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J Kapur

Publications and source records attributed to J Kapur.

At least 37 records · Page 2Linked to original sources
PubMed1996

Pharmacological properties of gamma-aminobutyric acidA receptors from acutely dissociated rat dentate granule cells.

The pharmacological properties of gamma-aminobutyric acid (GABA) type A receptor (GABAR) currents recorded from hippocampal dentate granule cells acutely dissociated from 28-35-day-old rats were characterized using the whole-cell patch-clamp technique. Granule cells were voltage-clamped to 0 mV, and GABA was applied using a modified U-tube rapid-application technique. All granule cells were moderately sensitive to GABA (EC50 = 47 microM). All granule cell GABAR currents were uniformly sensitive to Zn2+ (IC50 = 29 microM), diazepam (EC50 = 158 nM), zolpidem (EC50 = 75 nM), and dimethoxyl-4-ethyl-beta-carboline-3-carboxylate (IC50 = 60 nM). GABAR currents from only 50% of granule cells were sensitive to loreclezole (EC50 = 9 microM). These data suggest that hippocampal dentate granule cells expressed GABARs with distinctive pharmacological properties of two types: loreclezole-sensitive and -insensitive receptors. It is likely that these distinctive properties were due to the specific GABAR subtypes that assembled to produce distinct granule cell GABAR isoforms.

Allosteric Regulation↗
PubMed1995

Experimental status epilepticus alters gamma-aminobutyric acid type A receptor function in CA1 pyramidal neurons.

There is a reduction of gamma-aminobutyric acid (GABA)-mediated inhibition of the CA1 pyramidal region of the hippocampus during status epilepticus (SE). The cellular basis of this loss of GABA-mediated inhibition is not known. This study tested the possibility that GABA type A (GABAA) receptor function in CA1 pyramidal neurons was reduced or blocked during SE, at least in part by postsynaptic cellular mechanisms. GABAA receptor currents (IGABA) were studied by whole-cell patch-clamp techniques in CA1 pyramidal neurons acutely dissociated from rats undergoing lithium/pilocarpine-induced limbic status epilepticus (SE neurons) and from naive rats (naive neurons). SE neurons had more depolarized resting membrane potential (-17.3 mV) compared with naive neurons (-56 mV). IGABA was absent in 47% of SE neurons and reduced in 55% of the remainder, compared with naive neurons. The reduction in IGABA in SE neurons resulted from a combination of factors, including reduced potency and reduced efficacy of GABA in activating chloride channels, and diminished driving force for the GABA-induced chloride currents once activated. These postsynaptic cellular mechanisms resulted in a net reduction or loss in GABA-mediated inhibition and may explain previous in vivo findings reporting a loss of inhibition in hippocampus during limbic SE.

Animals↗
PubMed1995

Psychogenic elaboration of simple partial seizures.

Seizures that cause loss of consciousness (LOC) can be classified as epileptic or nonepileptic based on evaluation of ictal semiology and analysis of changes in EEG events, recorded with continuous scalp EEG and video monitoring. We report 3 patients who had hippocampal electrographic seizures documented with intracranial EEG recording with no accompanying scalp EEG change immediately preceding psychogenic unresponsiveness. Each patient also had complex partial seizures (CPS) originating in the hippocampus. Some individuals can have complex interactions of epileptic and nonepileptic seizures.

Adult↗
PubMed1991

Secretion and excretion of endogenously synthesized lipids by adult Haemonchus contortus in vitro.

Results of the incorporation of carbon from 14C-glycerol into total, polar and nonpolar lipids in Haemonchus contortus (Nematoda: Trichostrongylidae) reveal that the radioactivity lost into the medium as lipids decreased during the first 3 h of incubation. This was followed by a drastic increase during the 4th h. Again, there was a decline by 75% during the 5th h. However, there was a slight increase in the nonpolar lipids during the 5th h.

Animals↗
PubMed1990

NMDA receptor activation mediates the loss of GABAergic inhibition induced by recurrent seizures.

Previously we have shown that delivery of rapidly recurring hippocampal seizures (RRHS) to awake rats causes a rapid kindling and that RRHS in urethane-anesthetized rats leads to a progressive lengthening of afterdischarges and diminution of paired pulse inhibition. The present experiments examined the relationship between the changes in afterdischarge durations and inhibition. Pre-treatment before RRHS with the non-competitive NMDA receptor antagonists MK-801 and ketamine blocked afterdischarge lengthening. MK-801 also prevented RRHS-induced changes in paired pulse inhibition. For pharmacodynamic and pharmacokinetic reasons the ability of ketamine to counteract RRHS-induced changes of paired pulse inhibition was not examined. MK-801 also blocked the rightward shift of stimulus intensity vs. population spike curves which RRHS caused. We suggest that RRHS leads to an enduring diminution of GABAergic inhibition and that this accounts, at least in part, for the lengthening of afterdischarges seen with recurrent hippocampal seizures. In addition, NMDA receptor activation appears to play a role in this decrease of the potency of GABAergic inhibition. However, mechanisms which are not dependent on NMDA receptor activation also play a critical role in hippocampal epileptogenesis.

Animals↗
PubMed1990

Recurrent spontaneous hippocampal seizures in the rat as a chronic sequela to limbic status epilepticus.

A period of continuous hippocampal stimulation (CHS) establishes an acute condition of self-sustaining limbic status epilepticus (SSLSE) which is followed by chronic neuropathological changes reminiscent of hippocampal sclerosis encountered in epileptic patients. In the chronic (greater than or equal to 1 month) condition following CHS-induced SSLSE, extended electrographic monitoring in the hippocampus revealed spontaneous recurrent paroxysmal discharges. All 6 animals studied had persistent interictal spiking; 3 had multiple fully developed electrographic seizures. There was a marked diminution of paired pulse inhibition, demonstrated by a protocol known to reflect the potency of inhibition mediated by GABAA receptors. Hippocampal slices from animals that had previously experienced CHS-induced SSLSE demonstrated an increased excitability relative to slices from control animals as evidenced by epileptiform bursting in increased extracellular potassium ([K+]0) and decreased extracellular calcium ([Ca2+]0). These studies establish that CHS-induced SSLSE in rats provides an experimental model with recurrent spontaneous hippocampal seizures. Based on electrophysiological data we suggest that a decrease in GABA-mediated inhibition and/or altered sensitivity to extracellular ions may play roles in the development of such seizures.

Action Potentials↗
PubMed1989

Reduction of paired pulse inhibition in the CA1 region of the hippocampus by pilocarpine in naive and in amygdala-kindled rats.

Subconvulsant doses (20 mg/kg) of pilocarpine administered to a kindled rat convert a kindled seizure to status epilepticus. The hippocampus is involved in such status epilepticus. Furthermore, evidence is accumulating that GABA-mediated inhibition in the hippocampus is chronically diminished by kindling. The studies presented here compared the electrophysiologic effects of pilocarpine in vivo in the CA1 region of the hippocampus in naive and amygdala-kindled rats. A paired pulse paradigm previously shown to quantify the potency of GABAergic inhibition was employed. Stimuli were delivered in the CA3 region of urethane-anesthetized rats and population spikes were recorded in the contralateral CA1 region. In naive rats, pilocarpine (6-60 mg/kg) caused a left shift in the input-output curve measuring stimulus intensity vs population spike amplitudes, indicating an increase in neuronal excitability. In addition, paired pulse inhibition was reduced for interpulse intervals less than 70 ms. In amygdala-kindled rats, neuronal excitability was also enhanced following pilocarpine administration. The potency of baseline paired pulse inhibition was decreased in kindled rats compared to naive controls. Following pilocarpine, inhibition for interpulse intervals less than 70 ms was further reduced, but to a lesser extent than in naive rats. These findings suggest that the ability of subconvulsive doses of pilocarpine to change a discrete kindled seizure triggered by one stimulus to status epilepticus depends on the suppression of GABAergic inhibition below a critical level.

Amygdala↗
PubMed1989

Evidence that repetitive seizures in the hippocampus cause a lasting reduction of GABAergic inhibition.

1. A method was developed to quantify paired-pulse depression of population spikes in the CA1 region of the hippocampus of urethane-anesthetized rats with paired stimuli to the contralateral CA3 region at various states of excitability of pyramidal cells. This method was applied to measure changes following recurrent seizures, a single seizure, or long-term potentiation (LTP). 2. In naive animals paired-pulse depression was highly variable at low stimulus intensities, but constant above a certain "threshold" stimulus intensity. The potency of paired-pulse depression also depended on the time between paired stimuli, being maximal at an interpulse interval of 20 ms. The general relationships of paired-pulse depression to stimulus intensity and to interpulse interval were unaltered after LTP, after a single seizure, and after recurrent seizures, but there were quantitative changes in the last two cases. 3. A variety of pharmacologic agents known to interact with GABAergic inhibition were studied for their effect on paired-pulse depression. These agents affected earlier phases of paired-pulse depression (interpulse intervals less than or equal to 100 ms). The GABA agonist muscimol and the benzodiazepine diazepam enhanced paired-pulse depression whereas the GABA antagonist bicuculline decreased it. 4. Repeated seizures elicited by trains (50-Hz, 10-s durations every 5 min) of electrical stimuli to the hippocampus were associated with progressive lengthening of afterdischarges. 5. Recurrent seizures caused a statistically significant reduction in the potency of earlier phases of paired-pulse depression. There was an increase in the potency of later phases of paired-pulse depression after recurrent seizures, but this was not statistically significant. These changes were present for at least 2 h after the last seizure. 6. An antidromic-orthdromic paired-pulse protocol was used to exclude slow conductance changes as the cause of paired-pulse depression. Paired-pulse depression measured with this method was also decreased by recurrent seizures. 7. A single seizure caused a small reduction in paired-pulse depression that dissipated in less than an hour. 8. A single seizure caused LTP of stimulus intensity versus population spike curves whereas recurrent seizures attenuated or even reversed the potentiation, leading to a rightward shift of the curves relative to control curves. When LTP was produced by a less intense stimulus train (50-Hz, 400-ms duration), there were no associated seizures nor was there any change in paired-pulse depression.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Loss of inhibition precedes delayed spontaneous seizures in the hippocampus after tetanic electrical stimulation.

1. The electrophysiological consequences of a "continuous" hippocampal stimulation protocol consisting of 10-s-long stimulus trains administered every 11 s for 90 min to the hippocampus of urethane-anesthetized rats were studied. During the period of stimulation, there was an initial phase with tonic discharges occurring every 1-2 min followed by a secondary phase in which there were well-demarcated recurrent clonic seizures. 2. At the end of the 90 min stimulation period, 7 out of a total of 14 animals studied show epileptiform activity that lasted one-half hour. The other half show disappearance of epileptiform activity within 2 min after terminating the stimulus. In all the animals a quiescent period then followed. In 11 of the animals studied, spontaneous seizures reappeared after the quiescent period had been present for several hours. 3. A paired-pulse method that in previous studies had been shown to reflect the functional state of GABAergic inhibition was employed. Paired-pulse depression in the CA1 region of the hippocampus was measured before administration of stimulus trains, in the quiescent period following the trains, and during and after spontaneous seizures. By comparing indices of maximal inhibition under the various experimental conditions, estimates of the relative amount of inhibition lost could be made. 4. All animals showed reduction of paired-pulse depression in the quiescent period following stimulation when compared with prestimulation values.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1987

Changes in lipids and free fatty acid fractions in adult Haemonchus contortus during incubation in vitro.

Adult Haemonchus contortus (Rud., 1803) has been investigated for its ability to utilize lipids with regard to the total lipids, sterols, free fatty acids, acylglycerols and phospholipids produced during incubation in vitro. All these components exhibit extensive fluctuations, decreasing at some times and increasing at others, thus indicating both biosynthesis and utilization. Also, changes in fatty acid components of total lipids have been analyzed by gas liquid chromatography. These observations indicate that H. contortus is capable of utilizing 16:0, 18:0, 18:1, 18:2, 20:0, 20:un1, 20:un2, 21:0, 21:un1, 21:1, 21:un2, 22:un1, 22:3, 22:?, 22:un2 and 24:3 fatty acids. At the same time, because of large increases in 15:0, 16:0, 18:0, 18:?, 18:1, 18:2, 20:0, 20:un1, 20:un2, 21:0, 21:un1, 21:1 and 21:un2 acids, it is postulated that these acids are synthesized by adult H. contortus.

Animals↗
PubMed1987

Biochemistry of Haemonchus--a review.

Haemonchus biochemistry has been reviewed under the subheadings chemical composition (carbohydrates, lipids, proteins, amino acids, nucleic acids, hormones, inorganic elements, pigments), absorption/transport, biosynthesis (carbohydrates, lipids, proteins, amino acids, nucleic acids), catabolism/utilization (carbohydrates-glycolysis, TCA cycle, CO2 fixation, electron transport system, pentose pathways, glyoxylate cycle, strain variations in energy metabolism; lipids, proteins), biochemistry in taxonomy and miscellaneous.

Amino Acids↗