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J Epelbaum

Publications and source records attributed to J Epelbaum.

At least 163 records · Page 9Linked to original sources
PubMed1981

Noradrenaline stimulates somatostatin release from incubated slices of the amygdala and the hypothalamic preoptic area.

Neurotransmitter effects were studied on in vitro release of immunoreactive somatostatin (SRIF) from slices prepared from several regions of the rat brain: mediobasal hypothalamus (MBH), preoptic anterior hypothalamic area (POA) and amygdaloid complex (AMY). Potassium (K+, 56 mM) stimulated SRIF release in all structures tested in a calcium dependent manner. Morphine, dopamine, GABA and serotonin did not modify SRIF release in any structure; noradrenaline (NA) was not effective on MBH slices, but elicited a dose-dependent stimulation of SRIF release from POA and AMY (ED50 = 6.4 +/- 1.4 nM and 3.6 +/- 1.2 nM respectively). Converse orders of potency of adrenergic agonists were observed in both structures (POA, adrenaline greater than noradrenaline greater than isoproterenol; AMY, isoproterenol greater than adrenaline greater than noradrenaline). Phentolamine blocked NA-induced SRIF release in the POA while propranolol was ineffective. On the contrary, propranolol, but not phentolamine, antagonized NA stimulation in the amygdala. The data suggest that NA acting through specific receptors modulate SRIF release from POA and AMY. In POA, NA effect seems mediated through alpha adrenergic receptors while in AMY, beta receptors are involved. The possibility that these interactions of NA with SRIF release are correlated with effects of NA on growth hormone secretion or on epileptic events is discussed.

Amygdala↗
PubMed1979

Vasoactive intestinal peptide inhibits release of somatostatin from hypothalamus in vitro.

The effect of vasoactive intestinal peptide (VIP) was studied on the release of somatostatin (SRIF) from slices of several regions of the rat brain in vitro. VIP induced a dose-dependent inhibition of SRIF release from mediobasal hypothalamic slices but did not interfere with SRIF release from preoptic area, amygdala or cortex. VIP inhibition had an apparent affinity: Kd = 6.8 +/- 3.9 x 10(-11) M. Secretin had a similar effect but at 600-fold higher concentrations (Kd secretin = 4.2 +/- 0.6 x 10(-8) M). Gucagon was ineffective in concentrations ranging from 10(-10) M to 10(-7) M. The data are consistent with a role of VIP in the hypothalamic control of growth hormone secretion.

Animals↗
PubMed1979

Chromatographic and biological properties of immunoreactive somatostatin in hypothalamic and extrahypothalamic brain regions of the rat.

A sheep antiserum to somatostatin was used to develop RIA and immunoaffinity chromatography methods for the study of immunoreactive somatostatin (IRS) in brain tissue. IRS extracted from rat median eminence, anterior hypothalamic-preoptic area, amygdala, and parietal cortex bound reversibly to immunoaffinity columns, providing a technique for concentration and partial purification. Immunoaffinity purified IRS from each of the four brain regions eluted as four peaks on gel filtration chromatography. Each peak possessed biological activity, as determined by inhibitory effects on the release of GH from cultured rat anterior pituitary cells. No differences were detected by the methods employed between IRS from the anterior hypothalamic-preoptic area, which is rich in IRS-containing neuronal cell bodies, and that from the median eminence, where IRS is localized predominantly in nerve terminals.

Animals↗
PubMed1978

Antiserum to somatostatin reverses starvation-induced inhibition of growth hormone but not insulin secretion.

The role of SRIF in starvation-induced inhibition of GH and insulin secretion was assessed by passive immunization with anti-SRIF serum. Six-hour secretory profiles obtained from chronically cannulated male rats deprived of food for 72 h showed marked suppression of GH secretory bursts and significant depression of plasma insulin levels. Administration of 1 ml SRIF antiserum (SRIF AS) iv to starved rats resulted in rapid (within 15 min) restoration of high amplitude GH pulses (600-800 ng/ml) and sighificant elevation of GH trough values. The mean 6-h GH level of starved SRIF, AS-treated rats (189.2 +/- 23.9 ng/ml) was significantly higher than that of starved, normal sheep serum-treated control animals (62.8 +/- 5.8 ng/ml) (P less than 0.005). In contrast to the effects on GH, plasma insulin levels in starved rats administered SRIF AS remained low. No significant difference was observed in the mean 6-h plasma insulin level of starved-SRIF, AS-treated rats when compared to starved, normal sheep serum-treated controls. These findings suggest that circulating SRIF is a physiological regulator of starvation-induced GH suppression but is not involved in mediating the inhibition of insulin.

Animals↗
PubMed1978

[Subcellular distribution of hypothalamic neurohormones and in vitro stimulation of their release].

Neuronal compartments can be separated by differential spinning or by centrifugation on continuous or discontinuous density gradients. Application of these fractionation techniques to brain structures containing neurosecretory neurons shows that LHRH, somatostatin and a non dopamine prolactin inhibiting factor (PIF) are exclusively recovered from synaptosomal fractions. This indicates that biologically and/or immunologically reactive forms of these hormones are almost entirely concentrated in nerve-endings of neurosecretory neurons. In contrast, other neuropeptides - posterior pituitary hormone, but also TRH, a vasoactive intestinal peptide (VIP), substance P or endorphins - are also found in supernatant fractions. The existence of multiple molecular forms of neuropeptides is likely to explain these differences. Current theories postulate that they are synthetized on ribosomes as precursor forms. Their active structure is only achieved by enzymatic splitting of the pre- or the prohormone within nerve endings. This mode of synthesis is probably common to all neuropeptides, although it has only been well substantiated in a few cases, in particular for the hormones of the posterior pituitary. Thus, the lack of immunologically detectable LHRH or SRIF outside the synaptosomal fraction may reflect masking of the active immunological sites by inert peptide chains associated with prohormonal forms. Fractionation methods can also be applied to physiological or pharmacological experiments. In particular, they permit to characterize, on presynaptic membranes of neurosecretory neurons, specific receptors to neurotransmitters involved in the control of neurohormone secretion. Interaction of dopamine and acetylcholine with LHRH and CRF release are presented as examples of such applications.

Animals↗
PubMed1977

Subcellular distribution of radioimmunoassayable somatostatin in rat brain.

A specific, sensitive and reproducible radioimmunoassay is described for measurement of somatostatin in brain tissue. The sensitivity of the assay is 10 pg/tube and recovery of synthetic somatostatin added to brain homogenates was 95.8 +/- 6.2%. Dilution of tissue extracts from various brain regions showed parallelism in standard curves with labelled somatostatin. Somatostatin is shown to be widespread in the central nervous system with highest concentrations in hypothalamus, particularly the median eminence. Subcellular preparations of medial basal hypothalamus, preoptic area and amygdala indicate that over 70% of somatostatin immunoreactivity is localized to the synaptosome fraction. Recovery of activity in the P2 pellet prior to separation on sucrose gradient is approximately 100%. It is hypothesized that somatostatin, in addition to being released into blood vessels of the median eminence, may also be liberated from nerve terminals in other brain regions.

Amygdala↗