bluuebunny/crossref_metadata_2025 huggingface dataset:
Contribution of Outward Currents to Spike-Frequency Adaptation in Hypoglossal Motoneurons of the Rat
Authors: Sawczuk Andrea , Powers Randall K. , Binder Marc D.
Published: December 2017

Sawczuk, Andrea, Randall K. Powers, and Marc D. Binder. Contribution of outward currents to spike-frequency adaptation in hypoglossal motoneurons of the rat. J. Neurophysiol. 78: 2246–2253, 1997. Spike-frequency adaptation has been attributed to the actions of several different membrane currents. In this study, we assess the contributions of two of these currents: the net outward current generated by the electrogenic Na+-K+pump and the outward current that flows through Ca2+-activated K+channels. In recordings made from hypoglossal motoneurons in slices of rat brain stem, we found that bath application of a 4–20 μM ouabain solution produced a partial block of Na+-K+pump activity as evidenced by a marked reduction in the postdischarge hyperpolarization that follows a period of sustained discharge. However, we observed no significant change in either the initial, early, or late phases of spike-frequency adaptation in the presence of ouabain. Adaptation also has been related to increases in the duration and magnitude of the medium-duration afterhyperpolarization (mAHP) mediated by Ca2+-activated K+channels. When we replaced the 2 mM Ca2+in the bathing solution with Mn2+, there was a significant decrease in the amplitude of the mAHP after a spike. The decrease in mAHP amplitude resulted in a decrease in the magnitude of the initial phase of spike-frequency adaptation as has been reported previously by others. However, quite unexpectedly we also found that reducing the mAHP resulted in a dramatic increase in the magnitude of both the early and late phases of adaptation. These changes could be reversed by restoring the normal Ca2+concentration in the bath. Our results with ouabain indicate that the Na+-K+pump plays little, if any, role in the three phases of adaptation in rat hypoglossal motoneurons. Our results with Ca2+channel blockade support the hypothesis that initial adaptation is, in part, controlled by conductances underlying the mAHP. However, our failure to eliminate initial adaptation completely by blocking Ca2+channels suggests that other membrane mechanisms also contribute. Finally, the increase in both the early and late phases of adaptation in the presence of Mn2+block of Ca2+channels lends further support to the hypothesis that the initial and later (i.e., early and late) phases of spike-frequency adaptation are mediated by different cellular mechanisms.
Decoding Visual Information From a Population of Retinal Ganglion Cells
Authors: Warland David K. , Reinagel Pamela , Meister Markus
Published: December 2017

Warland, David K., Pamela Reinagel, and Markus Meister.Decoding visual information from a population of retinal ganglion cells. J. Neurophysiol. 78: 2336–2350, 1997. This work investigates how a time-dependent visual stimulus is encoded by the collective activity of many retinal ganglion cells. Multiple ganglion cell spike trains were recorded simultaneously from the isolated retina of the tiger salamander using a multielectrode array. The stimulus consisted of photopic, spatially uniform, temporally broadband flicker. From the recorded spike trains, an estimate was obtained of the stimulus intensity as a function of time. This was compared with the actual stimulus to assess the quality and quantity of visual information conveyed by the ganglion cell population. Two algorithms were used to decode the spike trains: an optimized linear filter in which each action potential made an additive contribution to the stimulus estimate and an artificial neural network trained by back-propagation to match spike trains with stimuli. The two methods performed indistinguishably, suggesting that most of the information about this stimulus can be extracted by linear operations on the spike trains. Individual ganglion cells conveyed information at a rate of 3.2 ± 1.7 bits/s (mean ± SD), with an average information content per spike of 1.6 bits. The maximal possible rate of information transmission compatible with the measured spiking statistics was 13.9 ± 6.3 bits/s. On average, ganglion cells used 22% of this capacity to encode visual information. When a decoder received two spike trains of the same response type, the reconstruction improved only marginally over that obtained from a single cell. However, a decoder using an on and an off cell extracted as much information as the sum of that obtained from each cell alone. Thus cells of opposite response type encode different and nonoverlapping features of the stimulus. As more spike trains were provided to the decoder, the total information rate rapidly saturated, with 79% of the maximal value obtained from a local cluster of just four neurons of different functional types. The decoding filter applied to a given neuron's spikes within such a multiunit decoder differed substantially from the filter applied to that same neuron in a single-unit decoder. This shows that the optimal interpretation of a ganglion cell's action potential depends strongly on the simultaneous activity of other nearby cells. The quality of the stimulus reconstruction varied greatly with frequency: flicker components below 1 Hz and above 10 Hz were reconstructed poorly, and the performance was optimal near 2.5 Hz. Further analysis suggests that temporal encoding by ganglion cell spike trains is limited by slow phototransduction in the cone photoreceptors and a corrupting noise source proximal to the cones.
Quantal Organization of Reflex and Conditioned Eyelid Responses
Authors: Domingo José A. , Gruart Agnes , Delgado-García José M.
Published: December 2017

Domingo, José A., Agnes Gruart, and José M. Delgado-Garcı́a. Quantal organization of reflex and conditioned eyelid responses. J. Neurophysiol. 78: 2518–2530, 1997. Upper lid movements and the electromyographic activity of the orbicularis oculi muscle were recorded in behaving cats during spontaneous and experimentally evoked reflex blinks, and conditioned eyelid responses. Reflex blinks evoked by the presentation of air puffs, flashes, or tones consisted of a fast downward lid movement followed by late, small downward waves, recurring at ≈50-ms intervals. The latency, maximum amplitude, peak velocity, and number of late waves depended on the modality, intensity, and duration of the evoking stimulus. The power spectra of acceleration records indicated a dominant frequency of ≈20 Hz for air puff–evoked blinks. Flashes and tones usually evoked small and easily fatigable reflex responses of lower dominant frequencies (14–17 and 9–11 Hz, respectively). A basic ≈20-Hz oscillation was also noticed during lid fixation, and ramplike lid displacements evoked by optokinetic stimuli. Five classical conditioning paradigms were used to analyze the frequency-domain properties of conditioned eyelid responses. These learned lid movements differed in latency, maximum amplitude, and profile smoothness depending on the modality (air puff, tone), intensity (weak, strong), and presentation site (ipsi-, contralateral to the unconditioned stimulus) of the conditioned stimulus. It was found that the characteristic ramplike profile of a conditioned response was not smooth, but appeared to be formed by a succession of small waves at a dominant frequency of ≈20 Hz. The amplitude (and number) of the constituting waves depended on the characteristics of the conditioned stimulus and on the time interval until unconditioned stimulus presentation. Thus conditioned responses seemed to be formed from lid displacements of 2–6° in amplitude and ≈50 ms in duration, which increased in number throughout conditioning sessions, until a complete (i.e., lid closing) conditioned response was reached. It is suggested that a ≈20-Hz oscillator underlies the generation of reflex and conditioned eyelid responses. The oscillator is susceptible to being neurally modulated to modify the velocity of a given quantum of movement, and the total duration of the lid response. Learned eyelid movements are probably the result of a successively longer release of the oscillator as a function of the temporal-spatial needs of the motor response.
Conditions for the Induction of Long-Term Potentiation and Long-Term Depression by Conjunctive Pairing in the Dentate Gyrus In Vitro
Authors: Wang Yue , Wu Jianqun , Rowan Michael J. , Anwyl Roger
Published: December 2017

Wang, Yue, Jianqun Wu, Michael J. Rowan, and Roger Anwyl. Conditions for the induction of long-term potentiation and long-term depression by conjunctive pairing in the dentate gyrus in vitro. J. Neurophysiol. 78: 2569–2573, 1997. The conditions under which long-term potentiation (LTP) and long-term depression (LTD) of excitatory postsynaptic currents were induced by the conjunctive pairing-type protocol of afferent stimulation and postsynaptic depolarization were studied in the medial perforant pathway-granule cell synapse of the dentate gyrus in vitro. The conjunctive pairing of 1-Hz afferent stimulation and steady state postsynaptic depolarization to 0 mV did not induce LTP or LTD. Inhibition of LTD induction with a phosphatase inhibitor or ruthenium red resulted in induction of LTP after the conjunctive pairing. Such LTP induction was N-methyl-d-aspartate dependent. Conversely, inhibition of LTP induction with a kinase inhibitor resulted in LTD induction after the conjunctive pairing. Thus the failure to induce LTP or LTD with the pairing protocol involving depolarization to 0 mV membrane potential was due to simultaneous activation of intracellular processes that generate the induction of LTP and LTD. Increasing the frequency of afferent stimulation to 200 Hz, even for just eight stimuli, resulted in LTP induction. The studies show that two factors govern the induction of LTP/LTD, membrane potential and frequency of afferent stimulation, with either increased depolarization or increased afferent stimulation favoring LTP induction.
Ionic Mechanisms of Spontaneous GABAergic Events in Rat Hippocampal Slices Exposed to 4-Aminopyridine
Authors: Lamsa Karri , Kaila Kai
Published: December 2017

Lamsa, Karri and Kai Kaila. Ionic mechanisms of spontaneous GABAergic events in rat hippocampal slices exposed to 4-aminopyridine. J. Neurophysiol. 78: 2582–2591, 1997. Ion-selective (H+ and K+) microelectrode techniques as well as conventional extra- and intracellular recordings were used to study the ionic mechanisms of propagating spontaneous GABAergic events (SGEs) in rat hippocampal slices exposed to 4-aminopyridine (4-AP, 50–100 μM). All experiments were made in the presence of antagonists of ionotropic glutamate receptors [10 μM 6-nitro-7-sulphamoylbenzoquinoxaline-2,3-dione (NBQX) and 40 μM dl-2-amino-5-phosphonopentanoic acid (AP5)]. The SGEs were composed of a negative-going change in field potential with a temporally coincident increase (0.7 ± 0.3 mM; mean ± SE) in extracellular K+ ([K+]o) and an alkaline transient (0.01–0.08 units) in extracellular pH (pHo) in stratum radiatum of the area CA1. Simultaneous intracellular recordings showed a triphasic hyperpolarization-depolarization–late hyperpolarization response in pyramidal cells. Application of pentobarbital sodium (PB, 100 μM) decreased the interval between SGEs from a mean value of 35 to ∼20 s and shortened the period of refractoriness of stimulus-evoked propagating events. This was accompanied by an increase in the amplitude of the field potential response of the [K+]o and the pHo shifts and of the depolarizing phase of the pyramidal-cell response. The SGEs were completely blocked by the γ-aminobutyric acid-A (GABAA) receptor antagonist, picrotoxin (PiTX; 100 μM). The amplitudes of the negative-going field potential and of the depolarizing phase of the pyramidal-cell response as well as the ionic shifts associated with SGEs were strongly suppressed in the nominal absence of CO2/HCO− 3. There was a five-fold increase in the interevent interval, and propagating SGEs could not be evoked by stimuli given at intervals shorter than ∼2–3 min. Exposure to inhibitors of carbonic anhydrase, benzolamide (BA; 10 μM) or ethoxyzolamide (EZA; 50 μM) fully blocked the alkaline pHo transients and turned them into acid shifts. The poorly membrane-permeant BA had no discernible effect on the other components of the SGEs, but application of EZA had effects reminiscent to those of CO2/HCO− 3-free medium. Addition of the GABAA receptor–permeant weak-acid anion, formate (20 mM) reestablished the SGEs that were first suppressed by exposure to the CO2/HCO− 3-free medium. No SGEs were seen in the presence of a similar concentration of the GABAA receptor–impermeant anion propionate. Unlike the alkaline transients associated with HCO− 3-driven SGEs, those supported by formate were not blocked by BA. The present data suggest that an inward current carried by bicarbonate is necessary for the generation of SGEs and that the GABAA receptor–mediated excitatory coupling among GABAergic interneurons is essentially dependent on the availability of intracellular bicarbonate.
Ca2+-Activated K+Currents in Rat Locus Coeruleus Neurons Induced by Experimental Ischemia, Anoxia, and Hypoglycemia
Authors: Murai Yoshinaka , Ishibashi Hitoshi , Koyama Susumu , Akaike Norio
Published: December 2017

Murai, Yoshinaka, Hitoshi Ishibashi, Susumu Koyama, and Norio Akaike. Ca2+-activated K+currents in rat locus coeruleus neurons induced by experimental ischemia, anoxia, and hypoglycemia. J. Neurophysiol. 78: 2674–2681, 1997. The effects of metabolic inhibition on membrane currents and N-methyl-d-aspartic acid (NMDA)-induced currents were investigated in dissociated rat locus coeruleus (LC) neurons by using the nystatin perforated patch recording mode under voltage-clamp conditions. Changes in the intracellular Ca2+concentration ([Ca2+]i) during the metabolic inhibition were also investigated by using the microfluometry with a fluorescent probe, Indo-1. Removal of both the oxygen and glucose (experimental ischemia), deprivation of glucose (hypoglycemia), and a blockade of electron transport by sodium cyanide (NaCN) or a reduction of the mitochondrial membrane potentialwith carbonyl cyanide- p-trifluoromethoxyphenyl-hydrazone(FCCP) as experimental anoxia all induced a slowly developing outward current ( IOUT) at a holding potential of −40 mV. The application of 10−4M NMDA induced a rapid transient peak and a successive steady state inward current and a transient outward current immediately after washout. All treatments related to metabolic inhibition increased the NMDA-induced outward current( INMDA-OUT) and prolonged the one-half recovery time of INMDA-OUT. The reversal potentials of both IOUTand INMDA-OUTwere close to the K+equilibrium potential ( EK) of −82 mV. Either charybdotoxin or tolbutamide inhibited the IOUTand INMDA-OUT, suggesting the contribution of Ca2+-activated and ATP-sensitive K+channels, even though the inhibitory effect of tolbutamide gradually diminished with time. Under the metabolic inhibition, the basal level of [Ca2+]iwas increased and the one-half recovery time of the NMDA-induced increase in [Ca2+]iwas prolonged. The IOUTinduced by NaCN was inhibited by a continuous treatment of thapsigargin but not by ryanodine, indicating the involvement of inositol 1,4,5-trisphosphate (IP3)-induced Ca2+release (IICR) store. These findings suggest that energy deficiency causes Ca2+release from the IICR store and activates continuous Ca2+-activated K+channels and transient ATP-sensitive K+channels in acutely dissociated rat LC neurons.
A Fast Synaptic Potential Mediated by NMDA and Non-NMDA Receptors
Authors: Wolszon Laura R. , Pereda Alberto E. , Faber Donald S.
Published: December 2017

Wolszon, Laura R., Alberto E. Pereda, and Donald S. Faber. A fast synaptic potential mediated by NMDA and non-NMDA receptors. J. Neurophysiol. 78: 2693–2706, 1997. Excitatory synaptic transmission in the CNS often is mediated by two kinetically distinct glutamate receptor subtypes that frequently are colocalized, the N-methyl-d-aspartate (NMDA) and non-NMDA receptors. Their synaptic currents are typically very slow and very fast, respectively. We examined the pharmacological and physiological properties of chemical excitatory transmission at the mixed electrical and chemical synapses between auditory afferents and the goldfish Mauthner cell, in vivo. Previous physiological data have suggested the involvement of glutamate receptors in this fast excitatory postsynaptic potential (EPSP), the chemical component of which decays with a time constant of <2 ms. We demonstrate here that the pharmacological and voltage-dependent characteristics of the synaptic currents are consistent with glutamatergic transmission and that both NMDA and non-NMDA receptors are involved. The two components surprisingly exhibit quite similar kinetics even at resting potential, with the NMDA response being only slightly slower. Due to its fast kinetics and characteristic voltage dependence, NMDA receptor-mediated transmission at these first-order synapses contributes significantly to paired pulse and frequency-dependent facilitation of successive fast EPSPs during high-frequency repetitive firing, a presynaptic impulse pattern that induces activity-dependent homosynaptic changes in both electrical and chemical transmission. Thus NMDA receptor kinetics in this intact preparation are suited to its functional requirements, namely speed of information transmission and the ability to trigger changes in synaptic efficacy.
Attenuation of Paired-Pulse Facilitation Associated With Synaptic Potentiation Mediated by Postsynaptic Mechanisms
Authors: Wang Jin-Hui , Kelly Paul T.
Published: December 2017

Wang, Jin-Hui and Paul T. Kelly. Attenuation of paired-pulse facilitation associated with synaptic potentiation mediated by postsynaptic mechanisms. J. Neurophysiol. 78: 2707–2716, 1997. The relationship between paired-pulse facilitation (PPF) and synaptic potentiation induced by various protocols and their cellular and molecular mechanisms were examined by extracellular field potential and current- or voltage-clamp recordings at CA1 synapses in rat hippocampal slices. Microelectrodes were used for both intracellular recordings and injections of modulators of calcium (Ca2+) and Ca2+/calmodulin (CaM) signaling pathways into postsynaptic neurons. Basal synaptic transmission was not accompanied by changes in PPF. Tetanic stimulation induced long-term potentiation (LTP) of synaptic transmission and attenuated PPF. Experiments stimulating two independent Schaffer collateral/commisural(S/C) pathways showed that PPF attenuation and tetanus-LTP were pathway specific. Postsynaptic injections of pseudosubstrate inhibitors of CaM-dependent protein kinase II and protein kinase C (CaM-KII/PKC), [Ala286]CaMKII286–302plus PKC19–31, almost completely attenuated tetanus-LTP and reversed PPF attenuation but did not affect synaptic transmission and PPF under basal conditions. Postsynaptic injections of heparin and dantrolene (inhibitors of IP3and ryanodine receptors at intracellular Ca2+stores) prevented tetanus-LTP induction and PPF attenuation. Postsynaptic injections of calcineurin (CaN) inhibitors, CaN autoinhibitory peptide (CaN-AIP) or FK-506, enhanced synaptic transmission and decreased PPF. CaN-inhibited synaptic potentiation and PPF attenuation were unaffected by d(-)-a-Amino-5-phosphonopentanoic, but blocked by coinjecting 1,2-bis(2-aminophenoxy)-ethane- N,N,N′,N′-tetraacetic acid, heparin plus dantrolene, calmodulin-binding peptide, or [Ala286]CaMKII281–302plus PKC19–31. PPFattenuation associated with tetanus-LTP or CaN-inhibited synaptic potentiation resulted from smaller increases in the potentiation of the second synaptic responses (R2) compared with the potentiation of the first responses (R1). Our results indicate that PPF attenuation is associated with synaptic potentiation mediated by postsynaptic mechanisms, and postsynaptic Ca2+/CaM signaling pathways play a dual role in synaptic plasticity. CaN activity limits synaptic transmission under basal conditions, whereas the activation of Ca2+-dependent protein kinases enhances synaptic transmission and attenuates PPF at central synapses.
Coding for Auditory Space in the Nucleus of the Brachium of the Inferior Colliculus in the Ferret
Authors: Schnupp Jan W. H. , King Andrew J.
Published: December 2017

Schnupp, Jan W. H. and Andrew J. King. Coding for auditory space in the nucleus of the brachium of the inferior colliculus in the ferret. J. Neurophysiol. 78: 2717–2731, 1997. The nucleus of the brachium of the inferior colliculus (BIN) projects topographically to the deeper layers of the superior colliculus (SC), which contain a two-dimensional map of auditory space. In this study, we have used broadband stimuli presented in the free field to investigate how auditory space is represented in the BIN of the ferret. Response latencies and temporal firing patterns were comparable with those in the SC, and both properties showed some variation with stimulus location. We obtained spatial response profiles at two sound levels (5–15 and 25–35 dB above unit threshold). A large proportion of azimuth profiles (41% in the suprathreshold condition, 80% in the near-threshold condition) presented a single peak, indicating that they were tuned to single regions in space. For some of these units, the preferred speaker position varied considerably with sound level. The remaining units showed predominantly either broad “hemifield” or spatially ambiguous “bilobed” response profiles. At suprathreshold sound levels, the preferred azimuths of the tuned cells were ordered topographically along the rostrocaudal axis of the BIN, although this representation is considerably more scattered than that in the SC. In contrast to the SC, we observed no systematic variation in the distribution of near-threshold best azimuths, which were instead concentrated around the interaural axis in the contralateral hemifield. The azimuth tuning of individual units in the BIN was generally broader at both sound levels than that in the SC. Many units also were tuned for the elevation of the sound source (48% for supra-, 77% for near-threshold stimulation), but there was no evidence for topographic order in the distribution of preferred elevations within the BIN. These results suggest that the BIN sends inputs to the SC that are already selective for sound azimuth and elevation and that show some degree of topographic order for sound azimuth. These inputs then presumably are sharpened and their topography refined by a mechanism that is likely to involve convergence of other inputs and activity-dependent fine tuning of terminal connections, to result in a precise two-dimensional map of auditory space in the SC.
Visual Response Properties and Visuotopic Representation in the Newborn Monkey Superior Colliculus
Authors: Wallace M. T. , McHaffie J. G. , Stein B. E.
Published: December 2017

Wallace M. T., J. G. McHaffie, and B. E. Stein. Visual response properties and visuotopic representation in the newborn monkey superior colliculus. J. Neurophysiol. 78: 2732–2741, 1997. Visually responsive neurons were recorded in the superior colliculus (SC) of the newborn rhesus monkey. The receptive fields of these neurons were larger than those in the adult, but already were organized into a well-ordered map of visual space that was very much like that seen in mature animals. This included a marked expansion of the representation of the central 10° of the visual field and a systematic foveal to peripheral increase in receptive field size. Although newborn SC neurons had longer response latencies than did their adult counterparts, they responded vigorously to visual stimuli and exhibited many visual response properties that are characteristic of the adult. These included surround inhibition, within-field spatial summation, within-field spatial inhibition, binocularity, and an adult-like ocular dominance distribution. As in the adult, SC neurons in the newborn preferred a moving visual stimulus and had adult-like selectivities for stimulus speed. The developmentally advanced state of the functional circuitry of the newborn monkey SC contrasts with the comparative immaturity of neurons in its visual cortex. It also contrasts with observations on the state of maturation of the newborn SC in other developmental models (e.g., cat). The observation that extensive visual experience is not necessary for the development of many adult-like SC response properties in the monkey SC may help explain the substantial visual capabilities shown by primates soon after birth.
Epileptogenesis Following Neocortical Trauma From Two Sources of Disinhibition
Authors: Yang Lie , Benardo Larry S.
Published: December 2017

Yang, Lie and Larry S. Benardo. Epileptogenesis following neocortical trauma from two sources of disinhibition. J. Neurophysiol. 78: 2804–2810, 1997. Intracellular and field potential recordings were obtained from superficial and deep neurons from both intact coronal rat somatosensory slices, and from slices which had been acutely divided into a superficial strip of cortex (∼450 μm from the pia) and a deep segment. Membrane properties for cells in the traumatized slices were similar to those of their counterparts in intact slices. However, synaptic hyperexcitability developed in the deep segments in which a majority of cells likely underwent dendrotomy. This hyperexcitability was manifested by epileptiform activity in 54% of traumatized slices. Measurements of fastGABAergic inhibitory strength showed these slices were disinhibited. Superficial delivery of tetrodotoxin to the upper 450 μm of intact slices led to disinhibition of fast GABAergic transmission as well as an attendant increase in excitatory postsynaptic potential strength but not epileptogenesis. Pharmacological maneuvers aimed at preventing glutamate-triggered increases in intracellular calcium [glutamate ionotropic antagonists, dantrolene, and bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA)-AM] showed that a 1 h treatment in these agents conferred protection against epileptogenesis. These results demonstrate that the seizure-like activity developing in deep dendrotomized cortical segments resulted from two sources of GABAergic disinhibition: the physical removal of important superficial inhibitory circuits and glutamate-triggered increases in intracellular calcium.
Role of Neuropeptides Encoded on CDCH-1 Gene in the Organization of Egg-Laying Behavior in the Pond Snail,Lymnaea stagnalis
Authors: Hermann Petra M. , de Lange Robert P. J. , Pieneman Anton W. , ter Maat Andries , Jansen Rene F.
Published: December 2017

Hermann, Petra M., Robert P. J. de Lange, Anton W. Pieneman, Andries ter Maat, and Rene F. Jansen. Role of neuropeptides encoded on CDCH-1 gene in the organization of egg-laying behavior in the pond snail, Lymnaea stagnalis. J. Neurophysiol. 78: 2859–2869, 1997. Egg laying in the pond snail Lymnaea stagnalis is triggered by a discharge of the neuroendocrine caudodorsal cells (CDCs). The CDCs expresses three different caudorsal cell hormone (CDCH) genes. This gene family expresses, in total, 11 different peptides among which is the ovulation hormone. Besides the CDCs, the CDCH gene family is expressed in other central and peripheral neurons. In this study, we investigated the roles the different CDCH peptides play in the organization of egg-laying behavior. Egg-laying behavior is a sequence of stereotyped movements in which three phases can be distinguished: resting, turning, and oviposition. We have used the excitation of right pedal N (RPeN) motor neurons as a simple analogue of shell-turning behavior, one of the elements of egg-laying behavior. RPeN motor neurons were inhibited during the resting phase of egg laying but were subsequently excited at the onset of and during the turning phase. The excitatory effect could be evoked by application of beta3-CDCP on RPeN motor neurons in the CNS as well as in isolation but not by the ovulation hormone, alpha-CDCP or Calfluxin, the other CDCH-1 peptides tested. The ovulation hormone itself caused inhibition of RPeN motor neurons. Anti-CDCH–1 positive fiber tracts were found close to the cell bodies and axons of the RPeN motor neurons. Electrical stimulation of a nerve that contains these fibers resulted in excitation of the RPeN motor neurons. The effects of injection of CDCH-1 peptides into intact animals correlated well with the effects of these peptides on RPeN motor neurons. Injection of beta3-CDCP or alpha-CDCP into intact animals resulted in immediate turning behavior in the absence of egg laying itself. The ovulation hormone and Calfluxin had no immediate effect on the behavior. Furthermore, our data indicate that the individual CDCH-1 peptides act on different targets.
Estimating the Distribution of Synaptic Reliabilities
Authors: Huang Emily P. , Stevens Charles F.
Published: December 2017

Huang, Emily P. and Charles F. Stevens. Estimating the distribution of synaptic reliabilities. J. Neurophysiol. 78: 2870–2880, 1997. Using whole cell recording from CA1 hippocampal pyramidal neurons in slices, we examined the progressive decrease of N-methyl-d-aspartate receptor-mediated synaptic responses in the presence of the open-channel blocker MK-801. Previous studies analyzing this decrease have proposed that hippocampal synapses fall into two distinct classes of release probabilities, whereas studies based on other methods indicate a broad distribution of synaptic reliabilities exists. Here we derive the theoretical relationship between the MK-801–mediated decrease in excitatory postsynaptic current amplitudes and the underlying distribution of synaptic reliabilities. We find that the MK-801 data are consistent with a continuous distribution of synaptic reliabilities, in agreement with studies examining individual synapses. In addition, changes in the MK-801–mediated decrease in response size as a consequence of altering release probability are consistent with this continuous distribution of synaptic reliabilities.
Neural Circuit Mediating Tentacle Withdrawal inHelix aspersa,With Specific Reference to the Competence of the Motor Neuron C3
Authors: Prescott Steven A. , Gill Nishi , Chase Ronald
Published: December 2017

Prescott, Steven A., Nishi Gill, and Ronald Chase. Neural circuit mediating tentacle withdrawal in Helix aspersa, with specific reference to the competence of the motor neuron C3. J. Neurophysiol. 78: 2951–2965, 1997. The tentacle withdrawal reflex in the terrestrial snail Helix aspersa involves bending and retraction of the tentacles. When elicited by mechanical stimulation of the tentacle, the reflex is mediated by the conjoint action of the central and peripheral nervous systems. The neural circuit underlying the stimulus-response pathways was studied in vitro using a combination of morphological and physiological techniques. Sensory input caused by stimulation of the nose (situated at the superior tentacle's tip) first passes into the tentacle ganglion. Motor fibers are likely excited in the tentacle ganglion to form a peripheral stimulus-response pathway. While still in the tentacle ganglion, the excitation caused by a brief stimulus is transformed into a prolonged neuronal discharge. This modified signal travels, via the olfactory nerve, to the cerebral ganglion where it excites the giant motor neuron C3 along with numerous smaller motor neurons. Afferent input to C3 also arrives from several other sources. The afferent convergence is followed by a marked divergence of C3's output. C3 innervates the muscles mediating both tentacle retraction and tentacle bending through multiple cerebral nerves. Thus C3's pattern of effector innervation allows this single cell to elicit and coordinate both components of the tentacle withdrawal reflex. Lesion experiments indicate that C3 is responsible for 85% of the central contribution to tentacle retraction, though C3 is actually sufficient to mediate maximal muscle contraction as evidenced by intracellular stimulation. In addition to C3, three groups of putative central motor neurons were identified through nerve backfills and nerve recordings. The additional motor neurons mediating tentacle retraction are important for maximizing the rate of muscle contraction, whereas those mediating tentacle bending are likely more important for nondefensive behaviors. These neurons are arranged in parallel with C3, but unlike C3, each of these neurons innervates only a single effector or portion thereof. Given C3's direct innervation of multiple effectors and its sufficiency to evoke strong responses in those effectors, we conclude that C3 is paramount in eliciting and coordinating tentacle withdrawal.
Metabotropic Glutamate Receptors Regulate N-Methyl-d-Aspartate–Mediated Synaptic Transmission in Nucleus Accumbens
Authors: Martin Gilles , Nie Zhiguo , Siggins George R.
Published: December 2017

Martin, Gilles, Zhiguo Nie, and George R. Siggins. Metabotropic glutamate receptors regulate N-methyl-d-aspartate–mediated synaptic transmission in nucleus accumbens. J. Neurophysiol. 78: 3028–3038, 1997. We recorded intracellularly from core nucleus accumbens (NAcc) neurons in brain slices to study the regulation by metabotropic glutamate receptors (mGluRs) of pharmacologically isolated N-methyl-d-aspartate–mediated excitatory postsynaptic currents (NMDA-EPSCs). Monosynaptic NMDA-EPSCs, evoked by local stimulation, were isolated by superfusion of the non-NMDA and γ-aminobutyric acid-A (GABAA) receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 μM) and bicuculline (15 μM), respectively. Trans-1-aminocyclopentane-1,3-decarboxylic acid ( trans-ACPD; 50 μM), a nonspecific group 1 and 2 mGluR agonist, had no effect on resting membrane potential (RMP) or input resistance of NAcc neurons. However, it consistently decreased NMDA-EPSC areas (time integrals) dose dependently (1–100 μM; EC50 = 8 μM) and reversibly. The specific group 1 mGluR agonists quisqualate (1–4 μM) and (RS)-3,5-dihydroxyphenylglycine (DHPG; 100 μM) did not mimic the trans-ACPD effect on NMDA-EPSCs, nor did exposure of the slice to the group 1 mGluR antagonist l(+)-2-amino-3-phosphonopropionic acid (l-AP3, 0.4 mM) inhibit the trans-ACPD effect. The putative mGluR1 and mGluR2 antagonist (+)-α-methyl-4-carboxyphenylglycine (MCPG) at 0.5 mM failed to antagonize trans-ACPD effects but at 1 mM blocked them. Both the group 2 mGluR agonist (2S,3S,4S)-α-(carboxycyclopropyl)-glycine (l-CCG-I, 2 μM) and the group 3 mGluR specific agonist l(+)-2-amino-4-phosphonobutyric acid (l-AP4, 20 μM) attenuated NMDA-EPSC areas; the effect of l-AP4 was blocked by the group 3 antagonist (S)-2-amino-2-methyl-4-phosphonobutanoic acid (MAP4; 0.5 mM). Exogenously applied NMDA, in the presence of tetrodotoxin to prevent presynaptic effects, induced inward currents that were decreased by 20 μM l-AP4 but not by 10 μM trans-ACPD. These findings suggest that NMDA receptor-mediated neurotransmission in NAcc is under dual inhibitory regulation by group 2 and 3 metabotropic receptor subtypes: l-AP4–sensitive receptors located postsynaptically and those sensitive to trans-ACPD located presynaptically.
Heterologous Expression of a P2 x-Purinoceptor in Rat Chromaffin Cells Detects Vesicular ATP Release
Authors: Hollins Bettye , Ikeda Stephen R.
Published: December 2017

Hollins, Bettye and Stephen R. Ikeda. Heterologous expression of a P2 x -purinoceptor in rat chromaffin cells detects vesicular ATP release. J. Neurophysiol. 78: 3069–3076, 1997. A cloned P2 x -purinoceptor was transiently expressed in single isolated rat adrenal chromaffin cells and evaluated for the detection of released ATP. After cytoplasmic injection of the P2 x complementary RNA (cRNA; 4–24 h), application of ATP produced an inwardly rectifying current over the voltage range −130 to −10 mV as measured by the whole cell patch-clamp technique. The dose-response curve for ATP was sigmoidal with a 50% effective concentration of 18.2 μM. Suramin, a P2 x -antagonist, attenuated the ATP-induced current. Depolarizing voltage pulses to 0 mV or application of histamine, stimuli that trigger exocytosis, resulted in the appearance of suramin-sensitive spontaneous transient inward currents (at −60 mV) that resembled excitatory postsynaptic currents although they were slower in time course. Concurrent detection of catecholamine release with a carbon fiber electrode often showed coincidence of the amperometric current with the synaptic currentlike events suggesting that ATP and catecholamines were released from the same vessicle. These data demonstrate that expression of a P2 x -purinoceptor in chromaffin cells produces a functional autoreceptor capable of detecting vesicular release of ATP. In combination with carbon fiber amperometry, simultaneous vesicular release of two neurotransmitters from a single chromaffin cell could be monitored. The P2 x -purinoceptor, however, produced a regenerative effect on release apparently resulting from the high Ca2+ permeability of the receptor. Thus modification of the P2 x -purinoceptor would be required before the system could be applied to examining processes involved in stimulus-release coupling.
Stability of Motor-Unit Force Thresholds in the Decerebrate Cat
Authors: Cope Timothy C. , Sokoloff Alan J. , Dacko Stan M. , Huot Rebecca , Feingold Eleanor
Published: December 2017

Cope, Timothy C., Alan J. Sokoloff, Stan M. Dacko, Rebecca Huot, and Eleanor Feingold. Stability of motor-unit force thresholds in the decerebrate cat. J. Neurophysiol. 78: 3077–3082, 1997. To further test the hypothesis that some fixed property of motoneurons determines their recruitment order, we quantified the variation in force threshold (FT) for motoneurons recruited in muscle stretch reflexes in the decerebrate cat. Motor axons supplying the medial gastrocnemius (MG) muscle were penetrated with micropipettes and physiological properties of the motoneuron and its muscle fibers, i.e., the motor unit, were measured. FT, defined as the amount of MG force produced when the isolated motor unit was recruited, was measured from 20 to 93 consecutive stretch trials for 29 motor units. Trials were selected for limited variation in base force and rate of rise of force, which have been shown to covary with FT, and in peak stretch force, which gives some index of motor-pool excitability. Under these restricted conditions, large variation in FT would have been inconsistent with the hypothesis. Analysis of the variation in FT employed the coefficient of variation (CV), because of the tendency for FT variance and mean to increase together. We found that CV was distributed with a median value of 10% and with only 2 of 29 units exceeding 36%. Some of this variation was associated with measurement error and with intertrial fluctuations in base, peak, and the rate of change of muscle force. CV was not significantly correlated with motor-unit axonal conduction velocity, contraction time, or force. In three cases FT was measured simultaneously from two motor units in the same stretch trials. Changes in recruitment order were rarely observed (5 of 121 stretch trials), even when FT ranges for units in a pair overlapped. We suggest that the large variation in recruitment threshold observed in some earlier studies resulted not from wide variation in the recruitment ranking of motoneurons within one muscle, but rather from variation in the relative activity of different pools of motoneurons. Our findings are consistent with the hypothesis that recruitment order is determined by some fixed property of α-motoneurons and/or by some unvarying combination of presynaptic inputs that fluctuate in parallel.
Topography and Reciprocal Activity of Cerebellar Purkinje Cells in the Uvula-Nodulus Modulated by Vestibular Stimulation
Authors: Fushiki H. , Barmack N. H.
Published: December 2017

Fushiki, H. and N. H. Barmack. Topography and reciprocal activity of cerebellar Purkinje cells in the uvula-nodulus modulated by vestibular stimulation. J. Neurophysiol. 78: 3083–3094, 1997. In the rabbit uvula-nodulus, vestibular and optokinetic information is mapped onto parasagittal zones by climbing fibers. These zones are related functionally to different pairs of vertical semicircular canals, otolithic inputs and horizontal optokinetic inputs. Vestibular stimulation restricted to one of these zones modulates climbing fiber responses (CFRs). Within each of these zones, simple spikes (SSs) are modulated reciprocally with CFRs. In rabbits anesthetized with chloralose-urethan, we have used vestibular and optokinetic stimulation to evoke CFRs within a parasagittal zone while recording from Purkinje cells in adjacent zones. We have examined whether the CFRs evoked by vestibular stimulation in one zone influence the SSs of an adjacent zone. CFRs and SSs were recorded during roll vestibular stimulation. The orientation of the head of the rabbit with respect to the axis of rotation was varied systematically so that a climbing fiber null plane could be determined. This null plane was the orientation of the head about the vertical axis at which no modulation of the CFR was observed during rotation about the longitudinal axis of the vestibular rate table. In the left uvula-nodulus, a medial sagittal strip extending through all the folia contained Purkinje cells with CFRs that had optimal planes of stimulation coplanar with the left posterior-right anterior semicircular canals (LPC-RAC). Lateral to this strip was a strip of Purkinje cells with CFRs that were characterized by optimal planes corresponding to stimulation of the left anterior-right posterior semicircular canals (LAC-RPC). SSs in Purkinje cells were modulated out of phase with CFRs from the same Purkinje cell. The depth of modulation of both CFRs and SSs was reduced during rotation in the climbing fiber “null plane”. The depth of modulation of SSs was greatest when recorded from Purkinje cells located at the center of semicircular canal-related strip. We observed that 1) all folia of the uvula-nodulus receive vestibular climbing fiber inputs; 2) these climbing fiber inputs convey information from the vertical semicircular canals and otoliths but not the horizontal semicircular canals; 3) CFRs evoked in a particular sagittal zone do not influence SSs in adjacent zones; 4) modulation of a CFRs in a particular Purkinje cell can occur without modulation of SSs in the same Purkinje cell, although modulation of SSs was not observed in the absence of CFR modulation; and 5) modulation of SSs sometimes preceded that of CFRs in the same cell, implying that interneuronal pathways may contribute to SS modulation. Climbing fiber-driven Golgi cells, the inhibitory axon terminals of which end on granule cell dendrites in the classic glomerular synapse, may provide this interneuronal mechanism.
Insensitivity of V1 Complex Cell Responses to Small Shifts in the Retinal Image of Complex Patterns
Authors: Kjaer Troels W. , Gawne Timothy J. , Hertz John A. , Richmond Barry J.
Published: December 2017

Kjaer, Troels W., Timothy J. Gawne, John A. Hertz, and Barry J. Richmond. Insensitivity of V1 complex cell responses to small shifts in the retinal image of complex patterns. J. Neurophysiol. 78: 3187–3197, 1997. An important role for neurons in the early visual system is to convey information about the structure of visual stimuli. However, neuronal responses show substantial variation across presentations of the same stimulus. In awake monkeys, it has been assumed that a great deal of this variation is related to the scatter in eye position (inducing scatter in the retinal position of the stimulus). Here we investigate the implied consequence of this assumption, i.e., that the scatter variation in eye position degrades the decodability of the neural response. We recorded from 50 complex cells in primary visual cortex of fixating monkeys while different complex stimuli were presented. Three types of retinal shifts were considered: natural scatter in the fixation, systematic fixation point shift, and systematic stimulus position shift. The stimulus pattern accounts for >50% of the response variance, always six times that accounted for by the scatter in eye position during fixation. The retinal location of a stimulus had to be shifted by 10–12 min of arc, an amount almost two times larger than the smallest picture element, before the responses changed systematically. Nonetheless, changes of the stimulus at the single pixel level often gave rise to discriminable responses. Thus complex cells convey information about the spatial structure of a stimulus, independent of rigid stimulus displacements on the order of the receptive field size or smaller.
Pharmacological Characterization of Na+Influx via Voltage-Gated Na+Channels in Spinal Cord Astrocytes
Authors: Rose Christine R. , Ransom Bruce R. , Waxman Stephen G.
Published: December 2017

Rose, Christine R., Bruce R. Ransom, and Stephan G. Waxman. Pharmacological characterization of Na+influx via voltage-gated Na+channels in spinal cord astrocytes. J. Neurophysiol. 78: 3249–3258, 1997. Spinal cord astrocytes display a high density of voltage-gated Na+channels. To study the contribution of Na+influx via these channels to Na+homeostasis in cultured spinal cord astrocytes, we measured intracellular Na+concentration ([Na+]i) with the fluorescent dye sodium-binding benzofuran isophthalate. Stellate and nonstellate astrocytes, which display Na+currents with different properties, were differentiated. Baseline [Na+]iwas 8.5 mM in these cells and was not altered by 100 μM tetrodotoxin (TTX). Inhibition of Na+channel inactivation by veratridine (100 μM) evoked a [Na+]iincrease of 47.1 mM in 44% of stellate and 9.7 mM in 64% of nonstellate astrocytes. About 30% of cells reacted to veratridine with a [Na+]idecrease of ∼2 mM. Qualitatively similar [Na+]ichanges were caused by aconitine. The effects of veratridine were blocked by TTX, amplified by (α-)scorpion toxin and usually were readily reversible. Veratridine-induced [Na+]iincreases were reduced upon membrane depolarization with elevated extracellular [K+]. Recovery to baseline [Na+]iwas unaltered during blocking of K+channels with 4-aminopyridine. [Na+]iincreases evoked by the ionotropic non- N-methyl-d-aspartate receptor agonist kainate were not altered by TTX. Our results indicate that influx of Na+via voltage- gated Na+channels is not a prerequisite for glial Na+,K+-ATPase activity in spinal cord astrocytes at rest nor does it seem to be involved in [Na+]iincreases evoked by kainate. During pharmacological inhibition of Na+channel inactivation, however, Na+channels can serve as prominent pathways of Na+influx and mediate large perturbations in [Na+]i, suggesting that Na+channel inactivation plays an important functional role in these cells.