- 90%). Much of this increase was due to an increase in the bursts of EPSCs. 7. Neurons in the basolateral amygdala therefore appear to receive both excitatory (glutamatergic) and inhibitory (GABAergic) synaptic input from local neurons. The activity of the neurons responsible for these inputs are themselves largely regulated by glutamatergic and GABAergic inputs. The relevance of this local circuitry to seizures and epilepsy is discussed briefly.
Opioids modulate N-methyl-D-aspartic acid (NMDA)-evoked responses of trigeminothalamic neurons
Authors: Wang X. M. , Mokha S. S.
Published: December 2017

1. The present study investigated opioid-mediated modulation of N-methyl-D-aspartic acid (NMDA)-evoked responses of trigeminothalamic neurons in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in rats anesthetized with urethane. 2. Microiontophoretic application of NMDA activated 18/19 trigeminothalamic neurons. Administration of [D-Ala2, N-Me-Phe4,Gly5-ol]-Enkephalin, a selective mu-opioid receptor agonist, reduced the NMDA-evoked responses in 77% of trigeminothalamic neurons. [D-Pen2,5]-Enkephalin, a selective delta-opioid receptor agonist, produced inhibition of NMDA-evoked responses in 36% of neurons. 3. We suggest that 1) NMDA-receptor activation excites trigeminothalamic nociceptive neurons and may, therefore, mediate nociceptive transmission in the medullary dorsal horn; and 2) the predominantly inhibitory modulation of NMDA-receptor-mediated responses of nociceptive trigeminothalamic neurons by activation of mu- and delta-opioid receptors may provide a neural mechanism for the antinociceptive actions of opioids.
Oscillatory and burst discharge across electrosensory topographic maps
Authors: Turner R. W. , Plant J. R. , Maler L.
Published: December 2017

1. Three parallel maps of the distribution of tuberous electroreceptor inputs are found in the medullary electrosensory lateral line lobe (ELL) of weakly electric fish. Pyramidal cells in each map are known to respond differentially to the frequency of amplitude modulations (AMs) of external electric fields in vivo. We used an in vitro ELL slice preparation of Apteronotus leptorhynchus to compare the characteristics of spontaneously active single units across the three tuberous maps. It was our objective to determine whether spontaneous bursting activity of pyramidal cells in each map correlates with the known AM frequency selectivities of pyramidal cells in vivo. 2. Single-unit discharges were recorded from the pyramidal cell layer of the centromedial segment (CMS), centrolateral segment (CLS), and lateral segment (LS) of the ELL. Stochastic analysis of interspike intervals (ISIs) was used to identify bursting and nonbursting unit activity, and to separately analyze intra- and interburst ISIs. Four ISI patterns were identified as 1) bursting, 2) regular spiking, 3) irregular spiking, and 4) highly irregular spiking. This work focuses primarily on the characteristics of bursting units across the ELL segments. 3. Spontaneous bursting discharge was identified in all three maps (68 of 97 units), with several characteristics changing in a gradual manner across the maps. The coefficient of variation (CV) of ISIs and intraburst ISIs decreased significantly from the CMS to the LS, whereas the CV of burst periods increased significantly from the CMS to the LS. Autocorrelations and power spectral density analysis identified units discharging in an oscillatory manner with the following ratio: CMS, 75%; CLS, 4%; LS, 8%. 4. The mean period of spike bursts decreased significantly across the segments (CMS, 2.7 s; CLS, 1.2 s; LS, 1.1 s) primarily because of a shortening of mean burst duration (CMS, 1.0 s; CLS, 0.1 s; LS, 0.05 s). The average number of spikes per burst decreased significantly across the maps (CMS, 61; CLS, 8; LS, 8), whereas the average frequency of spikes per burst increased (CMS, 90 Hz; CLS, 130 Hz; LS, 178 Hz), mainly through an increase in the maximal frequencies attained by units within each map. 5. Bursts in the CMS were unstructured in that the intraburst ISIs were serially independent, whereas for many units in the CLS and especially the LS there were serial dependencies of successive spikes, with alternating short and long ISIs during the burst. 6. These data reveal that the characteristics of bursting unit activity differ between the CMS, CLS, and LS maps in vitro, implying a modulation of the factors underlying burst discharge across multiple sensory maps. Because the pattern of change in burst activity between these maps parallels that of pyramidal cell AM frequency selectivity in vivo, oscillatory and burst discharge may represent the cellular mechanism used to tune these cells to specific frequencies of afferent input during electrolocation and electrocommunication.
Somatosensory cortical activity in relation to arm posture: nonuniform spatial tuning
Authors: Tillery S. I. , Soechting J. F. , Ebner T. J.
Published: December 2017

1. Single unitary activity in primate somatosensory cortex (SI) was recorded while monkeys maintained a range of static arm postures. Unit discharge was related to parameters defining the posture of the arm by multiple linear regression techniques. 2. Two monkeys were trained to grasp a manipulandum presented at locations distributed throughout their workspace. The discharge of single units in SI was recorded for 3 s while the monkeys maintained contact with the manipulandum and the mean discharge rate over this hold time was related to the location of the hand and to the shoulder and elbow joint angles of the arm. 3. Unitary activity of 171 neurons in the proximal arm region of areas 3, 1, and 2 was recorded during the task. Of the total, 78 neurons had activity that varied with the location of the hand in space. Neuronal discharge typically varied monotonically with the target location, reaching a maximum at the borders of the work-space. The discharge rate in most of these neurons varied with both shoulder and elbow angles. 4. Discharge rate was related to the hand's location along three axes by means of a polynomial fit. In approximately half of the neurons, activity varied significantly only for displacements along a single axis in space. However, many neurons exhibited nonlinear relations between hand location along this preferred axis and discharge rate. Discharge rate did not vary for displacements of the hand in the plane perpendicular to this preferred axis (null plane). 5. In other neurons, discharge rate varied for hand displacements in a plane, i.e., along two perpendicular axes. Displacements of the hand along the axis perpendicular to this plane (null axis) did not affect the discharge rate. In only a small minority of neurons did discharge rate vary for hand displacements along all three axes in space. 6. The distribution of the sensitivity of the neural population to hand displacements along arbitrary directions in space was not uniform. On average, hand displacement along a vertical axis led to the smallest modulation of neural discharge, and displacement of the hand along the anteroposterior direction led to the largest modulation of activity.
Imaging NMDA- and kainate-induced intrinsic optical signals from the hippocampal slice
Authors: Andrew R. D. , Adams J. R. , Polischuk T. M.
Published: December 2017

1. Brain ischemia causes excess release and accumulation of glutamate that binds to postsynaptic receptors. This opens ionotropic channels that mediate neuronal depolarization and ionic fluxes that can lead to neuronal death. 2. The CA1 pyramidal cell region of the hippocampus is particularly susceptible to this neurotoxic process. Brain cell swelling is considered an early excitotoxic event, but remains poorly under stood and documented. As cells swell, light transmittance (LT) increases through brain tissue, so we hypothesized that brief exposure to glutamate agonists would elicit cell swelling that could be imaged in real time in the hippocampal slice. 3. A 1-min bath application of 100 microM N-methyl-D-aspartate (NMDA) or 100 microM kainate at 22 degrees C greatly increased LT, particularly in the dendritic regions of CA1. The response peaked by 2-3 min and slowly reversed over the subsequent 20 min following exposure. Peak LT increases were > 50% in CA1 stratum radiatum and > 20% in both CA1 stratum oriens and the dendritic region of the dentate gyrus, all areas with a high concentration of NMDA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors. The CA3 stratum radiatum, which contains fewer of these receptors, showed a comparatively small LT increase. 4. The NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP-5) [but not 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)] blocked the CA1 response to NMDA, whereas the non-NMDA receptor antagonist CNQX (but not AP-5) blocked the response to kainate. The relative tissue resistance measured across CA1 stratum radiatum increased after NMDA or kainate exposure with a time course similar to the LT change described above. The increase in relative tissue resistance was blocked by kynurenate, a nonspecific glutamate antagonist. Increases in both LT and tissue resistance provide two independent lines of evidence that cell swelling rapidly developed in CA1 dendritic areas after activation of NMDA or AMPA receptors. 5. This swelling at 22 degrees C was accompanied by a temporary loss of the evoked CA1 field potential. However, at 37 degrees C the dendritic swelling rapidly progressed to an irreversible LT increase (swelling) of the CA1 cell bodies accompanied by a permanent loss of the evoked field. 6. We propose that dendritic swelling mediated by NMDA and AMPA receptors is an early excitotoxic event that can herald permanent damage to CA1 neurons, those cells most vulnerable to ischemic insult.
Modulation of the human vestibuloocular reflex during saccades: probing by high-frequency oscillation and torque pulses of the head
Authors: Tabak S. , Smeets J. B. , Collewijn H.
Published: December 2017

1. We probed the gain and phase of the vestibuloocular reflex (VOR) during the execution of voluntary gaze saccades, with continuous oscillation or acceleration pulses, applied through a torque helmet. 2. Small-amplitude (< 1 degree), high-frequency (10-14 Hz) head oscillations in the horizontal or vertical plane were superimposed on ongoing horizontal gaze saccades (40-100 degrees). Torque pulses to the head (“with” or “against” gaze) were superimposed on 40 degrees horizontal saccades. Eye and head movements were precisely measured with sensor coils in magnetic fields. 3. Techniques were developed to separate the oscillatory (horizontal or vertical) component from the gaze shift and obtain VOR gain and phase with Fourier techniques from the relation between eye-in-head and head oscillations. These involved either subtraction of exactly matching saccades with and without oscillation (drawback: low yield) or time shifting of successive trials to synchronize the oscillations (drawback: slight time blurring of saccades). 4. The results of these matching and synchronization methods were essentially identical and consistent. Presaccadic gain values of the horizontal VOR (typically about unity) were reduced by, on average, approximately 20 and 50% during horizontal saccades of 40 and 100 degrees, respectively. These percentages may be truncated because of methodological limitations, but even after taking these into account (on the basis of simulation experiments with 2 different, theoretical profiles of suppression) our results do not support a complete saccadic VOR suppression for any substantial fraction of saccadic duration. Qualitatively similar changes were found when the vertical VOR was probed during 100 degrees horizontal saccades. 5. Concomitantly with the reductions in gain, VOR phase was advanced by approximately 20 degrees during the saccade. 6. In the wake of gaze saccades, VOR gain was consistently elevated (to approximately 1.0) above the presaccadic level (approximately 0.9). We submit that this mechanism ensures stable fixation of the newly acquired target at a time when the head is still moving substantially. 7. Although the responses to head torque pulses showed idiosyncratic asymmetries, analysis of the differences in eye and head movements for pulses with and against consistently showed a sharp fall of VOR gain at saccadic onset, following an approximately exponential course with a time constant of approximately 50 ms. This decay may be assumed to reflect VOR gain for a period of approximately 50 ms, after which secondary gaze control mechanisms become dominant. 8. The time course of the gain decay and phase shift of the VOR suggest that suppression of the “integrative (position) loop” of the VOR circuit was more complete than suppression of the direct, “velocity” pathway.
Nociceptin (orphanin FQ), an endogenous ligand for the QRL1 (opioid-receptor-like1) receptor; modulates responses of trigeminal neurons evoked by excitatory amino acids and somatosensory stimuli
Authors: Wang X. M. , Zhang K. M. , Mokha S. S.
Published: December 2017

1. This is the first in vivo electrophysiological evidence demonstrating the effects of Phe-Gly-Gly-Phe-Thr-Gly-Ala-Arg-Lys-Ser-Ala-Arg-Lys-Leu-Ala-Asn-Gln (nociceptin or orphanin FQ), an endogenous ligand for the orphan ORL1 receptor, on nociceptive neurons in the CNS. The effects of nociceptin were tested on the responses of neurons recorded in the superficial and deeper dorsal horn of the medulla (trigeminal nucleus caudalis) in the rat. 2. Nociceptin applied microiontophoretically produced a predominantly long-lasting (5–30 min) inhibitory modulation of the N-methyl-D-aspartic acid (NMDA)-evoked responses of 24 of 31 nociceptive and 12 of 12 nonnociceptive neurons. Excitatory or biphasic effects of nociceptin were also observed in 6 of 43 neurons. Responses evoked by (+/-)-alpha-amino-3-hydroxy-5-methylisox-azole-4-propionic acid (AMPA) were reduced in eight of nine nociceptive and nonnociceptive neurons. 3. The inhibitory effect of nociceptin was not modality specific; responses to both noxious and nonnoxious stimuli were reduced. 4. Although naloxone applied iontophoretically blocked or reduced the peak inhibitory effect of [D-Ala2,N-Me-Phe4, Gly5-ol]-Enkephalin (DAMGO) or trans-(+/-)-3,4-dicholoro-N-methyl-N-(2-1-pyrrolidinyl-cyclo hexyl)-benzene acetamide (U50, 488H), it did not produce a significant alteration in the peak inhibitory effect of nociceptin. 5. Nociceptin administered intracerebroventricularly produced a long-lasting (20–35 min) reduction in the NMDA-evoked responses of three of three nociceptive neurons. 6. Nociceptin produces a predominantly antinociceptive action in the trigeminal system.
Postural Control of Three-Dimensional Prehension Movements
Authors: Desmurget Michel , Prablanc Claude
Published: December 2017

Desmurget, Michel and Claude Prablanc. Postural control of three-dimensional prehension movements. J. Neurophysiol. 77: 452–464, 1997. This experiment was carried out to test the hypothesis that three-dimensional upper limb movements could be initiated and controlled in the joint space via a mechanism comparing an estimate of the current postural state of the upper arm with a target value determined by one specific inverse static transform converting the coordinates of the object into a set of arm, forearm, and wrist angles. This hypothesis involves two main predictions: 1) despite joint redundancy, the posture reached by the upper limb should be invariant for a given context; and 2) a movement programmed in joint space should exhibit invariant characteristics of the joint covariation pattern as well as a corresponding variable hand path curvature in the task space. To test these predictions, we examined prehension movements toward a cylindrical object presented at a fixed spatial location and at various orientations without vision of the moving limb. Once presented, the object orientation was either kept constant (unperturbed trials) or suddenly modified at movement onset (perturbed trials). Three-dimensional movement trajectories were analyzed in both joint and task spaces. For the unperturbed trials, the task space analysis showed a variable hand path curvature depending on object orientation. The joint space analysis showed that the seven final angles characterizing the upper limb posture at hand-to-object contact varied monotonically with object orientation. At a dynamic level, movement onset and end were nearly identical for all joints. Moreover, for all joints having a monotonic variation, maximum velocity occurred almost simultaneously. For the elbow, the only joint presenting a reversal, the reversal was synchronized with the time to peak velocity of the other joint angles. For the perturbed trials, a smooth and complete compensation of the movement trajectory was observed in the task space. At a static level the upper limb final posture was identical to that obtained when the object was initially presented at the orientation following the perturbation. This result was particularly remarkable considering the large set of comfortable postures allowed by joint redundancy. At a dynamic level, the joints' covariation pattern was updated to reach the new target posture. The initial synergies were not disrupted by the perturbation, but smoothly modified, the different joints' movements ending nearly at the same time. Taken together, these results support the hypothesis that prehension movements are initiated and controlled in the joint space on the basis of a joint angular error vector rather than a spatial error vector.