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Biomedical subjects

J R Dave

Publications and source records attributed to J R Dave.

63 records · Page 4Linked to original sources
PubMed1981

Indomethacin causes a simultaneous decrease of both prolactin binding and fluidity of mouse liver membranes.

Indomethacin suppressed the numbers of prolactin receptors detectable in the liver membranes of both male and female C3H mice. This occurred in a dose-dependent fashion with 7.5 mug/gm body weight injected every 4 hours exerting a maximal effect within 20 hours. While injection of 50 mug prolactin every 4 hr increased the number of prolactin receptors in control animals it could not in the indomethacin-treated animals. Membrane fluidity was estimated by fluorescence polarization techniques using the lipid probe 1, 6-diphenylhexatriene. Indomethacin caused a decrease in membrane fluidity, whereas, exogenous prolactin increased the fluidity of the recipients' liver membranes but again could not overcome these suppressive effects of indomethacin. The data suggest that prolactin induces its own membrane-associated receptor by means of the prostaglandin cascade, perhaps by altering the fluidity of the supporting lipid bilayer.

Animals↗
PubMed1980

Prostaglandin I2 modifies both prolactin binding capacity and fluidity of mouse liver membranes.

The objective of this study was to determine if prostaglandins alter the fluidity of hepatic membranes and if this, in turn, modifies their ability to bind prolactin. Liver homogenates of adult C3H female mice incubated with 1-1000 nM prostaglandin A1, A2, B2, F1 alpha, 6-keto-F1 alpha, E1, E2, I2, or thromboxane B2 provided the 100,000 X g membrane pellets for subsequent ovine prolactin binding and membrane fluidity studies. Only membrane preparations treated with prostaglandin I2 showed an increase in specific binding of ovine prolactin. The effect (40-50%) was maximal at 100 nM prostaglandin I2 after 30 min of incubation and was due to an increase in the number of receptor sites. Under the same conditions, prostaglandin I2 induced a 17% decrease in membrane microviscosity. These data suggest that specific prostaglandins may modulate the number of prolactin receptors in vivo by modifying the fluidity of the lipid bilayer and the subsequent ease with which receptors can assume active configurations within the matrix.

Animals↗
PubMedDate not supplied

Dodecylglycerol provides partial protection against glutamate toxicity in neuronal cultures derived from different regions of embryonic rat brain.

Primary cultures enriched in neurons dissociated from embryonic rat cerebral cortex, cerebellum, or hippocampus were treated in a chemically defined serum-free media with either vehicle, dodecylglycerol (DDG, 3 microM), or glutamate (75 microM), or preincubated with DDG for 4 or 24 h, and further incubated with glutamate. Their morphological and biochemical assessments (lactate dehydrogenase [LDH] release in the culture media, neuronal viability and intracellular Ca2+ mobilization) were made. Neurotoxic effects of glutamate and glutamate-mediated increases in intracellular Ca2+ were maximal in neurons from cerebellum and minimal in neurons from cortex. Cotreatment of cells with DDG and glutamate failed to provide significant neuronal protection against glutamate in the three brain regions. Pretreatment of cells with DDG for 4 or 24 h prior to glutamate treatment provided significant neuroprotection as judged by morphological changes and a decrease in LDH activity. Neuroprotection of approximately 15-35% was observed following 4 h of DDG pretreatment, increasing to 60-85% protection after 24 h of DDG pretreatment. Although the mechanism of DDG's neuroprotective action remains to be elucidated, these results demonstrate that both glutamate and DDG have differential specificity for anatomical regions of the brain.

Animals↗
PubMedDate not supplied

Changes in the prolactin-binding capacity of mouse hepatic membranes with development and aging.

The objective of this study was to document the developmental changes in the prolactin-binding capacity of hepatic membranes of the female mouse. Prolactin-binding capacity was measured in the microsomal membranes of liver obtained from C3H female mice at various ages. Binding capacity of these membranes remained low until 21 days of age after which it increased and reached the adult levels by 44 days of age. Additional studies were made to observe this parameter in male and female mice during aging. Both female and male mice at 450-470 days of age had values of prolactin binding that were 66% and 79% that of the 77-day-old animals, respectively. A significant increase in membrane lipid microviscosity was observed in animals from both sexes at 450-470 days of age. This was in agreement with earlier studies that showed that prolactin receptors of hepatic membranes are modulated by changes in the membrane lipid microviscosity. These changes suggest that such modifications of cellular membranes are interrelated and that changes in the membrane microviscosity with aging may be a factor modulating cellular responses in older animals.

Age Factors↗
PubMedDate not supplied

Nicotinic receptor stimulation activates enkephalin release and biosynthesis in adrenal chromaffin cells.

Neuroendocrine cells release a portion of their stored secretory hormone content when exposed to tissue-specific secretagogues. In the case of the adrenal medulla, catecholamines and enkephalin peptides, as well as other secretory proteins, are secreted in response to acetylcholine, which is released onto cholinergic receptors on chromaffin cells upon splanchnic nerve stimulation in vivo. Secretagogue stimulation thus depletes intracellular stores of exportable hormone. We were interested to know whether the signal for exportable hormone release might also function as a signal for compensatory hormone repletion by enhancing the biosynthesis of the released hormone(s). Accordingly, we have investigated the effect of nicotinic receptor stimulation on Met-enkephalin peptide biosynthesis and expression of proenkephalin messenger RNA in primary cultures of bovine chromaffin cells. Our results, reported here, suggest a model for stimulus-secretion-synthesis coupling in which nicotinic receptor occupancy activates two pathways. One pathway, dependent on calcium and not mimicked by increased intracellular cyclic AMP, leads to exocytotic hormone release; the other, probably via a calcium-dependent increase in intracellular cyclic AMP, leads to a compensatory increase in intracellular enkephalin through activation of transcription of the proenkephalin structural gene.

Adrenal Medulla↗
PubMedDate not supplied

Chronic ethanol treatment decreases specific nonopiate beta-endorphin binding to hepatic and kidney membranes and lowers plasma beta-endorphin in the rat.

In a previous study we reported the presence of specific nonopiate beta-endorphin (BE) binding sites in peripheral tissues of the rat (Dave JR, Rubinstein N, Eskay RL: Evidence that beta-endorphin binds to specific receptors in rat peripheral tissue and stimulates the adenylate cyclase-adenosine 3',5'-monophosphate system. Endocrinology 117:1389-1396, 1985). The objective of this study was to determine the effect of chronic ethanol administration in vivo on specific nonopiate binding of BE in hepatic and kidney membranes. Experimental animals were exposed continuously for 14 days to ethanol vapor in an inhalation chamber at vapor levels sufficient to maintain blood ethanol levels greater than 120 mg/100 ml, whereas control animals were maintained in ethanol-free chambers. Chronic ethanol treatment decreased [125I]BE binding to hepatic and kidney membranes by approximately 35%, which was due to a decrease in the number of BE binding sites. Chronic ethanol treatment decreased immunoreactive BE in plasma by greater than 80%. In vitro exposure of hepatic and kidney membranes from control animals to ethanol resulted in a dose-related enhancement of BE binding with maximal enhancement of 50-65% being observed at 0.2% ethanol concentration. In contrast, the addition of ethanol in vitro to hepatic and kidney membranes derived from rats chronically exposed to ethanol in vivo did not affect BE binding. Our findings demonstrate that chronic alcohol exposure lowers immunoreactive BE in plasma and reduces BE binding in hepatic and kidney membranes. The observed reduction of BE binding may be due to ethanol-induced changes in membrane composition.

Alcoholism↗