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Biomedical subjects

H Datta

Publications and source records attributed to H Datta.

At least 19 recordsLinked to original sources
PubMed1994

A novel technique for isolation of pure sperm heads from disintegrated mammalian spermatozoa.

The phenomenon of differential charge distribution on sperm surface membrane has been utilised here in a low e.m.f. (electro motive force) capillary electrophoresis system to effect separation of sperm heads from disintegrated mixed spermatozoal subfractions. Washed caudal sperm of goat (Black Bengal variety) and ejaculated washed human sperm were fractionated by sonication into head, mid-piece and tail portions. Routine techniques of density gradient centrifugation on Percoll and/or sucrose were performed with sonicated spermatozoa for separation into their respective subfractions. The products obtained were not free of contamination in either case. Mixed sperm fractions when subjected to the afore mentioned modified capillary electrophoresis technique only the head pieces exhibited high affinity for migration towards the cathode terminal. With this method around 50% of the total sperm heads were separated and collected in absolutely pure form at the cathode side within 2 hrs. at 150 volts (V) and 1.5 milliampere (mA) current at 37.5 degrees C. A 4 cm. long capillary tube with a bore size 1.2 mm. was used for this purpose.

Animals↗
PubMed1991

Alkaline phosphatase isoforms in bile and serum and their generation from cells in vitro.

Alkaline phosphatase is anchored to cell membranes by a glycosyl-phosphatidylinositol anchor and is present in bile and plasma in various isoforms. The formation of these isoforms depends upon mechanisms of release and subsequent complex formation. Evidence is presented for an enzymatic activity possibly a glycosyl-phosphatidylinositol-specific phospholipase D (GPI-PLD), in serum that releases an isoform incapable of further complex formation, whereas such an activity is absent from bile.

Alkaline Phosphatase↗
PubMed1991

Enhancement of memory retrieval and attenuation of scopolamine-induced amnesia following administration of 5-HT3 antagonist ICS 205-930.

Experimental evidence suggests an important role of serotonin in the process of learning and memory. The present study investigated the effect of 5HT3-receptor antagonist (ICS 205-930) on retrieval of a previously learned aversive habit in the mouse. The effect of ICS 205-930 on scopolamine (3 mg/kg) induced amnesia was also studied. ICS 205-930 (1, 10 & 100 micrograms/kg) produced a dose-dependent increase in latency to cross into the dark chamber. The scopolamine induced memory impairment was significantly attenuated by ICS 205-930 (10 micrograms/kg). These results suggest that memory deficits may be susceptible to attenuation with non-cholinergic treatments.

Amnesia↗
PubMed1991

Effects of morphine on memory: interactions with naloxone, propranolol and haloperidol.

The effects of morphine on memory have been shown to be dependent on the strain of animal used and on the experimental parameters. Memory was assessed in a passive avoidance task using Swiss albino (ICRC) mice. Morphine at doses of 1, 3 and 10 mg kg-1 was administered immediately after foot shock (memory retention) or 23.5 h after foot shock (memory retrieval). Retest step-down latencies measured 24 h later showed that morphine did not affect memory retention but dose-dependently impaired retrieval of memory. Administration of naloxone 0.1 mg kg-1 antagonised the effects of morphine and impaired memory retention. Propranolol 0.3 mg kg-1 along with morphine 3 mg kg-1 impaired memory retention only while haloperidol 0.1 mg kg-1 improved the impairment of memory retrieval caused by morphine 3 mg kg-1. Glucose did not alter the effects of morphine on memory. There was no per se effect of morphine, naloxone, propranolol, glucose and haloperidol on memory at the doses used. The effect of morphine on memory retention is mediated by opioid mechanisms; however, adrenergic and dopaminergic mechanisms possibly modulate retention and retrieval of memory, respectively.

Animals↗
PubMed1990

Intracellular calcium in the control of osteoclast function. II. Paradoxical elevation of cytosolic free calcium by verapamil.

We report here for the first time that verapamil elevates cytosolic calcium. We have found that in the isolated rat osteoclast, verapamil at low micromolar concentrations did not block the elevation of cytosolic free calcium ([Ca++]i) in response to elevated extracellular calcium concentrations ([Ca++]e). However, high micromolar concentrations of verapamil (300 microM or above) led to a rapid sustained elevation of [Ca++]i. These concentrations of verapamil had effects on osteoclast morphology and resorptive activity that were similar to those produced by elevated [Ca++]e: there was a marked dose-dependent fall in cell spread area and osteoclastic bone resorption. The sensitivity of osteoclasts to high micromolar concentrations of verapamil is unique and could not be mimicked in macrophages and lymphocytes.

Animals↗
PubMed1990

Kidney: a target organ for calcitonin gene-related peptide.

In the present study we have evaluated the effect of calcitonin gene-related peptide (CGRP) on cyclic AMP levels in intact mouse kidneys. We have used an in vivo bioassay based on microwave irradiation as a means of rapid tissue fixation, followed by the determination of cyclic AMP concentration using a protein binding assay. CGRP was found to cause a dose-dependent elevation of renal cyclic AMP levels, and despite being slightly less potent than calcitonin (CT), the action of CGRP was significantly more prolonged. The extended time course of action of CGRP is in sharp contrast to its known effect on bone cyclic AMP levels and could be of physiological relevance. CGRP may act on a receptor different from that of CT to produce distinct functional effects.

Animals↗
PubMed1990

Interactions of verapamil and diltiazem with ketamine: effects on memory and sleeping time in mice.

The effects of ketamine (3, 10 and 30 mg/kg) alone and in combination with verapamil (10 mg/kg) or diltiazem (30 mg/kg) on the acquisition, consolidation and retrieval of memory using a passive avoidance task in mice were studied. Ketamine significantly inhibited the acquisition and consolidation of memory at 10 and 30 mg/kg dose levels and these effects were antagonized by diltiazem 30 mg/kg but not by verapamil 10 mg/kg. Studies of sleeping time demonstrated that pretreatment with verapamil 10 mg/kg increased the duration of sleeping time. Diltiazem, however, did not potentiate the effects of ketamine on sleeping time. The present findings indicate that diltiazem can counter the effects of ketamine on memory. The data also indicates that pretreatment of surgical patients with verapamil may reduce the dose of ketamine required for anesthesia.

Animals↗
PubMed1990

Effects of morphine, buprenorphine, pentazocine and nalorphine on acquisition and extinction of active avoidance responses in rats.

The effects of subcutaneous administration of morphine, buprenorphine, pentazocine and nalorphine were studied at two dose levels in rats (low dose x 10 and high dose x 20 of equivalent human dose) on the performance of active avoidance responses using a shuttle box. Pretraining injections of both doses of pentazocine and low dose nalorphine impaired acquisition on day 1 and day 2. Morphine and buprenorphine (at both dose levels) and high dose nalorphine did not affect the acquisition process. Post-training administration of morphine (high dose) and buprenorphine (both doses) delayed extinction of active avoidance responses. Low dose of morphine, high dose of pentazocine and both doses of nalorphine did not appreciably affect the extinction process. Mu opioid receptor agonists probably act as reinforcers to facilitate memory.

Animals↗
PubMed1989

The lung as a target organ for thyroxine.

The isolated perfused in situ rat lung preparation was used to investigate the chronic effect of thyroxine on the intermediary metabolism in the mammalian lung. Treatment with thyroxine caused stimulation of the rate of glucose utilization (91 +/- 11 mumol/g dry weight/hr versus 54 +/- 5 mumol/g dry weight/hr). The increase in the rate of glucose uptake was not accompanied by a similar increase in lactate output. Alanine and pyruvate release were also similar in both groups. The implication is that oxidative metabolism of glucose was increased. This study provides the first unequivocal evidence that the mammalian lung is a target organ for thyroxine.

Alanine↗
PubMed1980

A possible mechanism for the anti-ketogenic action of alanine in the rat.

1. The anti-ketogenic effect of alanine has been studied in normal starved and diabetic rats by infusing l-alanine for 90min in the presence of somatostatin (10mug/kg body wt. per h) to suppress endogenous insulin and glucagon secretion. 2. Infusion of alanine at 3mmol/kg body wt. per h caused a 70+/-11% decrease in [3-hydroxybutyrate] and a 58+/-9% decrease in [acetoacetate] in 48h-starved rats. [Glucose] and [lactate] increased, but [non-esterified fatty acid], [glycerol] and [3-hydroxybutyrate]/[acetoacetate] were unchanged. 3. Infusion of alanine at 1mmol/kg body wt. per h caused similar decreases in [ketone body] (3-hydroxybutyrate plus acetoacetate) in 24h-starved normal and diabetic rats, but no change in other blood metabolites. 4. Alanine [3mmol/kg body wt. per h] caused a 72+/-9% decrease in the rate of production of ketone bodies and a 57+/-8% decrease in disappearance rate as assessed by [3-(14)C]acetoacetate infusion. Metabolic clearance was unchanged, indicating that the primary effect of alanine was inhibition of hepatic ketogenesis. 5. Aspartate infusion at 6mmol/kg body wt. per h had similar effects on blood ketone-body concentrations in 48h-starved rats. 6. Alanine (3mmol/kg body wt. per h) caused marked increases in hepatic glutamate, aspartate, malate, lactate and citrate, phosphoenolpyruvate, 2-phosphoglycerate and glucose concentrations and highly significant decreases in [3-hydroxybutyrate] and [acetoacetate]. Calculated [oxaloacetate] was increased 75%. 7. Similar changes in hepatic [malate], [aspartate] and [ketone bodies] were found after infusion of 6mmol of aspartate/kg body wt. per h. 8. It is suggested that the anti-ketogenic effect of alanine is secondary to an increase in hepatic oxaloacetate and hence citrate formation with decreased availability of acetyl-CoA for ketogenesis. The reciprocal negative-feedback cycle of alanine and ketone bodies forms an important non-hormonal regulatory system.

Alanine↗
PubMed1980

Substrate utilization by the lung.

Intermediary metabolism of the lung and its regulation have received relatively little attention in the past, partly because of difficulty in producing suitable models for study. An in situ perfused rat lung preparation is described which remains viable for four hours or more. Concentration-dependent glucose utilization has been found with this model, associated with marked lactate production. More than half the glucose used appears as lactate, despite the high PO2 and maintenance of normal ATP concentrations. The high rates of glycolysis may be related to glycerol-3-phosphate requirements for lipid synthesis. Glucose clearance from the perfusion medium is dependent on nutritional status, clearance by lungs from 48-hour starved animals being decreased by comparison with lungs of fed controls. Lactate is taken up actively at concentrations of 2 mmol/l or above but is produced at an initial lactate concentration of 0.4 mmol/l. Non-esterified fatty acids (1 mmol/l in the perfusate) are also cleared by lung and may be important as an energy source even though 80% is used for synthetic reactions. Alanine, glycerol and 3-hydroxybutyrate are unimportant as substrates. The lung responds to metabolically important hormones. Insulin and adrenaline cause an acute increase in glucose utilization whereas corticosterone and noradrenaline are inhibitory. Utilization of glucose is also diminished in lungs from diabetic ketoacidotic rats. Further work is required to establish the relative importance of oxidative and synthetic routes for added substrates and the mechanisms of hormonal regulation.

Adenosine Triphosphate↗