bluuebunny/crossref_metadata_2025 huggingface dataset:
Postnatal Maturation of Rat Hypothalamoneurohypophysial Neurons: Evidence for a Developmental Decrease in Calcium Entry During Action Potentials
Authors: Widmer H. , Amerdeil H. , Fontanaud P. , Desarménien M. G.
Published: December 2017

Widmer, H., H. Amerdeil, P. Fontanaud, and M. G. Desarménien. Postnatal maturation of rat hypothalamoneurohypophysial neurons: evidence for a developmental decrease in calcium entry during action potentials. J. Neurophysiol. 77: 260–271, 1997. Action potentials and voltage-gated currents were studied in acutely dissociated neurosecretory cells from the rat supraoptic nucleus during the first three postnatal weeks (PW1–PW3), a period corresponding to the final establishment of neuroendocrine relationships. Action potential duration (at half maximum) decreased from 2.7 to 1.8 ms; this was attributable to a decrease in decay time. Application of cadmium (250 μM) reduced the decay time by 43% at PW1 and 21% at PW3, indicating that the contribution of calcium currents to action potentials decreased during postnatal development. The density of high-voltage-activated calcium currents increased from 4.4 to 10.1 pA/pF at postnatal days 1–5 and 11–14, respectively. The conductance density of sustained potassium current, measured at +20 mV, increased from 0.35 (PW1) to 0.53 (PW3) nS/pF. The time to half-maximal amplitude did not change. Conductance density and time- and voltage-dependent inactivation of the transient potassium current were stable from birth. At PW1, the density and time constant of decay (measured at 0 mV) were 0.29 nS/pF ( n = 12) and 17.9 ms ( n = 10), respectively. Voltage-dependent properties and density (1.1 nS/pF) of the sodium current did not change postnatally. During PW1, fitting the mean activation data with a Boltzmann function gave a half-activation potential of −25 mV. A double Boltzman equation was necessary to adequately fit the inactivation data, suggesting the presence of two populations of sodium channels. One population accounted for ∼14% of the channels, with a half-inactivation potential of −86 mV; the remaining population showed a half-inactivation potential of −51 mV. A mathematical model, based on Hodgkin-Huxley equations, was used to assess the respective contributions of individual currents to the action potential. When the densities of calcium and sustained potassium currents were changed from immature to mature values, the decay time of the action potentials generated with the model decreased from 2.85 to 1.95 ms. A similar reduction was obtained when only the density of the potassium current was increased. Integration of the calcium currents generated during mature and immature action potentials demonstrated a significant decrease in calcium entry during development. We conclude that the developmental reduction of the action potential duration 1) is a consequence of the developmentally regulated increase in a sustained potassium current and 2) leads to a reduction of the participation of calcium currents in the action potential, resulting in a decreased amount of calcium entering the cell during each action potential.
Startle Phase of Escape Swimming Is Controlled by Pedal Motoneurons in the Pteropod MolluskClione limacina
Authors: Satterlie Richard A. , Norekian Tigran P. , Robertson Kirk J.
Published: December 2017

Satterlie, Richard A., Tigran P. Norekian, and Kirk J. Robertson. Startle phase of escape swimming is controlled by pedal motoneurons in the pteropod mollusk Clione limacina. J. Neurophysiol. 77: 272–280, 1997. Escape swimming in the pteropod mollusk Clione limacina includes an initial startle response in which one or two powerful wing beats propel the animal up to 18 body lengths per second, followed by a variable period of fast swimming with a maximal speed of 6 body lengths per second. The initial startle response is the focus of this report. Two pairs of large pedal neurons (50–60 μm) initiate wing contractions that are several times stronger than those produced during slow or fast swimming. These “startle” neurons are silent, with very low resting potentials and high activation thresholds. Each startle neuron has widespread innervation fields in the ipsilateral wing, with one pair of neurons innervating the dorsal musculature and producing dorsal flexion of the wing (d-phase) and the other innervating the ventral musculature and producing a ventral flexion of the wing (v-phase). Startle neurons are motoneurons, because they produce junctional potentials or spikelike responses in both slow-twitch and fast-twitch muscle cells with 1:1 ratios of spikes to excitatory postsynaptic potentials. Muscle activation persists in high-divalent saline, suggesting monosynaptic connections. The musculature innervated by startle neurons is the same used during normal slow and fast swimming. However, startle neuron activity is independent of normal swimming activity: startle neurons do not influence the activity of swim pattern generator interneurons or motoneurons, nor do swim neurons alter the activity of startle neurons. The startle response shows significant response depression with repetitive mechanical stimulation of the tail or wings. A major focus for this depression is at the neuromuscular junction. In reduced preparations, repetitive direct stimulation of a startle neuron does not result in a significant decrease in spike number or frequency, but does produce a decrease in force generation (decrease to 20% of original value after 5 stimuli delivered at 3-s intervals). Inputs that activate the wing retraction reflex as well as swim inhibition inhibit startle neurons. The inhibition appears to originate in the retraction interneurons, because direct connections from retraction sensory cells or retraction motoneurons are not found. Mechanical stimulation of a wing or the tail, which usually initiates startle response in intact animals, produces spikes or large EPSPs in startle neurons. The startle neurons appear to be likely candidates for direct control of the swim musculature during the startle phase of escape swimming in Clione.
Mediation by Intracellular Calcium-Dependent Signals of Hypoxic Hyperpolarization in Rat Hippocampal CA1 Neurons In Vitro
Authors: Yamamoto S. , Tanaka E. , Higashi H.
Published: December 2017

Yamamoto, S., E. Tanaka and H. Higashi. Mediation by intracellular calcium-dependent signals of hypoxic hyperpolarization in rat hippocampal CA1 neurons in vitro. J. Neurophysiol. 77: 386–392, 1997. In response to oxygen deprivation, CA1 pyramidal neurons show a hyperpolarization (hypoxic hyperpolarization), which is associated with a reduction in neuronal input resistance. The role of extra- and intracellular Ca2+ ions in hypoxic hyperpolarization was investigated. The hypoxic hyperpolarization was significantly depressed by tolbutamide (100 μM); moreover, the response was reversed in its polarity in medium containing tolbutamide (100 μM), low Ca2+ (0.25 mM), and Co2+ (2 mM), suggesting that the hypoxic hyperpolarization is mediated by activation of both ATP-sensitive K+ (KATP) channels and Ca2+-dependent K+ channels. The hypoxic depolarization in medium containing tolbutamide, low Ca2+, and Co2+ is probably due to inhibition of the electrogenic Na+-K+ pump and concomitant accumulation of interstitial K+. Hypoxic hyperpolarizations were depressed in either low Ca2+ (0.25 or 1.25 mM) or high Ca2+ (5 or 7.5 mM) medium (control: 2.5 mM), indicating that there is an optimal extracellular Ca2+ concentration required to producethe hypoxic hyperpolarization. Bis-( o-aminophenoxy)- N,N,N′,N′tetraacetic acid (BAPTA)-AM (50–100 μM), procaine (300 μM), or ryanodine (10 μM) significantly depressed the hypoxic hyperpolarization, suggesting that Ca2+ released from intracellular Ca2+ stores may have an important role in the generation of hypoxic hyperpolarization. The high-affinity calmodulin inhibitor N-(6-amino-hexyl)-5-chloro-1-naphthalenesulfonomide hydrochloride (W-7) (5 μM) completely blocked, whereas the low-affinity calmodulin inhibitor N-(6-aminohexyl)-1-naphthalenesulfonomide hydrochloride (W-5) (50 μM) did not affect, the hypoxic hyperpolarization. The calmodulin inhibitor trifluoperazine (50 μM) also suppressed the hypoxic hyperpolarization. In addition, calcium/calmodulin kinase II inhibitor 1-[N,O-bis(1,5-isoquinol-inesulfonyl)- N-methyl-l-tyrosyl]-4-phenyl-piperazine (KN-62) (10 μM) markedly depressed the amplitude and net outward current of the hypoxic hyperpolarization without affecting the reversal potential. In contrast, neither the myosin light chain kinase inhibitor 1-(5-iodonaphthalene-1-sulfonyl)-1H-hexa-hydro-1,4-diazepin hydrochloride (ML-7) (10 μM) nor the protein kinase A inhibitorN-[2-(p-bromocinnamyl-amino)ethyl]-5-isoquinolinesulfonamide(H-89) (1 μM) significantly altered the hypoxic hyperpolarization. These results suggest that calmodulin kinase II, which is activated by calmodulin, may contribute to the generation of the hypoxic hyperpolarization. In conclusion, the present study indicates that, in the majority of hippocampal CA1 neurons, the hypoxic hyperpolarization is due to activation of both KATP channels and Ca2+-dependent K+ channels.
High-Voltage-Activated Calcium Currents in Neurons Acutely Isolated From the Ventrobasal Nucleus of the Rat Thalamus
Authors: Kammermeier Paul J. , Jones Stephen W.
Published: December 2017

Kammermeier, Paul J. and Stephen W. Jones. High-voltage-activated calcium currents in neurons acutely isolated from the ventrobasal nucleus of the rat thalamus. J. Neurophysiol. 77: 465–475, 1997. We studied the high-voltage-activated (HVA) calcium currents in cells isolated from the ventrobasal nucleus of the rat thalamus with the use of the whole cell patch-clamp technique. Low-voltage-activated current was inactivated by the use of long voltage steps or 100-ms prepulses to −20 mV. We used channel blocking agents to characterize the currents that make up the HVA current. The dihydropyridine (DHP) antagonist nimodipine (5 μM) reversibly blocked 33 ± 1% (mean ± SE), and ω-conotoxin GVIA (1 μM) irreversibly blocked 25 ± 5%. The current resistant to DHPs and ω-conotoxin GVIA was inhibited almost completely by ω-conotoxin MVIIC (90 ± 5% at 3–5 μM) and was partially inhibited by ω-agatoxin IVA (54 ± 4% block at 1 μM). We conclude that there are at least four main HVA currents in thalamic neurons: N current, L current, and two ω-conotoxin MVIIC-sensitive currents that differ in their sensitivity to ω-agatoxin IVA. We also examined modulation of HVA currents by strong depolarization and by G protein activation. Long (∼1 s), strong depolarizations elicited large, slowly deactivating tail currents, which were sensitive to DHP antagonists. With guanosine 5′-O-(3-thiotriphosphate) (GTP-γ-S) in the intracellular solution, brief (∼20 ms), strong depolarization produced a voltage-dependent facilitation of the current (44 ± 5%), compared with cells with GTP (22 ± 7%) or guanosine 5′-O-(2-thiodiphosphate) (7 ± 4%). However, the HVA current was inhibited only weakly by 100 μM acetylcholine (8 ± 4%). Effects of the γ-aminobutyric acid-B agonist baclofen were variable (3–39% inhibition, n = 12, at 10–50 μM).
Spatiotemporal Distribution of Intracellular Calcium Transients During Epileptiform Activity in Guinea Pig Hippocampal Slices
Authors: Albowitz B. , König P. , Kuhnt U.
Published: December 2017

Albowitz, B., P. König, and U. Kuhnt. Spatiotemporal distribution of intracellular calcium transients during epileptiform activity in guinea pig hippocampal slices. J. Neurophysiol. 77: 491–501, 1997. Calcium ions are known to play an important role in epileptogenesis. Although there is clear evidence for increased neuronal calcium influx during epileptiform potentials, direct measurements of the corresponding intracellular calcium transients are rare and the origin of calcium influx is not known. Therefore the spatial and temporal distribution of intracellular calcium transients during epileptiform activity in guinea pig hippocampal slices was monitored with the use of the indicator Calcium-Green and a fast optical recording method. Two models of epilepsy (bicuculline and low Mg2+) were compared. In both models, single epileptiform events were evoked by electrical stimulation of the Schaffer collaterals in CA1 or of stratum pyramidale in area CA3. Intracellular calcium transients during epileptiform activity were ∼5 times larger than during control stimulation. Calcium transients during epileptiform activity were present across at least the entire CA1 area, whereas presynaptic calcium transients from stimulated fibers were only seen at a distance up to 1 mm from the stimulation site. dl-2-amino-5-phosphonovaleric acid (APV), a specific antagonist of the N-methyl-d-aspartate (NMDA) receptor, abolished low-Mg2+ epileptiform activity and reduced bicuculline-induced epileptiform activity; it reduced calcium transients following stimulation of CA1 by only 29% (bicuculline) and 38% (low Mg2+). For comparison, calcium transients during control stimulation were 78% (bicuculline) and 69% (low Mg2+) smaller than epileptiform calcium transients. At a distance from the stimulation site, calcium transients and their NMDA-receptor-dependent components were largest in stratum pyramidale in the bicuculline model and in stratum oriens in the low-Mg2+ model. In both models, minimal onset latencies of calcium influx shifted with increasing distance to the stimulation electrode from stratum radiatum to stratum oriens. APV reduced the extent of spread of calcium transients in the low-Mg2+ model. In the bicuculline model, the spatial extent of spread of epileptiform calcium transients was not affected by application of APV; however, the mean velocity of spread was reduced from 0.20 to 0.12 m/s. In conclusion, the large size of calcium transients and of their NMDA-receptor-dependent components in stratum pyramidale or stratum oriens as well as shortest onset latencies of calcium transients at these sites suggest an important role of cell somata, basal dendrites, and possibly local circuit excitatory interactions for the generation and spread of epileptiform activity.
Comparison of Onset Time and Magnitude of Activity for Proximal Arm Muscles and Motor Cortical Cells Before Reaching Movements
Authors: Scott Stephen H.
Published: December 2017

Scott, Stephen H. Comparison of onset time and magnitude of activity for proximal arm muscles and motor cortical cells before reaching movements. J. Neurophysiol. 77: 1016–1022, 1997. The activity of motor cortical cells and proximal arm muscles during the initiation of planar reaching movements were analyzed to identify whether features of coordinated motor patterns of muscles spanning the elbow and shoulder were evident in the discharge patterns of motor cortical cells. Shoulder and elbow muscles were divided into four groups, flexors and extensors at each joint. Features of the initial agonist activity, onset time and magnitude, at the shoulder and elbow were compared for movements in different spatial directions. As observed for human movements, differences in the onset time and the relative magnitude of electromyographic activity (EMG) of muscles acting about the shoulder and elbow were dependent on the direction of movement. Motor cortical cells were categorized as elbow or shoulder related on the basis of their response to passive movement of the joints. Differences in the onset time and the relative magnitude of activity of cells related to the shoulder and elbow were both dependent on the direction of movement and were similar to those observed for muscles spanning these joints. There was a modest, but significant correlation between the onset time and magnitude of EMG for individual muscles. A similar magnitude-time coupling was observed for individual motor cortical cells. Variations in the discharge pattern of motor cortical cells before movement that mirror those observed for muscles spanning the shoulder and elbow support the potential role of primary motor cortex in the selection, timing, and magnitude of agonist motor patterns at the shoulder and elbow to initiate reaching movements.
Neurotransmitter Interactions in the Stomatogastric System of the Spiny Lobster: One Peptide Alters the Response of a Central Pattern Generator to a Second Peptide
Authors: Dickinson Patsy S. , Fairfield Wesley P. , Hetling John R. , Hauptman Jane
Published: December 2017

Dickinson, Patsy S., Wesley P. Fairfield, John R. Hetling, and Jane Hauptman. Neurotransmitter interactions in the stomatogastric system of the spiny lobster: one peptide alters the response of a central pattern generator to a second peptide. J. Neurophysiol. 77: 599–610, 1997. Two of the peptides found in the stomatogastric nervous system of the spiny lobster, Panulirus interruptus, interacted to modulate the activity of the cardiac sac motor pattern. In the isolated stomatogastric ganglion, red-pigment-concentrating hormone (RPCH), but not proctolin, activated the bursting activity in the inferior ventricular (IV) neurons that drives the cardiac sac pattern. The cardiac sac pattern normally ceased within 15 min after the end of RPCH superfusion. However, when proctolin was applied within a few minutes of that time, it was likewise able to induce cardiac sac activity. Similarly, proctolin applied together with subthreshold RPCH induced cardiac sac bursting. The amplitude of the excitatory postsynaptic potentials from the IV neurons to the cardiac sac dilator neuron CD2 (1 of the 2 major motor neurons in the cardiac sac system) was potentiated in the presence of both proctolin and RPCH. The potentiation in RPCH was much greater than in proctolin alone. However, the potentiation inproctolin after RPCH was equivalent to that recorded in RPCH alone. Although we do not yet understand the mechanisms for these interactions of the two modulators, this study provides an example of one factor that can determine the “state” of the system that is critical in determining the effect of a modulator that is “state dependent,” and it provides evidence for yet another level of flexibility in the motor output of this system.
Differential Sensitivity to Intracellular pH Among High- and Low-Threshold Ca2+ Currents in Isolated Rat CA1 Neurons
Authors: Tombaugh Geoffrey C. , Somjen George G.
Published: December 2017

Tombaugh, Geoffrey C. and George G. Somjen. Differential sensitivity to intracellular pH among high- and low-threshold Ca2+ currents in isolated rat CA1 neurons. J. Neurophysiol. 77: 639–653, 1997. The effects of intracellular pH (pHi) on high-threshold (HVA) and low-threshold (LVA) calcium currents were examined in acutely dissociated rat hippocampal CA1 neurons with the use of the whole cell patch-clamp technique (21–23°C). Internal pH was manipulated by external exposure to the weak base NH4Cl or in some cases to the weak acid Na-acetate (20 mM) at constant extracellular pH (7.4). Confocal fluorescence measurements using the pH-sensitive dye SNARF-1 in both dialyzed and intact cells confirmed that NH4Cl caused a reversible alkaline shift. However, the external TEA-Cl concentration used during I Ca recording was sufficient to abolish cellular acidification upon NH4Cl wash out. With 10 mM N-2-hydroxyethylpiperazine- N′-2-ethanesulfonic acid (HEPES) in the pipette, NH4Cl exposure reversibly enhanced HVA currents by 29%, whereas exposure to Na-acetate markedly and reversibly depressed HVA Ca currents by 62%. The degree to which NH4Cl enhanced HVA currents was inversely related to the internal HEPES concentration but was unaffected when internal ethylene glycol-bis(β-aminoethyl ether)- N,N,N′,N′-tetraacetic acid (EGTA) was replaced by equimolar bis-( o-aminophenoxy)- N,N,N′,N′-tetraacetic acid (BAPTA). When depolarizing test pulses were applied shortly after break-in ( V h = −100 mV), NH4Cl caused a proportionally greater increase in the sustained current relative to the peak. The dihydropyridine Ca channel antagonist nifedipine (5 μM) blocked nearly all of this sustained current. A slowly inactivating nifedipine-sensitive (L-type) HVA current could be evoked from a depolarized holding potential of −50 mV; NH4Cl enhanced this current by 40 ± 3% (mean ± SE) and reversibly shifted the tail-current activation curve by +6–8 mV. L-type currents exhibited more rapid rundown than N-type currents; HVA currents remaining after prolonged cell dialysis, or in the presence of nifedipine, inactivated rapidly and were depressed by ω-conotoxin (GVIA). NH4Cl enhanced these N-type currents by 76 ± 9%. LVA Ca currents were observed in 32% of the cells and exhibited little if any rundown. These amiloride-sensitive currents activated at voltages negative to −50 mV, were enhanced by extracellular alkalosis and depressed by extracellular acidosis, but were unaffected by exposure to either NH4Cl or NaAC. These results demonstrate that HVA Ca currents in hippocampal CA1 neurons are bidirectionally modulated by internal pH shifts, and that N-type currents are more sensitive to alkaline shifts than are L- or T-type (N > L > T). Our findings strengthen the idea that distinct cellular processes governed by different Ca channels may be subject to selective modulation by uniform shifts in cytosolic pH.
Pharmacology of Directionally Selective Ganglion Cells in the Rabbit Retina
Authors: Kittila Christopher A. , Massey Stephen C.
Published: December 2017

Kittila, Christopher A. and Stephen C. Massey. Pharmacology of directionally selective ganglion cells in the rabbit retina. J. Neurophysiol. 77: 675–689, 1997. In this report we describe extracellular recordings made from on and on-off directionally selective (DS) ganglion cells in the rabbit retina during perfusion with agonists and antagonists to acetylcholine (ACh), glutamate, and γ-aminobutyric acid (GABA). Nicotinic ACh agonists strongly excited DS ganglion cell in a dose-dependent manner. Dose-response curves showed a wide range of potencies, with (±)-exo-2-(6-chloro-3pyridinyl)-7-azabicyclo[2.2.1] heptane dihydrochloride (epibatidine) ≫ nicotine > 1,1-dimethyl-4-phenylpiperazinium iodide = carbachol. In addition, the mixed cholinergic agonist carbachol produced a small excitation, mediated by muscarinic receptors, that could be blocked by atropine. The specific nicotinic antagonists hexamethonium bromide (100 μM), dihydro-β-erythroidine (50 μM), mecamylamine (50 μM), and tubocurarine (50 μM) blocked the responses to nicotinic agonists. In addition, nicotinic antagonists reduced the light-driven input to DS ganglion cells by ∼50%. However, attenuated responses were still DS. We deduce that cholinergic input is not required for directional selectivity. These experiments reveal the importance of bipolar cell input mediated by glutamate. N-methyl-d-aspartic acid (NMDA) excited DS ganglion cells, but NMDA antagonists did not abolish directional selectivity. However, a combined cholinergic and NMDA blockade reduced the responses of DS ganglion cells by >90%. This indicates that most of the noncholinergic excitatory input appears to be mediated by NMDA receptors, with a small residual made upb y  α - a m i n o - 3 - h y d r o x y - 5 - m e t h y l - 4 - i s o x a z o l e p r o p i o n i c  a c i d(AMPA)/kainate (KA) receptors. Responses to AMPA and KA were highly variable and often evoked a mixture of excitation and inhibition due to the release of ACh and GABA. Under cholinergic blockade AMPA/KA elicited a strong GABA-mediated inhibition in DS ganglion cells. AMPA/KA antagonists, such as 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)quinoxaline dione and GYKI-53655, promoted null responses and abolished directional selectivity due to the blockade of GABA release. We conclude that GABA release, mediated by non-NMDA glutamate receptors, is an essential part of the mechanism of directional selectivity. The source of the GABA is unknown, but may arise from starburst amacrine cells.
Modulatory Effects of Regional Cortical Activation on the Onset Responses of the Cat Medial Geniculate Neurons
Authors: He Jufang
Published: December 2017

He, Jufang. Modulatory effects of regional cortical activation on the onset responses of the cat medial geniculate neurons. J. Neurophysiol. 77: 896–908, 1997. Corticofugal modulation on activity of the medial geniculate body (MGB) was examined by locally activating the primary auditory cortex (AI) and looking for effects on the onset responses of MGB neurons to acoustic stimuli. Of 103 MGB neurons recorded from 13 hemispheres of 11 animals, 91 neurons (88%) showed either a facilitatory or inhibitory effect or both; of these neurons, 72 showed facilitatory effects and 25 inhibitory effects. The average facilitatory effect was large, with a mean increase of 62.4%. Small inhibitory effects (mean: −16.2%) were obtained from a few neurons (6 of 103) when a pure tone stimulus was used, whereas the effect became larger and more frequent when a noise burst stimulus was used (mean: −27.3%, n = 22 of 27 neurons). Activation of an AI site having the same best frequency (BF) as the MGB neuron being recorded from produced mainly a facilitatory effect on MGB neuronal responses to pure tones. Activation of AI at a site neighboring the BF site produced inhibitory effects on the MGB response when noise burst stimuli were used. We found that the effective stimulation sites in AI that could modulate MGB activity formed patchlike maps with a diameter of 1.13 ± 0.09 (SE) mm (range 0.6–1.9 mm, n = 15) being larger than the patches of thalamocortical terminal fields. Examining the effects of sound intensities, of 18 neurons tested 9 neurons showed a larger effect for low-sound-intensity stimuli and small or no effects for high-sound-intensity stimuli. These were named low-sound-intensity effective neurons. Five neurons showed high sound intensity effectiveness and four were non-intensity specific. Most low-sound-intensity effective neurons were monotonic rate-intensity function neurons. The AI cortical modulatory effect was frequency specific, because 15 of 27 neurons showed a larger facilitatory effect when a BF stimulus was used rather than a stimulus of any other frequency. The corticothalamic connection between the recording site in MGB and the most effective stimulation site in AI was confirmed by injecting wheat germ agglutinin–horseradish peroxidase tracer at the stimulation site and producing a small lesion in the recording site. The results suggest that 1) the large facilitation effects obtained by AI activation at the region that directly projected to the MGB could be the result mainly of the direct projection terminals to the MGB relay neurons; 2) the large size patches of the effective stimulation site in AI could be due to widely ramifying corticothalamic projections; and 3) the corticofugal projection selectively gates auditory information mainly by a facilitatory effect, although there is also an inhibitory effect that depends on the sound stimulus used.
Eye Position Effects in Monkey Cortex. II. Pursuit- and Fixation-Related Activity in Posterior Parietal Areas LIP and 7A
Authors: Bremmer F. , Distler C. , Hoffmann K.-P.
Published: December 2017

Bremmer, F., C. Distler, and K.-P. Hoffmann. Eye position effects in monkey cortex. II. Pursuit- and fixation-related activity in posterior parietal areas LIP and 7A. J. Neurophysiol. 77: 962–977, 1997. We studied the effect of eye position on pursuit-related discharges and activity during fixation in darkness for neurons of monkey visual cortical areas (lateral intraparietal area) LIP and 7A. In a first step, neurons were tested for direction-specific activity related to pursuit eye movements while the monkey tracked a moving target. In consecutive trials the pursuit target moved in random order in one of four directions on a translucent screen. For 39% of the neurons, located mostly in a dorsoposterior region of area LIP, as well as 42% of the neurons tested in area 7A, a direction-specific pursuit-related activity could be found. To test whether responsiveness of these neurons was modulated by eye position, we employed a pursuit paradigm. In this paradigm, the monkey had to track a target that started to move in the preferred direction with constant speed from five different locations on the screen in random order. For the majority of cells in both areas, pursuit-related activity was modulated by eye position. Most of the neurons tested also revealed an influence of eye position on their spontaneous activity during fixation in darkness (fixation paradigm). For the majority of cells (>50%) recorded in both areas, two-dimensional regression planes could be approximated significantly ( P < 0.05) or nearly significantly ( P < 0.1) to the neuronal discharges observed on the fixation paradigm and pursuit paradigm. For 79% of the LIP neurons and 83% of the 7A neurons tested in both experimental paradigms, the directions of the gradients of the regression planes pointed into the same hemifield, suggesting a common neuronal mechanism mediating the eye position effect regardless of the behavioral task the monkey was performing. The observed effects very much resemble the effects of eye position on light-sensitive and saccade-related responses already described for areas LIP and 7A. Regarding also our results observed for the middle temporal and medial superior temporal areas, it is suggested that the observed modulatory effect of eye position on neuronal activity is a common phenomenon in the macaque visual cortical system subserving an internal representation of the external space in a nonretinocentric frame of reference.
Anatomy of Motor Learning. I. Frontal Cortex and Attention to Action
Authors: Jueptner M. , Stephan K. M. , Frith C. D. , Brooks D. J. , Frackowiak R.S.J. , Passingham R. E.
Published: December 2017

Jueptner, M., K. M. Stephan, C. D. Frith, D. J. Brooks, R.S.J. Frackowiak, and R. E. Passingham. Anatomy of motor learning. I. Frontal cortex and attention to action. J. Neurophysiol. 77: 1313–1324, 1997. We used positron emission tomography to study new learning and automatic performance in normal volunteers. Subjects learned sequences of eight finger movements by trial and error. In a previous experiment we showed that the prefrontal cortex was activated during new learning but not during automatic performance. The aim of the present experiment was to see what areas could be reactivated if the subjects performed the prelearned sequence but were required to pay attention to what they were doing. Scans were carried out under four conditions. In the first the subjects performed a prelearned sequence of eight key presses; this sequence was learned before scanning and was practiced until it had become overlearned, so that the subjects were able to perform it automatically. In the second condition the subjects learned a new sequence during scanning. In a third condition the subjects performed the prelearned sequence, but they were required to attend to what they were doing; they were instructed to think about the next movement. The fourth condition was a baseline condition. As in the earlier study, the dorsal prefrontal cortex and anterior cingulate area 32 were activated during new learning, but not during automatic performance. The left dorsal prefrontal cortex and the right anterior cingulate cortex were reactivated when subjects paid attention to the performance of the prelearned sequence compared with automatic performance of the same task. It is suggested that the critical feature was that the subjects were required to attend to the preparation of their responses. However, the dorsal prefrontal cortex and the anterior cingulate cortex were activated more when the subjects learned a new sequence than they were when subjects simply paid attention to a prelearned sequence. New learning differs from the attention condition in that the subjects generated moves, monitored the outcomes, and remembered the responses that had been successful. All these are nonroutine operations to which the subjects must attend. Further analysis is needed to specify which are the nonroutine operations that require the involvement of the dorsal prefrontal and anterior cingulate cortex.
Calcium Flux Through Predominantly Independent Purinergic ATP and Nicotinic Acetylcholine Receptors
Authors: Rogers Marc , Colquhoun Lorna M. , Patrick James W. , Dani John A.
Published: December 2017

Rogers, Marc, Lorna M. Colquhoun, James W. Patrick, and John A. Dani. Calcium flux through predominantly independent purinergic ATP and nicotinic acetylcholine receptors. J. Neurophysiol. 77: 1407–1417, 1997. Ligand-gated nicotinic acetylcholine receptors (nAChRs) and purinergic ATP receptors are often expressed in the same peripheral and central neurons, and ATP and acetylcholine (ACh) are stored together in some synaptic vesicles. Evidence has suggested that nAChRs and ATP receptors are not independent and that some agonists strongly cross-activate and desensitize both receptor types. Rat sympathetic neurons and nAChRs expressed in Xenopus oocytes were studied to determine the significance of the interactions caused by the two agonist types. Current amplitudes induced with separate or combined applications of ATP and nicotine are >90% additive and independent. Half of all neurons tested responded to either ATP or nicotine but not to both, indicating differences in the expression of the two receptors. In neurons that expressed both receptor types, the nAChRs were inhibited by the activity-dependent open-channel blocker chlorisondamine. If the purinergic and nicotinic receptors were significantly dependent and coactivated, then blocking the ion channels opened by a nicotinic agonist should diminish the current activated by a purinergic agonist. That result was not seen; rather, complete open-channel block of nAChRs with chlorisondamine did not significantly alter the amplitude or kinetics of ATP-induced currents in the same neurons. Finally, when cloned nAChR subunits were expressed in oocytes, ATP activated only very small currents compared with the current activated by ACh. For the 13 different nAChR subunit combinations that were studied, ATP (50–500 μM) activated a current that ranged from 0 to 4% of the size of the current activated by 100 μM ACh. In summary, we find that there is little cross reactivity, and nAChRs and purinergic ATP receptors are predominately independent, acting with separable physiological characteristics. Therefore the quantitative Ca2+flux could be separately determined for nAChRs and ATP receptors. The fraction of total current that is carried by Ca2+was quantitatively determined by simultaneously measuring the whole cell current and the associated change in intracellular Ca2+with fura-2. For sympathetic neurons bathed in 2.5 mM Ca2+at a holding potential of −50 mV, Ca2+carries 4.8 ± 0.3% (mean ± SE) of the inward current through neuronal nAChRs and 6.5 ± 0.1% of the current through purinergic ATP receptors. In conclusion, activity-dependent Ca2+influx through predominately independent populations of nAChRs and ATP receptors can produce different intracellular signals at purinergic and cholinergic synapses.
Modulation of High-Voltage Activated Ca2+ Channels in the Rat Periaqueductal Gray Neurons by μ-Type Opioid Agonist
Authors: Kim Chang-Ju , Rhee Jeong-Seop , Akaike Norio
Published: December 2017

Kim, Chang-Ju, Jeong-Seop Rhee, and Norio Akaike. Modulation of high-voltage activated Ca2+ channels in the rat periaqueductal gray neurons by μ-type opioid agonist. J. Neurophysiol. 77: 1418–1424, 1997. The effect of μ-type opioid receptor agonist, D-Ala2,N-MePhe4,Gly5-ol-enkephalin (DAMGO), on high-voltage-activated (HVA) Ca2+ channels in the dissociated rat periaqueductal gray (PAG) neurons was investigated by the use of nystatin-perforated patch recording mode under voltage-clamp condition. Among 118 PAG neurons tested, the HVA Ca2+ channels of 38 neurons (32%) were inhibited by DAMGO (DAMGO-sensitive cells), and the other 80 neurons (68%) were not affected by DAMGO (DAMGO-insensitive cells). The N-, P-, L-, Q-, and R-type Ca2+ channel components in DAMGO-insensitive cells shared 26.9, 37.1, 22.3, 7.9, and 5.8%, respectively, of the total Ca2+ channel current. The channel components of DAMGO-sensitive cells were 45.6, 25.7, 21.7, 4.6, and 2.4%, respectively. The HVA Ca2+ current of DAMGO-sensitive neurons was inhibited by DAMGO in a concentration-, time-, and voltage-dependent manner. Application of ω-conotoxin-GVIA occluded the inhibitory effect of DAMGO ∼70%. So, HVA Ca2+ channels inhibited by DAMGO were mainly the N-type Ca2+ channels. The inhibitory effect of DAMGO on HVA Ca2+ channels was prevented almost completely by the pretreatment of pertussis toxin (PTX) for 8–10 h, suggesting that DAMGO modulation on N-type Ca2+ channels in rat PAG neurons is mediated by PTX-sensitive G proteins. These results indicate that μ-type opioid receptor modulates N-type HVA Ca2+ channels via PTX-sensitive G proteins in PAG neurons of rats.
Electrogenic Hyperpolarization-Elicited Chloride Transporter Current in Blue Cones of Zebrafish Retinal Slices
Authors: Fan Shih-Fang , Yazulla Stephen
Published: December 2017

Fan, Shih-Fang and Stephen Yazulla. Electrogenic hyperpolarization-elicited chloride transporter current in blue cones of zebrafish retinal slices. J. Neurophysiol. 77: 1447–1459, 1997. Voltage-activated currents in blue cones of the retinal slice of zebrafish were characterized using whole cell recording techniques. Depolarizing-elicited currents were recorded: an outward tetraethylammonium (TEA)-sensitive K+current ( IKx), an outward Ca2+-activated Cl−current ( ICl(Ca)), from which we inferred an inward Ca2+current ( ICa) as well as a hyperpolarizing-elicited nonselective inward cation current ( Ih). In addition, hyperpolarizing steps elicited an outward current ( Iout-h) in about one-third of the blue cones. Iout-hseems to be carried by inward transported Cl−because it was abolished by equimolar substitution of bath Cl−with acetate; equimolar substitution of Na+with choline or TEA had no effect; it was not affected by Cl−channel blockers, anthracene-9-carboxylic acid, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid, N-phenylanthranilic acid (DPC), niflumic acid, and 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid but was suppressed by Cl−transporter blockers acetalzolamide, bumetanide, N-ethylmaleimide, furosemide, and vanadate, and no reversal potential was found. In addition, this current was suppressed by ouabains but unrelated to their Na+-K+-ATPase inhibitory effect, was not suppressed by Co2+or nifedipine, was not affected by the gap junction decoupler, 2-octanol, was increased by bath application of Cs+, presumably due to suppression of Ih, which was masked by Iout-h, and was suppressed by intense light. Similar current also was found in the short cones and double cones. As Iout-hoperates over the same voltage range, and with similar magnitude and time course as Ih, we suggest that Iout-hcontributes to the modulation of the photoresponse of cones.
Properties of Voltage-Activated Ca2+ Currents in Acutely Isolated Human Hippocampal Granule Cells
Authors: Beck H. , Steffens R. , Heinemann U. , Elger C. E.
Published: December 2017

Beck, H., R. Steffens, U. Heinemann, and C. E. Elger. Properties of voltage-activated Ca2+ currents in acutely isolated human hippocampal granule cells. J. Neurophysiol. 77: 1526–1537, 1997. Properties of Ba2+ currents through voltage-dependent Ca2+ channels ( I Ba) were investigated in 61 dentate granule cells acutely isolated from the resected hippocampus of nine patients with therapy-refractory temporal lobe epilepsy (TLE). Currents with a high threshold of activation (HVA) peaked at 0 mV, and showed some time-dependent inactivation and a voltage of half-maximal steady-state inactivation ( V 1/2inact) of −16.4 mV. Application of saturating doses of ω-conotoxin (ω-CgTx) GVIA or nifedipine distinguished characteristic N-type (38%) and L-type (62% of HVA currents) Ca2+ currents. Combined application of both agents blocked HVA currents by >95%. In a 10-mo-old child but not in adult patients, an ω-agatoxin IVA (ω-AgaTx IVA)-sensitive but ω-CgTx MVIIC-insensitive, noninactivating component of HVA currents (∼24%) was present that most probably corresponds to a P-type current. A T-type Ca2+ current could be separated from HVA components on the basis of its steady-state voltage-dependent inactivation( V 1/2inact = −71.0 mV). The T-type Ca2+ current isolated by subtraction peaked at more negative potentials (−10 mV), showed a significantly more rapid time-dependent inactivation, and could be selectively blocked by low concentrations of Ni2+. It was insensitive to nifedipine and ω-CgTx GVIA. We conclude that L-, N-, and T-type currents are present in adult human dentate granule cells and an additional P-type current is present in neurons from a 10-mo-old patient. These data may provide a basis for comparison with animal models of epilepsy and for the elucidation of mechanisms of action of drugs intended for use in human disease.
Neural Selectivity and Tuning for Sinusoidal Frequency Modulations in the Inferior Colliculus of the Big Brown Bat, Eptesicus fuscus
Authors: Casseday John H. , Covey Ellen , Grothe Benedikt
Published: December 2017

Casseday, John H., Ellen Covey, and Benedikt Grothe. Neural selectivity and tuning for sinusoidal frequency modulations in the inferior colliculus of the big brown bat, Eptesicus fuscus. J. Neurophysiol. 77: 1595–1605, 1997. Most communication sounds and most echolocation sounds, including those used by the big brown bat ( Eptesicus fuscus), contain frequency-modulated (FM) components, including cyclical FM. Because previous studies have shown that some neurons in the inferior colliculus (IC) of this bat respond to linear FM sweeps but not to pure tones or noise, we asked whether these or other neurons are specialized for conveying information about cyclical FM signals. In unanesthetized bats, we tested the response of 116 neurons in the IC to pure tones, noise with various bandwidths, single linear FM sweeps, sinusoidally amplitude-modulated signals, and sinusoidally frequency-modulated (SFM) signals. With the use of these stimuli, 20 neurons (17%) responded only to SFM, and 10 (9%) responded best to SFM but also responded to one other test stimulus. We refer to the total 26% of neurons that responded best to SFM as SFM-selective neurons. Fifty-nine neurons (51%) responded about equally well to SFM and other stimuli, and 27 (23%) did not respond to SFM but did respond to other stimuli. Most SFM-selective neurons responded to a limited range of modulation rates and a limited range of modulation depths. The range of modulationrates over which individual neurons responded was 5–170 Hz( n = 20). Thus SFM-selective neurons respond to low modulation rates. The depths of modulations to which the neurons responded ranged from ±0.4 to ±19 kHz ( n = 15). Half of the SFM-selective neurons did not respond to the first cycle of SFM. This finding suggests that the mechanism for selective response to SFM involves neural delays and coincidence detectors in which the response to one part of the SFM cycle coincides in time either with the response to a later part of the SFM cycle or with the response to the first part of the next cycle. The SFM-selective neurons in the IC responded to a lower and more limited range of SFM rates than do neurons in the nuclei of the lateral lemniscus of this bat. Because the FM components of biological sounds usually have low rates of modulation, we suggest that the tuning of these neurons is related to biologically important sound parameters. The tuning could be used to detect FM in echolocation signals, modulations in high-frequency sounds that are generated by wing beats of some beetles, or social communication sounds of Eptesicus.
Selectivity and Response Characteristics of Human Olfactory Neurons
Authors: Rawson N. E. , Gomez G. , Cowart B. , Brand J. G. , Lowry L. D. , Pribitkin E. A. , Restrepo D.
Published: December 2017

Rawson, N. E., G. Gomez, B. Cowart, J. G. Brand, L. D. Lowry, E. A. Pribitkin, and D. Restrepo. Selectivity and response characteristics of human olfactory neurons. J. Neurophysiol. 77: 1606–1613, 1997. Transduction mechanisms were investigated in human olfactory neurons by determining characteristics of odorant-induced changes in intracellular calcium concentration ([Ca2+]i). Olfactory neurons were freshly isolated from nasal biopsies, allowed to attach to coverslips, and loaded with the calcium-sensitive indicator fura-2. Changes in [Ca2+]i were studied in response to exposure to individual odors, or odorant mixtures composed to distinguish between transduction pathways mediated by adenosine 3′5′-monophosphate (cAMP; mix A) or inositol 1,4,5-trisphosphate (InsP3; mix B). Overall, 52% of biopsies produced one or more odorant-responsive olfactory neurons, whereas 24% of all olfactory neurons tested responded to odorant exposure with a change in [Ca2+]i. As in olfactory neurons from other species, the data suggest that odorant exposure elicited calcium influx via second-messenger pathways involving cAMP or InsP3. Unlike olfactory neurons from other species that have been tested, some human olfactory neurons responded to odorants with decreases in [Ca2+]i. Also in contrast with olfactory neurons from other species, human olfactory neurons were better able to discriminate between odorant mixtures in that no neuron responded to more than one type of odor or mixture. These results suggest the presence of a previously unreported type of olfactory transduction mechanism, and raise the possibility that coding of odor qualities in humans may be accomplished to some degree differently than in other vertebrates, with the olfactory neuron itself making a greater contribution to the discrimination process.
Dendritic Spine Density and LTP Induction in Cultured Hippocampal Slices
Authors: Collin Carlos , Miyaguchi Katsuyuki , Segal Menahem
Published: December 2017

Collin, Carlos, Katsuyuki Miyaguchi, and Menahem Segal.Dendritic spine density and LTP induction in cultured hippocampal slices. J. Neurophysiol. 77: 1614–1623, 1997. Transverse hippocampal slices were cut from 8- to 9-day-old rats and maintained in an interface chamber for periods of 1–4 wk, in tissue culture conditions. Neurons in the slice preserved their spatial organization and connectivity. Dendritic spine density in CA1 neurons was very low at 1 wk in culture, and long, filopodia-like structures were abundant. Spine density increased in these neurons nearly threefold during the course of 3 wk in vitro, to approach values of those of the normal, in vivo hippocampus. The magnitude of long-term potentiation (LTP) of reactivity of CA1 to stimulation of CA3 neurons also increased during weeks in culture in parallel with the change in spine density. Chronic exposure of slices to drugs that interact with synaptic activity caused changes in their dendritic spine density. Blockade of the N-methyl-d-aspartate (NMDA) receptors with the receptor antagonist 2-aminophosphonovalerate (d-APV) or blockade of action potential discharges with tetrodotoxin (TTX) prevented dendritic spine development in immature cultures. Enhancing synaptic activity by blockade of GABAergic inhibition with picrotoxin did not affect spine density to a significant degree. d-APV-treated slices expressed larger LTP than controls. TTX-treated slices expressed smaller LTP than controls. Picrotoxin treated slices did not express LTP. It is proposed that LTP and dendritic spine density are correlated strongly during development, whereas they are not correlated in the more mature slice/culture of the hippocampus where spine density can be modulated by chronic exposure to blockers of synaptic activity, which will not affect LTP in a similar manner.