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J G Borst

Publications and source records attributed to J G Borst.

11 recordsLinked to original sources
PubMed1996

Calcium influx and transmitter release in a fast CNS synapse.

Calcium entry through presynaptic calcium channels controls the release of neurotransmitter. It is not known whether the putative calcium sensor that triggers this rapid neurotransmitter release is close enough to be activated by the large increase in the Ca2+ concentration (calcium 'domain') reached within nanometres of a single calcium channel or whether many channels have to open. We tested this in a calyx-type synapse in the rat medial nucleus of the trapezoid body. We compared the quantal content of postsynaptic currents with the presynaptic calcium current that flows during an action potential, and the results suggest that more than 60 calcium channels open for each vesicle that is released. In addition, we dialysed terminals with the slow calcium buffer EGTA, which reduced phasic transmitter release at concentrations as low as 1 mM. These results indicate that the distance that calcium ions must diffuse to reach the calcium sensor is relatively long, and that therefore Ca2+ entry through multiple calcium channels is needed to release a vesicle.

Action Potentials↗
PubMed1996

In situ recordings of presumed folliculo-stellate cells in the intermediate lobe of the pituitary gland of Xenopus laevis.

In situ whole cell voltage clamp recordings of presumed folliculo-stellate cells were made in the intermediate lobe of the clawed toad Xenopus laevis. Lucifer Yellow fillings revealed, in addition to the small, spherical melanotropes, a population of larger cells with many processes that were, to a limited extent, dye-coupled and are assumed to be folliculo-stellate cells. The presumed folliculo-stellate cells differed strongly from the melanotropes in electrophysiological properties. The cells had a membrane resistance of < 600 M omega (at -100 to -80 mV) and a membrane potential of ca. -90 mV, close to the equilibrium potential for K+. At potentials of > or = -20 mV, most of the cells displayed a rapidly activating and slowly inactivating outward K+ current. In all cells, hyperpolarizing pulses to < or = -100 mV activated an inward rectifying K+ current.

Animals↗
PubMed1996

Relation between rise times and amplitudes of GABAergic postsynaptic currents.

1. We recorded rise times and amplitudes of spontaneous GABAergic inhibitory postsynaptic currents (IPSCs) in melanotropes of Xenopus laevis. Average rise times did not vary with amplitude, but the rise times of larger IPSCs were less variable. A simple linear one-step Markov model for channel opening following the binding of a transmitter molecule can quantitatively account for the average rise time and its coefficient of variation as a function of amplitude. Our results indicate that the observed variations in the rise times are not due to variations in transmitter concentrations, but result from stochastic variations in the opening of the receptor channels.

Animals↗
PubMed1995

Pre- and postsynaptic whole-cell recordings in the medial nucleus of the trapezoid body of the rat.

1. Simultaneous whole-cell recordings in a rat brain slice preparation are described from presynaptic terminals (calyces of Held) and postsynaptic somata which form an axosomatic synapse in the medial nucleus of the trapezoid body (MNTB). 2. Presynaptic action potentials evoked suprathreshold excitatory postsynaptic potentials (EPSPs). The minimum synaptic delay was around 0.4 ms at 36 degrees C and 0.9 ms at 23-24 degrees C. The amplitude of the L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor-mediated component of the excitatory postsynaptic currents (EPSCs) was 2-13 nA (at -80 mV). 3. Current-voltage relations showed that presynaptic Ca2+ channels were of the high voltage-activated type. 4. A single action potential evoked a presynaptic fluorescence transient that decayed with a time constant of 0.3-0.7 s, depending on the concentration (60-200 microM) of the Ca2+ indicator Calcium Green-5N (CG-5N). The peak amplitude of the [Ca2+]i transient was severalfold larger in the terminal than in the preterminal axon. 5. EPSC peak amplitudes were stable for more than 30 min after establishing the whole-cell configuration in the presynaptic terminal when the pipette contained 50 microM BAPTA. In contrast, with 1 mM BAPTA, peak amplitudes of EPSCs were reduced to one-third. 6. Trains of presynaptic action potentials evoked EPSCs with progressively smaller amplitudes. Little change was observed in the depression when the terminals were dialysed with 50 microM BAPTA, whereas depression was reduced with 1 mM BAPTA. 7. In low (1 mM) [Ca2+]o, facilitation instead of depression of EPSCs was observed. 8. The effects of presynaptic BAPTA suggest that the endogenous mobile Ca2+ buffer capacity of giant presynaptic terminals in the MNTB is lower than in other terminals of fast transmitting synapses.

Action Potentials↗
PubMed1994

Variance analysis of gamma-aminobutyric acid (GABA)-ergic inhibitory postsynaptic currents from melanotropes of Xenopus laevis.

We have studied the variance in the decay of large spontaneous gamma-aminobutyric acid (GABA)-ergic inhibitory postsynaptic currents (IPSCs) in melanotropes of Xenopus laevis to obtain information about the number of GABAA receptor channels that bind GABA during the IPSCs. The average decay of the IPSCs is well described by the sum of two exponential functions. This suggests that a three-state Markov model is sufficient to describe the decay phase, with one of the three states being an absorbing state, entered when GABA dissociates from the GABAA receptor. We have compared the variance in the decay of large spontaneous IPSCs with the variance calculated for two different three-state models: a model with one open state, one closed state, and one absorbing state (I), and a model with two open states and one absorbing state (II). The data were better described by the more efficient model II. This suggests that the efficacy of GABA at synaptic GABAA receptor channels is high and that only a small number of channels are involved in generating the GABA-ergic IPSCs.

Analysis of Variance↗
PubMed1994

Large amplitude variability of GABAergic IPSCs in melanotropes from Xenopus laevis: evidence that quantal size differs between synapses.

1. We made in situ whole-cell recordings from melanotropes in the intermediate lobe of the pituitary gland of Xenopus laevis. Melanotropes received spontaneous synaptic inputs that had a fast rise time and a much slower decay. These inputs were GABAergic inhibitory postsynaptic currents (IPSCs): they followed the reversal potential for chloride ions and they were blocked by the gamma-aminobutyric acid-A (GABAA) receptor antagonist bicuculline. 2. Because of the very low baseline noise it was possible to see discrete levels in the tails of IPSCs that corresponded to the opening of one or more synaptic GABAA receptor channels. "All-points" histograms of the IPSCs showed that the chord conductance of the channels in the tails of the IPSCs was 21.6 +/- 0.6 pS (mean +/- SE, n = 6). 3. The amplitudes of the spontaneous IPSCs were very variable, ranging from 3 to 390 pA at a holding potential of -80 mV. The average of the median amplitudes was -67.5 +/- 5.9 pA (n = 28). The amplitude distributions of the IPSCs were well described by the sum of two lognormal distributions with large SDs. The average of the means of the first lognormal distribution was 27.8 +/- 5.3 pA (n = 10); the average of the SDs was 24.7 +/- 8.1 pA. For the second lognormal distribution these values were 87.0 +/- 13.4 and 33.7 +/- 7.4 pA. An average of 41.8 +/- 6.9% of the IPSCs originated from the first lognormal distribution. 4. The large variability in the amplitudes of spontaneous IPSCs was not the result of presynaptic action potentials because it was not reduced by tetrodotoxin (TTX), Ca(2+)-free extracellular solution, or the combined application of TTX and Mn2+. 5. The time course of the IPSCs from the first and the second lognormal distributions were very similar: averages of the median 20- to 80% rise times were 585 +/- 64 and 488 +/- 28 microseconds, respectively (n = 8), whereas the decays were well described by the sum of two exponential functions, with fast time constants of 8.9 +/- 1.1 (n = 7) and 9.3 +/- 3.3 ms and slow time constants of 29.5 +/- 3.3 and 31.7 +/- 2.6 ms, respectively. 6. The decay of the IPSCs was voltage dependent; it was approximately 3 times slower at a holding potential of +40 mV than at -80 mV (n = 5).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1987

Electrical activity of the cingulate cortex. I. Generating mechanisms and relations to behavior.

Spontaneous slow waves (EEG) and multiple unit activity (MUA) were recorded in the posterior cingulate cortex (area 29) and the dorsal hippocampus of the freely moving rat by means of chronically implanted electrodes. Three different wave patterns were discerned in the cingulate EEG. Irregular slow waves occurred during grooming, drinking, eating (Type II behavior) and slow-wave sleep (SWS). The irregular waves also contained sharp transients of about 20 ms duration called EEG-spikes. EEG-spikes reversed their polarity within the cingulate cortex and correlated with an increase in cingulate MUA. They were probably generated by deep (layer IV to VI) neurons in the cingulate cortex. Theta rhythm of 6-10 Hz accompanied walking, rearing, postural shifts, head movements (Type I behavior) and rapid-eye-movement sleep (REMS). MUA of low-amplitude units was phase-locked to the local theta waves, suggesting local generation of the slow waves. However, volume-conduction from the hippocampus would likely contribute to the cingulate theta since no reversal of the theta waves was found in the cingulate cortex. Fast waves of greater than 30 Hz were generally larger during Type I than during Type II behavior. Cellular generators for fast waves are not known. High-amplitude (greater than 100 microV) MUA only appeared during Type II behavior, and in particular during SWS. During REMS, these units were silent. Stimulation of the contralateral homotopic cingulate cortex gave antidromic and synaptic components in the average evoked potential (AEP). The long latency waves of the AEP varied with behaviors and appeared oscillatory (25-40 Hz) during Type I but not during Type II behavior. In summary, the cingulate cortex has a rich gamut of spontaneous and evoked electrical activities which bears some resemblance to that of the hippocampus.

Animals↗
PubMed1987

Electrical activity of the cingulate cortex. II. Cholinergic modulation.

The role of the cholinergic innervation in the modulation of cingulate electrical activity was studied by means of pharmacological manipulations and brain lesions. In the normal rat, an irregular slow activity (ISA) accompanied with EEG-spikes was recorded in the cingulate cortex during immobility as compared to walking. Atropine sulfate, but not atropine methyl nitrate, increased ISA and the frequency of cingulate EEG-spikes. Pilocarpine suppressed ISA and EEG-spikes during immobility, and induced a slow (4-7 Hz) theta rhythm. Unilateral or bilateral lesions of the substantia innominata and ventral globus pallidus area using kainic acid did not significantly change the cingulate EEG or its relation to behavior. Large electrolytic lesions of the medial septal nuclei and vertical limbs of the diagonal band generally decreased or abolished all theta activity in the cingulate cortex and the hippocampus. However, in 5 rats the cingulate theta rhythm increased while the hippocampal theta disappeared after a medial septal lesion. The large, postlesion cingulate theta, accompanied by sharp EEG-spikes during its negative phase, is an unequivocal demonstration of the existence of a theta rhythm in the cingulate cortex, independent of the hippocampal rhythm. Cholinergic afferents from the medial septum and diagonal band nuclei are inferred to be responsible for the behavioral suppression of cingulate EEG-spikes and ISA, and partially for the generation of a local cingulate theta rhythm. However, an atropine-resistant pathway and a theta-suppressing pathway, possibly coming from the medial septum or the hippocampus, may also be important in cingulate theta generation.

Acetylcholinesterase↗
PubMed1986

Differentiation antigens on rhesus monkey lymphocytes. I. Identification of T cells bearing CD3 and CD8, and of a subset of CD8-bearing cells.

Rhesus monkeys provide an excellent preclinical model to test the effect of monoclonal antibodies (mAb) in vitro and in vivo. So far, mostly mAb have been used which were originally raised against human cell surface antigens but cross-reacted reasonably well with homologous antigens on rhesus monkey cells. However, to optimize the model, it was necessary to produce mAb which react specifically with subsets of rhesus monkey lymphocytes. In this report, three mouse anti-rhesus monkey mAb are described, specific for different subsets of rhesus monkey T lymphocytes. None of the reagents cross-reacts with human lymphocytes. Characterization of these mAb was based upon indirect immunofluorescence, using a simultaneous staining technique, and immunoprecipitation of the specific target antigens. One antibody (GM9) reacts with the same subset as is recognized by mAb specific for human CD8+ cells. The second mAb (GM13) is specific for a subset of CD8+ cells. A third mAb (FN18) was of particular interest: it identifies a cell surface complex, RhT3, expressed on mature T lymphocytes, of which the polypeptide chains have a molecular mass of 22 and 27 kDa. The data strongly suggest that RhT3 is a CD3-like determinant, so far unidentified in the rhesus monkey.

Animals↗
PubMed1975

Paradoxical diuresis after vasopressin administration to patients with neurohypophyseal diabetes insipidus treated with chlorpropamide, carbamazepine or clofibrate.

1. Chlorpropamide, carbamazepine and clofibrate have an antidiuretic action in patients with neurohypophyseal diabetes insipidus which is qualitatively similar to that of antidiuretic hormone (ADH). 2. An additive antidiuretic effect is produced by combination of chlorpropamide and carbamazepine with small dosages of ADH. 3. After an immediate and transient antidiuresis, a single intravenous bolus injection of lysine vasopressin given during treatment with chlorpropamide, chlorpropamide with a continuous intravenous infusion of lysine vasopressin, carbamazepine or clofibrate, resulted in increased water diuresis for 12-24 h or longer. 4. This paradoxical diuresis was not observed during treatment with chlorothiazide. 5. It is suggested that the antidiuretic action of chlorpropamide, carbamazepine and clofibrate is localized at the receptor site for ADH in the distal renal tubular cell.

Adolescent↗