Biomedical subjects

E Arilla

Publications and source records attributed to E Arilla.

At least 19 recordsLinked to original sources

PubMed1992

Reduction of somatostatin receptors in rat hippocampus by treatment with 5,7-dihydroxytryptamine.

Several lines of evidence suggest that somatostatin (SS) may interact with serotonergic neurons in the central nervous system. To assess whether SS acts presynaptically on serotonin (5-hydroxytryptamine, (5-HT)) neurons, SS receptors were measured in membranes from the hippocampus, a brain region that receives dense serotonergic innervation and has a high number of SS receptors in control and 5,7-dihydroxytryptamine (5,7-DHT)-treated rats, at 1 and 3 weeks after injection. Intracerebroventricular (i.c.v.) injection of the 5-HT-specific neurotoxin 5,7-DHT (11 micrograms (free base) dissolved in 10 microliters of isotonic saline containing 0.01% ascorbic acid) produced a 70% reduction in hippocampal 5-HT content at 3 weeks after injection but not at 1 week. This change was associated with a significant decrease in SS receptor density in rat hippocampus only at 3 weeks following the injection, without influencing the apparent affinity of the receptors at any time. Administration of 5,7-DHT did not affect somatostatin-like immunoreactivity (SSLI) levels at both times studied. These results suggest that some of the hippocampal SS receptors may be localized presynaptically on the serotonergic nerve terminals.

5,7-Dihydroxytryptamine↗

PubMed1992

Desmethylimipramine pretreatment prevents 6-hydroxydopamine induced somatostatin receptor reduction in the rat hippocampus.

Several studies have shown anatomical and functional interconnections between catecholaminergic and somatostatinergic systems. To assess whether somatostatin (SS) may act presynaptically on catecholamine neurons, SS receptors were measured using radioligand test-tube binding assays on synaptosomes from hippocampus and frontoparietal cortex--areas that are innervated by catecholaminergic neurons with different densities and that have a high number of SS receptors--from control and 6-hydroxydopamine (6-OHDA)-treated rats. Intracerebroventricular (i.c.v.) injection of the catecholamine neurotoxin 6-OHDA (0.78 mg free base/kg of body weight in saline with 0.1% ascorbic acid) lowered hippocampal and frontoparietal cortical noradrenaline (NA) and dopamine (DA) levels at 1 week following the injection. Pretreatment of rats with desmethylimipramine (DMI) (40 mg/kg, intraperitoneal) prevented the drop in NA levels, but was not effective in attenuating DA depletion in the two brain areas studied. Treatment with 6-OHDA lowered the number of 125I-Tyr11-SS receptors in the hippocampus (130 +/- 19 vs. 266 +/- 16 fmol/mg protein, P < 0.001), whereas in the frontoparietal cortex a non significant 20% reduction in receptor number was found. The dissociation constants of 125I-Tyr11-SS binding to synaptosomes from frontoparietal cortex (0.65 +/- 0.06 vs. 0.60 +/- 0.04, P not significant) and hippocampus (0.44 +/- 0.04 vs. 0.63 +/- 0.14, P not significant) were similar in control and treated groups. Pretreatment with DMI reversed up to 80% of the effect of 6-OHDA on hippocampus SS receptors. DMI alone had no observable effect on the number and affinity of SS receptors. The 6-OHDA and the DMI treatment did not affect SLI levels in the brain areas studied. These results suggest that a portion of the hippocampal SS receptors may be localized presynaptically on the noradrenergic and dopaminergic nerve terminals.

Animals↗

PubMed1992

Somatostatin receptors increase in the olfactory bulb of developing pups after perinatal exposure to cocaine.

The effects of chronic prenatal and/or postnatal exposure to cocaine on somatostatin concentration and receptors were studied in the olfactory bulbs of rat pups at birth and at 15 days old. Wistar rats were injected subcutaneously with single daily doses of 40 mg cocaine hydrochloride/kg from days 7 to 19 of gestation, from day 7 of gestation to day 15 postpartum or from parturation to day 15 postpartum. Fetal exposure to cocaine decreased SS concentrations in the olfactory bulb of the newborn pups while prenatal-plus-postnatal exposure increased this parameter. Administration of cocaine only during lactation did not induce any change. Exposure during gestation or during nursing induced an increase in the total number of somatostatin receptors and a decrease in the affinity constant in the olfactory bulb of newborn and 15-day-old pups. These results suggest that the development of somatostatin receptors in the olfactory bulb can be altered by prenatal and/or nursing period exposure to cocaine.

Animals↗

PubMed1992

Vasoactive intestinal peptide receptors in rat liver after partial hepatectomy.

We describe the status of vasoactive intestinal peptide (VIP) receptors in regenerating liver. VIP-stimulated adenylate cyclase activity was markedly decreased in proliferating liver 3 days after partial (70%) hepatectomy. This was associated with a reduced efficacy of VIP (53% compared with controls), with no change in the potency of the peptide (ED50 0.8 nM). In contrast, forskolin- and guanosine 5'-[beta gamma-imido]triphosphate (Gpp[NH]p)-stimulated enzyme activities were not decreased after hepatectomy. The expression of Gs protein subunits (alpha and beta) was studied by cholera toxin-catalysed ADP ribosylation of alpha s and by immunoblotting of alpha s and beta subunits. Both subunits were increased in regenerating liver, further suggesting that the decreased response to VIP was not related to a decreased expression of Gs proteins. In fact, the reduced adenylate cyclase response to VIP in regenerating liver was associated with quantitative and structural changes in VIP receptors. Equilibrium binding data obtained with 125I-VIP indicated the presence of two classes of binding sites, the Kds of which were not altered after hepatectomy. In contrast, changes in binding capacity (Bmax.) were as follows: 0.11 +/- 0.01 and 0.05 +/- 0.01 pmol/mg of protein for high-affinity sites in control and hepatectomized rats respectively; and 2.3 +/- 0.2 and 0.65 +/- 0.03 pmol/mg of protein for low-affinity sites in control and hepatectomized rats respectively. Moreover, affinity labelling experiments showed that the M(r) value of 125I-VIP-receptor complexes was higher in regenerating liver than in quiescent hepatocytes, e.g. 58,000 and 53,000 respectively. It is concluded that VIP receptors are altered in regenerating liver, resulting in a decreased response of adenylate cyclase to the neuropeptide.

Adenosine Diphosphate Ribose↗

PubMed1992

Different response of astrocytes and Bergmann glial cells to portacaval shunt: an immunohistochemical study in the rat cerebellum.

The present study was performed in order to follow the response of rat cerebellum astroglial cells (Bergmann glial cells and astrocytes) to long-term portacaval shunt (PCS), by means of glial fibrillary acidic protein (GFAP) and vimentin immunoreactivities. Bergmann glia accumulated GFAP in response to PCS, whereas astrocytes decreased GFAP immunoreactivity when compared to control rats. The increase of GFAP occurs in cells located in the cerebellar layer where glutamate is mainly released. Since the vimentin content remained unaltered in response to PCS, when compared to control rats, it can be concluded that only the GFAP filaments are affected by PCS. Nevertheless, GFAP immunoreactivity presents regional differences in the cerebellar astroglial population, and the factors responsible for these variations are still unknown.

Animals↗

PubMed1992

Somatostatin binding reduced by ammonium acetate in the rat hippocampus can be reversed by treatment with N-carbamyl-L-glutamate plus L-arginine.

The effects of short-term (90 min), mid-term (5 days), and long-term (15 days) administration of ammonium acetate (5 mmol/Kg day i.p.) on the somatostatinergic neurotransmitter system of the rat hippocampus have been studied. Scatchard analysis of the binding of 125I-Tyr11-somatostatin to hippocampal dissociated cells indicated that administration of ammonium acetate at the times studied were associated with a decrease in the number of somatostatin receptors in this brain area, whereas the affinity of the same receptors remained unchanged. Administration of ammonium acetate did not affect the levels of somatostatin-like immunoreactivity in the hippocampus. Treatment with N-carbamyl-L-glutamate (1 mmol/Kg, i.p.) plus L-arginine (1 mmol/kg), which lead to the conversion of ammonia into urea, prevented the ammonium acetate-induced changes in somatostatin binding in this brain area. N-carbamyl-L-glutamate plus L-arginine alone had no observable effect on the somatostatinergic system. The decrease in the number of somatostatin receptors induced by ammonium acetate might reflect a decreased sensitivity of the target cells to somatostatin, a phenomenon that could contribute to the depressed neuronal excitability induced by ammonia in the rat hippocampus.

Acetates↗

PubMed1992

Acute nicotine administration increases somatostatin content and binding in the rat hypothalamus.

Within 4 minutes a single, intravenous injection of nicotine (0.3 mg/Kg) induced increases in somatostatin-like immunoreactivity concentrations in the rat hypothalamus but not in the striatum. These changes were associated with a significant increase in the specific binding of somatostatin to putative receptor sites in hypothalamic membranes, while no significant changes were found in striatum. The enhancement of somatostatin binding resulted from a rapid increase in the number of available receptors rather than a change in receptor affinity. This effect appears to be mediated by nicotinic cholinergic receptors, because pretreatment with a centrally active nicotinic receptor antagonist, mecamylamine (5.0 mg/Kg i.v.), prevented the nicotine-induced changes in somatostatin content and binding in the hypothalamus. Mecamylamine alone had no observable effect on the hypothalamic somatostatinergic system. These results suggest that the rat hypothalamic somatostatinergic system can be regulated by nicotine-like acetylcholine receptors.

Animals↗

PubMed1992

Somatostatin binding to a fresh rat astrocyte-enriched suspension.

Since there are conflicting reports regarding the effects of somatostatin (SS) on cyclic AMP levels in astrocytes derived from rat cerebral cortex and, to date, the SS binding to mature astrocytes is unknown, the present study has determined SS binding and its effect on cyclic AMP accumulation in a fresh astrocyte-rich suspension from rat cerebral cortex. 125I-Tyr11-SS binding was inhibited by SS in a dose-dependent manner. The Scatchard analysis of binding data was linear and yielded a dissociation constant of 0.95 +/- 0.15 nM with a maximal binding capacity of 122 +/- 13 fmol/mg protein. Vasoactive intestinal peptide (VIP) stimulated cyclic AMP accumulation up to 2.3 times above the basal levels whereas SS had no effect. This effect at any of the VIP concentrations. Likewise, SS did not inhibit the stimulation of cyclic AMP accumulation provoked by other effectors such as isoproterenol and forskolin. In view of our results and those of other authors, SS receptor localized in astrocytes must be able to couple with signal transduction systems other than adenylate cyclase, in order to carry out its biological actions in the cell.

Animals↗

PubMed1992

Somatostatin binding and modulation of adenylate cyclase in ovine retina membranes.

Somatostatin (SS) receptors in membranes from ovine retinas were examined using 125I-Tyr11-SS as a ligand. Receptor binding was rapid, specific, saturable, reversible and dependent on temperature and membrane concentration. Conditions of apparent equilibrium were obtained at 25 degrees C after a 45 min incubation in the presence of about 0.25 mg membrane protein/ml. Native SS competitively inhibited the binding of 125I-Tyr11-SS in the range of 0.01-10 nM, and half-maximal inhibition was observed at 0.2 nM SS. Scatchard analysis of these data suggested the existence of a single population of SS receptors with a dissociation constant of 0.23 +/- 0.03 nM and a maximum binding capacity of 84 +/- 6 fmol/mg protein. The binding of 125I-Tyr11-SS was inhibited by various synthetic SS analogs in a dose-dependent manner whereas peptides unrelated to SS did not show practically any effect even at concentrations as high as 10(-6) M. SS receptor occupancy appears to be coupled to inhibition of adenylate cyclase activity by a guanine nucleotide-binding regulatory protein, as suggested by the facts that: (a) SS noncompetitively inhibited the stimulatory effect of vasoactive intestinal peptide (VIP) (3 x 10(-7) M) on membrane adenylate cyclase activity but it did not alter basal enzyme activity; and (b) the addition of guanosine 5'-triphosphate (GTP) (10(-5) M) decreased the specific binding of 125I-Tyr11-SS to 26.6% of the control value due to a decrease in SS receptor affinity. The present results support the hypothesis that SS may contribute to the physiological regulation of the functions of the retina.

Adenylyl Cyclases↗

PubMed1992

Somatostatin receptor elevation in rat striatum after diisopropylfluorophosphate administration.

The acute and chronic administration of diisopropylfluorophosphate (DFP), an inhibitor of acetylcholinesterase or of atropine, a blocker of muscarinic cholinergic receptors, did not affect somatostatin-like immunoreactivity (SLI) content in the striatum of rats. Acute and chronic DFP administration increased the number of specific 125I-Tyr11-somatostatin (125I-Tyr11-SS) receptors in cells dissociated from the striatum without changing the affinity constant. Although the increase could be blocked by pretreatment with atropine, it was not due to a direct effect by DFP on somatostatin (SS) receptors, because no rise in 125I-Tyr11-SS binding was produced by high concentrations of DFP (10(-5) M) when added in vitro. The acute administration of atropine alone had no observable effect on the number of SS receptors. However, repeated atropine administration produced a significant decrease in the 125I-Tyr11-SS binding in cells dissociated from the striatum, although the affinity constant was unchanged. The results suggest that interactions between somatostatinergic and cholinergic receptors may be of importance in the rat striatum.

Animals↗

PubMed1991

Changes in striatal somatostatin receptors in pups after cocaine administration to pregnant and nursing dams.

Primiparous female Wistar rats were injected subcutaneously with single daily doses of 40 mg of cocaine hydrochloride/kg from day 7 to 19 of gestation, from day 7 of gestation to day 15 postpartum or from parturation to day 15 postpartum. At birth, some of the offspring were fostered to control mothers to limit the effect of cocaine to the prenatal period and some were left with their mothers with the aim of studying prenatal plus postnatal exposure to cocaine. Prenatal and/or postnatal cocaine exposure did not affect the content of somatostatin (SS)-like immunoreactivity (SLI) in the striatum of the offspring as compared with the control groups on day 15 in all experimental groups. Prenatal and prenatal-plus-postnatal exposure to cocaine increased the total number of binding sites for 125I-Tyr11-SS in the rat striatum at 15 days of age. Prenatal exposure to cocaine also decreased the apparent affinity of the receptors. Postnatal exposure to cocaine alone had no such post-treatment effect on 125I-Tyr11-SS binding. These results suggest that the development of SS receptors in the rat striatum can be altered by prenatal exposure to cocaine.

Animals↗

PubMed1991

Heterogeneous astroglial response in the rat spinal cord to long-term portacaval shunt: an immunohistochemical study.

Glial fibrillary acidic protein (GFAP) immunoreactivity has been used to study the astroglial response in the rat spinal cord to long-term portacaval shunt (PCS). The astroglial response in PCS rats is heterogeneous. In general, astrocytes show a loss of GFAP immunoreactivity, as well as shrinking and pyknosis in their nuclei; however, while GFAP reactivity was unchanged in the periependymal region, it was strongly increased in the dorsolateral region of the spinal cord (lateral spinal nucleus, dorsal root entry zone, and the most dorsal region of the dorsal horn). Three possibilities are postulated to explain how astrocytes, in the periependymal and dorsolateral regions, can support the effects of PCS: a) astrocytes related to glutamatergic pathways ought to possess a more efficient ammonia uptake and detoxification system, b) long-term PCS can activate nociceptive pathways (substancePergic fibers), and c) astrocytes located in periependymal and dorsolateral regions can be exposed to lower concentrations of ammonia because of its diffusion into the cerebro-spinal fluid close to these regions.

Ammonia↗

PubMed1991

Effect of maternal exposure to nicotine in the rat on level and binding of somatostatin in brain of developing offspring.

The effect of maternal exposure to nicotine on the level of somatostatin and specific binding in frontoparietal cortex and hippocampus of developing offspring was investigated. Sprague-Dawley rats were injected subcutaneously, throughout the pregnancy and the nursing period, with either: 3 mg/kg nicotine base or saline vehicle. In the offspring of control rats, the level of somatostatin-like immunoreactivity peaked at day 10 in the frontoparietal cortex, whereas the level of immunoreactivity in the hippocampus was the highest on day 30. Maternal exposure to nicotine caused enhanced levels of immunoreactivity in the frontoparietal cortex, on the day of birth and in the hippocampus, up to day 10. The maximum specific binding of somatostatin to the receptors in membranes from the frontoparietal cortex, peaked at 10 days of age in the offspring of control rats. The number of somatostatin receptors in cortical (but not in hippocampal) membranes was significantly decreased in the 0- to 10-day-old offspring of the nicotine-treated rats. Despite transient alterations in the number of somatostatin receptors, the affinity of the sites for somatostatin was consistently unchanged. The levels of somatostatin-like immunoreactivity and the number of somatostatin receptors in the frontoparietal cortex and hippocampus was comparable in the 30-day-old offspring of the control and nicotine-treated rats.

Aging↗

PubMed1991

Maternal ethanol ingestion and somatostatin level and binding in developing rat brain.

The effect of maternal ethanol ingestion on 125I-labeled [Tyr11]somatostatin (SS) binding and somatostatin-like immunoreactivity (SLI) in the rat frontoparietal cortex and hippocampus of developing offspring was explored. Female Sprague-Dawley rats were given ethanol in the drinking water before pregnancy, during gestation, and while nursing, whereas controls received a standard diet and fresh water ad libitum. In the ethanol group, food intake decreased as ethanol consumption augmented, with the ethanol calories comprising greater than 30% of the total energy intake during pregnancy. Total energy intake was similar for the ethanol group and normal controls. Maternal alcohol ingestion is associated with an enhanced SLI level in the frontoparietal cortex and hippocampus on the day of birth. This study provided evidence of a selective decrease in SS receptor binding in frontoparietal cortex but not in hippocampus in the 0- to 10-day-old offspring of the ethanol-fed rats. The SS receptor number increased from day 0 to 10 in both control and ethanol groups. However, the affinity appeared to decrease significantly in the ethanol group during this period. At day 30, no differences were found between offspring of control and ethanol-treated rats in any of the parameters. These results suggest that the development of SS receptors in the rat frontoparietal cortex can be transitorily delayed by maternal ethanol ingestion.

Animals↗

PubMed1990

Effects of acute nicotine and mecamylamine administration on somatostatin concentration and binding in the rat brain.

Since nicotine and somatostatin have regulatory effects on locomotor activity it was of interest to determine whether the receptors for somatostatin are modulated by the cholinergic nicotine-like effects. An i.v. dose of 0.3 mg/kg nicotine induced an increase in the concentrations of somatostatin-like immunoreactivity at 4 min in the parietal cortex and at 15 min in the hippocampus. These changes were associated with a significant increase in the total number of specific somatostatin receptors in the parietal cortex at 15 min and in the hippocampus at 30 min following injection. To determine if the above mentioned changes are related to the nicotine activation of central nicotine-like acetylcholine receptors, a cholinergic nicotinic blocking agent, mecamylamine, was administered before the nicotine injection. Pretreatment with mecamylamine (5.0 mg/kg i.v.) prevented the nicotine-induced changes in somatostatin level and binding in both brain areas. Mecamylamine alone had no observable effect on the somatostatinergic system. These results suggest that the somatostatinergic system can be regulated by nicotine-like acetylcholine receptors and may be involved in some of the behavioral central effects of nicotine.

Animals↗

PubMed1990

Effect of bilateral adrenalectomy on VIP receptor/effector system in rat intestinal epithelial cells.

The number of vasoactive intestinal peptide (VIP) receptors and the efficiency of VIP in the stimulation of cyclic AMP accumulation in rat jejunal epithelial cells increased after bilateral adrenalectomy. However, this condition increased neither receptor affinity nor VIP potency. In addition, jejunal VIP levels followed a parallel increase. These changes reversed to control conditions after glucocorticoid replacement with dexamethasone indicating that adrenalectomy modifies the intestinal VIP receptor/effector system and suggest a relationship between corticosteroids and VIP in the functions of intestinal epithelium.

Adrenalectomy↗

PubMed1990

Effect of haloperidol withdrawal on somatostatin level and binding in rat brain.

The effects of withdrawal on the level and specific binding of somatostatin in the frontoparietal cortex and hippocampus of the rat after chronic haloperidol treatment were examined using 125I-Tyr11 somatostatin as tracer. One week after haloperiodol withdrawal the number of specific somatostatin receptors in both brain areas returned to control values, after having decreased as the result of chronic administration. Neither administration of haloperidol nor withdrawal of it affected the levels of somatostatin-like immunoreactivity (SLI) in the two brain areas studied. The return of the somatostatin receptor number to control values after haloperidol withdrawal may be related to the motor side-effects that are clinically observed when the haloperidol treatment is terminated.

Animals↗

PubMed1990

Somatostatin content and binding in small intestinal mucosa from fed, fasted, and refed rabbits.

The present study is an investigation of the effects of 12- to 96-hours' starvation and 96-hours' starvation plus 48-hours' refeeding on both somatostatin-like immunoreactivity (SLI) and cytosolic somatostatin binding sites in rabbit small intestinal mucosa. The SLI concentration increased after 24 h in duodenal and jejunal mucosa, but not in ileal mucosa, and reached its highest value after 96 h of fasting. The number of specific high and low-affinity somatostatin binding sites, but not their affinity, decreased with the duration of fasting in the same gut segments, refeeding of fasted animals resulted in a return to normal control values for small intestine mucosal SLI and somatostatin binding.

Animals↗