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N Akaike

Publications and source records attributed to N Akaike.

At least 289 records · Page 16Linked to original sources
PubMed1989

Change of intracellular K+ activity in rat soleus muscle during hypokalemia.

The relationship between intracellular total K+ concentration [( K]i) as determined by a flame spectrophotometer and intracellular K+ activity (aKi) as determined by an ion-selective microelectrode was studied in soleus muscle of rats on a diet deficient in K+ for 40 days. [K]i began to fall immediately from the initial stage of hypokalemia, while aKi was well-maintained for 15 days. Then, aKi decreased gradually. The measured resting potential (Em) hyperpolarized beyond the EK was calculated from aKi in hypokalemic rat muscle from day 20 to 40. A rapid increase in aKi occurred over 3 hours in soleus muscle of hypokalemic rats for 5 to 6 weeks. It was concluded that the bound intracellular K+ acts as a buffer for aKi in hypokalemic rat muscle, that Em exceeds EK because the Na+-K+ pump is stimulated by increased [Na]i and that the increase in aKi after denervation is due to the removal of a Na+-K+ pump inhibitor normally released from nerve ending.

Aging↗
PubMed1989

Delayed activation of large-conductance Ca2+-activated K channels in hippocampal neurons of the rat.

We applied a fast concentration jump system to produce step changes in Ca2+ concentration [( Ca2+]i) on the cytoplasmic side of the inside-out membrane patch, excised from isolated rat hippocampal pyramidal neurons, and examined the time course of the activation phase of the large-conductance K channel (the BK channel; approximately 266 pS) after a step rise in [Ca2+]i. Diffusion of Ca2+ from the electrode tip to the cytoplasmic surface of the patch was estimated to be almost completed in 10 ms. After a step increase in [Ca2+]i from 0.04 to 3.2-1,000 microM, the activation of the K channel started after a clear latency of 280-18 ms and proceeded along a sigmoidal function. This was in sharp contrast with the rapid deactivation that began without delay and that was completed within 50 ms. The latency in activation was not accounted for by the binding of Ca2+ to EGTA in unstirred layers in the patch, since this binding was reported to be slow, taking up to seconds at physiological pH. Calmodulin (1 microM) did not affect the delay, the activation rate, or the steady-state current level. The calmodulin inhibitors W-7 and W-5 caused flickering of the single-channel current. These results indicate a delayed activation of the BK channel after a step rise in [Ca2+]i, suggesting that the BK current does not contribute to the repolarization of the action potential. Calmodulin is probably not involved in the activation process of the channel.

Animals↗
PubMed1989

What confers specificity on glycine for its receptor site?

1. The structural requirements for activation of the glycine receptor were studied in isolated ventromedial hypothalamic neurones of rats by use of a 'concentration-clamp' technique under single-electrode voltage-clamp conditions. 2. alpha-Amino acids (L-alpha-alanine, and D-alpha-alanine, and L-serine), and glycine-methylester, glycine-ethylester and beta-amino acids (beta-alanine and taurine) produced a transient inward Cl- current, which was similar to that induced by glycine. 3. The responses to individual alpha- and beta-amino acids were selectively antagonized by strychnine, but were not affected by bicuculline, picrotoxin or the taurine antagonist, TAG (6-aminomethyl-3-methyl-4H,1,2,4-benzothiadiazine-1,1-dioxide hydrochloride), suggesting that alpha- and beta-amino acids activate the same glycine receptor. 4. beta-Amino acids were slightly more potent than the alpha-amino acids in causing cross-desensitization of the glycine response. 5. From the results of the structure-activity analysis of the optical isomers of alpha-alanine, serine and cysteine, a tentative structure of the glycine receptor is proposed.

Amino Acids↗
PubMed1989

Effects of benzodiazepines and non-benzodiazepine compounds on the GABA-induced response in frog isolated sensory neurones.

1. The effects of benzodiazepines and non-benzodiazepine compounds on the gamma-aminobutyric acid (GABA)-induced chloride current (ICl) were studied in frog isolated sensory neurones by use of a concentration-jump (termed 'concentration-clamp') technique, under single-electrode voltage-clamp conditions. The drugs used were classified into four categories as follows: full benzodiazepine receptor agonists (diazepam, clonazepam, nitrazepam, midazolam, clotiazepam and etizolam), partial agonists (CL 218,872, Ro 16-6028, Ro 17-1812 and Ro 23-0364), inverse agonists (Ro 15-3505, FG 7142 and beta-CCE) and a benzodiazepine receptor antagonist, Ro 15-1788 (flumazenil). 2. All full agonists at concentrations of 3 x 10(-6) M or less increased dose-dependently the peak amplitude of ICl elicited by 3 x 10(-6) M GABA to twice to three times larger than the control. However, no further augmentation of the GABA response was observed at concentrations of 1 x 10(-5) M or higher. Partial agonists also showed a dose-dependent augmentation of the GABA response at concentrations ranging from 3 x 10(-8) M to 3 x 10(-5) M, but their efficacies of augmentation of the GABA response were only about half or less of those of full agonists. Of the inverse agonists, beta-CCE had a unique dose-dependent effect on the GABA response. Beta-CCE reduced dose-dependently the GABA response at concentrations of less than 3 x 10(-6) M, but augmented it at concentrations of 3 x 10(-5) M and 6 x 10(-5) M. The inverse agonists reduced dose-dependently the GABA response. The benzodiazepine antagonist, flumazenil, slightly augmented the GABA response at concentrations between 3 x 10 7M and 3 x 10 5 M. 3. These results show clear differences in the effects on the GABA response between these four categories of compounds known to affect the benzodiazepine recognition site of the GABA/ benzodiazepine receptor-chloride channel complex. Our experimental system of frog isolated sensory neurones and a 'concentration-clamp' technique appears to be useful for evaluating efficacy of compounds on responses mediated by the GABA/benzodiazepine receptor-chloride channel complex.

Animals↗
PubMed1989

Different time courses of the blockade of sodium current by lignocaine and SUN 1165 in single myocytes isolated from guinea-pig atrium.

1. The time course of the blockade of sodium currents (INa) by the antiarrhythmic agents, lignocaine and SUN 1165, was studied in single myocytes isolated enzymatically from guinea-pig atrium, by a new concentration-jump termed as a 'concentration-clamp' technique. This technique combines an intracellular perfusion and a rapid exchange of external solution surrounding the voltage-clamped myocyte within 2 ms. 2. Lignocaine (3.7 x 10(-5) M to 3.7 x 10(-4) M) inhibited the peak amplitude of INa in a concentration-dependent fashion. It took 2 to 5s to reach apparent steady-state inhibition at the concentrations used. Complete recovery from the inhibition also took 2 to 5s after washing out the agent. In contrast, the inhibitory effect of SUN 1165 (1 x 10(-5) M) on the peak INa gradually progressed and reached a steady-state level about 2 min after the start of drug-application. The recovery required more than 10 min after washing out of the agent. 3. In cardiomyocytes treated with scorpion toxin (5 micrograms ml-1), the inactivation of INa was greatly inhibited, resulting in the relatively persistent Na inward current (persistent INa) during the depolarizing pulse. Lignocaine (1.1 x 10(-4) M) applied during the depolarizing pulse, reduced in a single-exponential fashion the amplitude of the persistent INa in milliseconds. On the other hand, lignocaine applied several tens of milliseconds before the depolarizing pulse induced only a small reduction of the peak amplitude of the first persistent INa. When SUN 1165 (1 x 10- M) was applied during the depolarizing pulse, there was only a small instantaneous reduction of the amplitude of the persistent I'N, although it did inhibit time-dependently, the peak IN.. Both agents accelerated the decay phase of the persistent IN in a time-dependent manner. 4. These results suggest that lignocaine and SUN 1165 may preferentially interact with the openstate of the sodium channel rather than with the rested one, although SUN 1165 does so much more slowly.

Animals↗
PubMed1989

Dihydropyridine-sensitive low-threshold calcium channels in isolated rat hypothalamic neurones.

1. Low-voltage-activated Ca2+ channels which produce a transient inward current were studied in neurones freshly isolated from the ventromedial hypothalamic region of the rat. Membrane currents were recorded using a suction-pipette technique which allows for internal perfusion under a single-electrode voltage clamp. A concentration-jump technique was also used for rapid drug application. 2. In most cells superfused with 10 mM-Ca2+, a transient inward Ca2+ current was evoked by a step depolarization to potentials more positive than -65 mV from a holding potential of -100 mV. Such a low-threshold Ca2+ current could easily be separated from a high-threshold, steady type of Ca2+ current by selecting the holding and test potential levels, as well as by resistance to the wash-out during cell dialysis. 3. Activation and inactivation processes of the low-threshold Ca2+ current were highly potential dependent at 20-22 degrees C. For a test potential change from -60 to +20 mV, the time to peak of the current decreased from 45 to 9 ms, and the time constant of the current decay decreased from 90 to 40 ms. The steady-state inactivation occurred at very negative potentials, reaching a 50% level at -93 mV. Recovery from inactivation showed a time constant between 2.63 and 0.94 s for a potential change from -80 to -120 mV. 4. The amplitude of the low-threshold Ca2+ current depended on the external Ca2+ concentration [( Ca2+]o), approaching saturation at 100 mM [Ca2+]o. Ba2+ substituted for Ca2+ reduced the current amplitude by 30-50% while Sr2+ produced no definite changes in the current amplitude. 5. The low-threshold Ca2+ current was blocked by various di- or trivalent cations in the sequence of La3+ greater than Zn2+ greater than Cd2+ greater than Ni2+ greater than Co2+. The corresponding apparent dissociation constants (KD) were 7 x 10(-7), 1 x 10(-4), 3 x 10(-4), 6 x 10(-4) and 3 x 10(-3) M. 6. Various organic Ca2+ antagonists were effective in blocking the low-threshold Ca2+ current in the following sequence: flunarizine greater than nicardipine greater than nifedipine greater than nimodipine greater than D600 (methoxyverapamil) greater than diltiazem. The corresponding KDs were 7 x 10(-7), 3.5 x 10(-6), 5 x 10(-6), 7 x 10(-6), 5 x 10(-5) and 7 x 10(-5) M. These Ca2+ antagonists induced a use-dependent decrease in the current amplitude.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Caffeine affects four different ionic currents in the bull-frog sympathetic neurone.

1. Ionic mechanisms related to the caffeine-induced current (Icaffeine) were examined in the single isolated sympathetic neurones of the bull-frog. We used the 'concentration-jump' technique in combination with intracellular perfusion and a rapid external solution change, under single-electrode voltage-clamp conditions. 2. Icaffeine was pharmacologically separated into a tetraethylammonium (TEA)-sensitive transient outward current (ITO), a picrotoxin (PTX)-sensitive transient inward current (ITI) and a TEA- and PTX-insensitive sustained inward current (ISI). At low concentrations of caffeine, a sustained outward current (ISO) was observed instead of ISI. 3. All components of Icaffeine were abolished by intracellular perfusion of 30 mM-EGTA. Pre-treatment with A23187 or ryanodine or the simultaneous application of procaine either reduced or abolished all the components of Icaffeine in a dose-dependent manner. The concentration causing 50% inhibition (IC50) was 10(-8) M for A23187 and 2 mM for procaine. 4. The peak response of ITO increased abruptly at caffeine concentrations between 3 and 6 mM followed by saturation above 30 mM. A notch was observed on the rising phase of ITO. 5. The reversal potential (Ecaffeine) of ITO shifted 58 mV for a tenfold change of the extracellular K+ concentration. External application of TEA blocked ITO with an IC50 of 1 mM. ITO was relatively insensitive to apamin, 4-aminopyridine and muscarine. 6. In external solution containing 2 mM-Ca2+, ITO induced by 10 mM-caffeine recovered completely within 3 min from a previous exposure to caffeine. In the absence of extracellular Ca2+, there was little such recovery. A 5 min treatment in a Ca2+-free solution reduced ITO induced by the first application of caffeine by 5%. With a continuous application of 3 mM-caffeine, the amplitude of ITO induced by 10 mM-caffeine reduced in 1 min, and showed a partial recovery in 3 min. The amplitude of ITO increased by increasing the concentration of intracellular Cl-. 7. ITI was activated around the peak of ITO and was rapidly inactivated. ITI was evoked at caffeine concentrations of about 6-10 mM. When the intracellular Cl- concentration was changed, the amplitude of ITI behaved like a Cl- electrode. The Ecaffeine of ITI was close to the Cl- equilibrium potential (ECl). 8. ISI was a 'plateau' response and persisted for over 3 min. ISI was due to a decrease in K+ conductance. In the presence of muscarine (3 x 10(-5) M), ISI was occluded.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Low-voltage-activated calcium current in rat aorta smooth muscle cells in primary culture.

1. Electrical and pharmacological properties of the low-voltage-activated Ca2+ current (ICa, LVA) in rat aorta smooth muscle cells (SMC) in primary culture were examined, particularly in comparison with the high-voltage-activated Ca2+ current (ICa, HVA). Both types of Ca2+ currents were recorded in external solution containing 20 mM-Ca2+, using the whole-cell voltage-clamp technique. 2. ICa, LVA was evoked by step depolarizations to potentials more positive than -60 mV from a holding potential of -100 mV, and reached a peak in the current-voltage (I-V) relationship around -30 mV. ICa, HVA was activated at -20 mV, and reached a peak at +20 mV. 3. The intracellular dialysis of 5 mM-F- irreversibly suppressed ICa, HVA, with time, while it has little effect on the ICa, LVA. The ICa, LVA could be separated from the ICa, HVA by either selecting the holding and test potential levels or by perfusing intracellularly with F-. 4. The ratio of peak amplitude of Ba2+, Sr2+ and Ca2+ currents in the respective I-V relationship was 1.6:1.2:1.0 for high-voltage-activated Ca2+ channels and was 1.0:1.4:1.0 for low-voltage-activated ones. 5. The inactivation phase of ICa, HVA was fitted by a sum of double-exponential functions, the time constants of which were larger when the current was carried by Ba2+ than by Ca2+. The inactivation time course of ICa, LVA was fitted by a single-exponential function, and the time constant was practically the same when the current was carried by Ba2+ or by Ca2+. Activation and inactivation processes of ICa, LVA were potential-dependent. 6. The steady-state inactivation curve of ICa, LVA was fitted by the Boltzmann equation, having a mid-potential of -80 mV and a slope factor of 5.0. The recovery time course from steady-state inactivation was fitted by a sum of two exponential functions. The time constants of the faster phase were 230 and 380 ms, and those of slower phase were 2.8 and 1.8 s at the repolarization potentials of -120 and -100 mV, respectively. 7. The amplitude of ICa, LVA depended on the external Ca2+ concentration ([Ca2+]o), approaching saturation at 95 mM [Ca2+]o. 8. Various polyvalent cations blocked both types of Ca2+ current reversibly in the order (IC50 in M): La3+ (8 x 10(-8)) greater than Cd2+ (6 x 10(-6)) greater than Ni2+ (1 x 10(-5)) greater than Zn2+ (2 x 10(-5)) for ICa, HVA, and La3+ (6 x 10(-7)) greater than Zn2+ (3 x 10(-5)) greater than Cd2+ (4 x 10(-4)) greater than Ni2+ (6 x 10(-4)) for ICa, LVA.(ABSTRACT TRUNCATED AT 400 WORDS)

4-Aminopyridine↗
PubMed1989

GABA-induced chloride current in rat isolated Purkinje cells.

Electrical and pharmacological properties of the gamma-aminobutyric acid (GABA)-induced current in the rat isolated cerebellar Purkinje cell bodies were studied using a concentration-jump method, which is termed as a "concentration-clamp" technique. This technique enables the rapid exchange of external solution around the neurons to be perfused internally under a voltage-clamp condition. The peak amplitude of GABA response increased sigmoidally with the increase of the concentration of GABA. The value of the GABA concentration that evokes a half-maximal response (Ka) was 5 X 10(-5) M, and the Hill coefficient was 1.8. The current-voltage relationship for the GABA response showed nonlinearity at membrane potentials more negative than -40 mV. The reversal potential of GABA-evoked current was close to the equilibrium potential of Cl- (ECl), indicating that the current elicited by GABA is carried by Cl-. Both the activation and inactivation phases of GABA-induced Cl- current (ICl) consisted of fast and slow components. These time constants in both phases decreased as the concentration of GABA increased. Strychnine and bicuculline inhibited the GABA-induced ICl in a dose-dependent manner, and the inhibition of the GABA response by bicuculline was competitive. Pentobarbital sodium augmented the GABA response and modified the inactivation phase. The augmentation of the GABA response by pentobarbital was more profound at lower concentrations of GABA and was accompanied by a change in the Hill coefficient from 2 to 1. The properties of the GABA response in cerebellar Purkinje cells were thought to be basically similar to those previously reported in other preparations.

Animals↗
PubMed1989

Activation kinetics of the acetylcholine-gated potassium current in isolated atrial cells.

Processes involved in activation of the acetylcholine (ACh) receptor-operated K+ current (IK) were examined in atrial cells isolated from guinea pig using a "concentration-clamp" technique. This approach allows for the intracellular perfusion and the rapid change of external solution (time constant 4 ms) with cell-attached condition under a single-electrode voltage-clamp condition. The ACh-induced IK increased in a sigmoidal fashion with increasing concentrations of ACh. The Ka value estimated from the concentration-response curve was 3 X 10(-7) M, and the Hill coefficient was 1.0. The activation phase was accelerated not only by increasing the concentration of ACh but also by elevating the temperature. Before activation of the current, there was a brief latent period after the application of ACh. The latent period was shortened considerably with the increase in ACh concentration and in temperature, i.e., 267 +/- 20 ms at 18 degrees C, 98 +/- 11 ms at 26 degrees C, and 44 +/- 6 ms at 37 degrees C for 10(-6) M ACh. These results suggest that the latent period of ACh response seems to be the time lag needed for the activation of K+ channels using remote sensor.

Acetylcholine↗
PubMed1989

Kinetic analysis of acetylcholine-induced current in isolated frog sympathetic ganglion cells.

1. Kinetic properties of activation and inactivation phases of the ACh-gated nicotinic current were investigated in isolated frog sympathetic ganglion cells using "concentration-clamp" technique under voltage-clamp conditions. This technique combines internal perfusion with a rapid change of the external solution within a few milliseconds. 2. The dose-response curve for the peak current induced by ACh showed a sigmoidal increase, in which the apparent dissociation constant Kd and Hill coefficient were 2.6 x 10(-5) M and 2.0, respectively. 3. The current-voltage relationship of ACh-induced currents were linear at potentials more negative than the reversal potential (EACh) of -5.5 +/- 1.3 mV (mean +/- SE) but showed a slight inward rectification at positive potentials over +20 mV. Since this current could be generated predominantly by an increase of Na+ and K+ conductances, the value of EACh was close to the theoretical potential, -1.3 mV, for the total amount of both Na+ and K+ or Cs+ in the extracellular and intracellular solutions. 4. There was no difference between the dose-response curves of ACh- and nicotine-induced currents. The ACh-induced current was suppressed in a competitive manner by the nicotinic antagonists, d-tubocurarine and hexamethonium, but muscarine did not induce any response, indicating that the ACh-gated current might be mediated by the nicotinic ACh receptor-ionophore complex. 5. There was a latent period of the order of milliseconds in the ACh receptor activation phase before attaining exponential increase of activation process.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1989

Differential effects of extra- and intracellular anions on GABA-activated currents in bullfrog sensory neurons.

1. Kinetic properties of gamma-aminobutyric acid (GABA)-gated inward and outward anion currents were investigated in the frog sensory neurons perfused internally and externally with various anions with the use of a rapid concentration-jump (termed as 'concentration-clamp') technique. 2. Extracellular Br- [( Br-]o) shifted the dose-response curves of GABA-induced inward anion currents to the left without affecting the maximum values, whereas [Cl-]o, [I-]o, [No3-]o, [HCOO-]o, and [CH3COO-]o altered the rate of desensitization differently without shifting the GABA dose-response curves, indicating that the kinetics of desensitization phase are affected differently by various extracellular anions. 3. [CH3COO-]o suppressed the maximum current of the dose-response curve of the GABA-induced inward ICl without affecting Kd. 4. Both activation and desensitization phases of GABA-induced ICl consisted of fast and slow components, respectively. [Br-]o, [I-]o, and [NO3-]o significantly prolonged the slow desensitization component, whereas both [HCOO-]o and [CH3COO-]o shortened it. The fast desensitization and the fast and slow activation components were also affected by these foreign anions. 5. GABA dose-response curves of inward currents carried by various intracellular anions (Cl-, Br-, NO3-, I-, SCN-, HCOO-, F-, CH3COO-, CH3CH2COO-, BrO3-, and ClO3-) while keeping a constant [Cl-]o had a constant Kd value but different saturating maximum currents. There were no marked differences among their current kinetics except in the case of SCN-, indicating that the current kinetics is not affected by replacing intracellular Cl- [( Cl-]i) with various foreign anions. 6. The configuration and amplitude of GABA-gated outward anion currents at a constant [Cl-]i reflected the extracellular action of individual anions on the anion-binding site of GABA receptor associated with the anion-selective channel. 7. The relative conductances of the various anions, calculated from the maximum peak currents in dose-response curves of the GABA-induced inward anion currents at a constant [Cl-]o, was in the sequence: I- greater than Br- greater than or equal to NO3- greater than ClO3- greater than SCN- greater than or equal to Cl- greater than HCOO- greater than BrO3- greater than CH3COO- greater than F- greater than CH3CH2COO-.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Glycine-gated chloride current in acutely isolated rat hypothalamic neurons.

1. Electrical and pharmacologic properties of glycine-induced currents were investigated in single hypothalamic neurons acutely isolated from young and adult rats by the use of a "concentration-clamp" technique, which allows both internal perfusion and rapid application of an external solution under single-electrode voltage-clamp. 2. The glycine-induced current reversed at the Cl- equilibrium potential (ECl), and a 10-fold decrease of extracellular Cl- with a large impermeable anion resulted in a 53 mV shift of the glycine reversal potential (EGly). 3. Glycine-induced Cl- currents (ICl) increased sigmoidally in a concentration-dependent manner with a Kd of 9 X 10(-5) M at a Hill coefficient of 1.8. Current inactivation occurred completely at all concentrations within 10 s. EGly remained unchanged during continuous application of glycine, suggesting that the inactivation process is because of desensitization. 4. The glycine-induced conductance exhibited a striking voltage dependency at membrane potentials more negative than -50 mV and reached a steady state value when hyperpolarized beyond -110 mV. 5. Both the activation and inactivation phases of glycine-induced ICl are described by double exponential (fast and slow components) functions with the concentrations used. All four time constants decreased with increasing glycine concentration. 6. The slow time constant of the current decay induced by glycine increased with depolarization and decreased with hyperpolarization, indicating that the rate of desensitization is considerably voltage dependent. The fast decay showed little voltage dependency. 7. Recovery of the glycine response after complete desensitization consisted of two components. 8. The blockade of the glycine response by strychnine and picrotoxin was noncompetitive.

Animals↗
PubMed1989

[Blocking action of Nephila clavata spider toxin on ionic currents activated by glutamate and its agonists in isolated hippocampal neurons].

The blocking action of the Nephila clavata spider neurotoxin was studied using the concentration clamp method in isolated neurons of the rat hippocampus. Crude venom JSTX blocked L-glutamate-, quisqualate- and kainate-activated ionic currents mediated by activation of the non-N-methyl-D-aspartate (non-NMDA) membrane receptors. Ionic currents elicited by all agonists were depressed by crude JSTX venom to 34-35% of its initial amplitude with no recovery during prolonged washing. An active fraction of JSTX venom blocked ionic currents almost completely, but its action was partially reversible. The concentration dependences of blocking kinetics allowed determining the rate constants of JSTX interaction with glutamate receptors. It is supposed that JSTX blocks the non-NMDA ionic channels in some of their open states and may be one of useful tools in further biochemical and electrophysiological characterization of the glutamate-mediated synaptic transmission.

Animals↗
PubMed1988

Kinetic analysis of glutamate-induced chloride current in Aplysia neurones: a 'concentration clamp' study.

L-Glutamate (Glu) applied by the 'concentration clamp' technique to isolated neurones of Aplysia induced a chloride current (ICl) by activating a single population of the channel. The concentration-response curve for the peak ICl gave a dissociation constant of 1.3 x 10(-4) M and a Hill coefficient of 1.8. The current-voltage relationship was linear in the voltage range examined (-60 to +10 mV). The activation phase of the ICl followed a single-exponential time course and desensitization was complete with a double-exponential time course. The time constants for activation and desensitization decreased with increasing concentrations of Glu but were voltage-independent. The process of recovery from desensitization was also double-exponential. The single-channel conductance estimated by ensemble noise analysis was 50 +/- 4.7 pS (n = 4). These results suggest that the Glu receptor-Cl channel complex in Aplysia neurones consists of a single population with two binding sites for the agonist.

Animals↗
PubMed1988

The glutamate-induced chloride current in Aplysia neurones lacks pharmacological properties seen for excitatory responses to glutamate.

The pharmacological properties of the L-glutamate (Glu)-induced chloride current (ICl) in enzymatically isolated Aplysia neurones were examined using the 'concentration clamp' technique. The Glu-ICl did not cross-desensitize with the ICl evoked by gamma-aminobutyric acid or acetylcholine. Quisqualate, kainate (one out of eight) and N-methyl-D-aspartate (one out of nine) induced a small, non-desensitizing ICl in Glu-responding neurones. The quisqualate- and kainate-ICl did not cross-desensitize with the Glu-ICl. L-Aspartate did not induce a ICl in 11 neurones tested, which showed a Glu-ICl. Glutamate diethyl ester, Joro Spider toxin and ketamine did not suppress the Glu-ICl. Concanavalin A had no effect on the time course of desensitization. These results suggest that the Glu receptor-Cl channel complex in Aplysia neurones has pharmacological properties which differ from those of the excitatory Glu receptor-channel complexes in the crustacean muscle fibres and in the central neurones of vertebrates.

Acetylcholine↗