Glutamate Stimulates Somatostatin Release from Diencephalic Neurons in Primary Culture*

Tapia‐Arancibia, Lucía; Astier, H

doi:10.1210/endo-123-5-2360

Cited by 44 publications

(33 citation statements)

References 37 publications

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“…In fact, pharmacological evidence favours such a role for S R I F (26). Generally, although the present data is in keeping with our previous in vitro results (4) showing a direct GLU-SRIF interaction, we cannot totally exclude the involvement of intermediary steps in vivo particularly since GLU participates in a wide variety of metabolic processes. Growth hormone-releasing factor mediation could be a good candidate since this peptide originates in the arcuate nucleus (27) where an intricate interplay of SRIF/ growth hormone-releasing factor could explain the decreased output of hypothalamic growth hormone-releasing factor concomitant with the increased release of SRIF that has been observed (review in 24).…”

Section: Discussionsupporting

confidence: 66%

“…On the other hand, systemic administration of GLU to adult rats causes an immediate longlasting suppression of growth hormone secretion presumably via somatostatin (SRIF) release as estimated by decrease in its hypothalamic content (3). Most convincing evidence of this neuroendocrine role arises from our recent data showing that in primary culture of hypothalamic neurons, GLU exerts a stimulatory action on SRIF release involving N-methyl-D-aspartate (NMDA) receptor subtypes (4). The present work was designed to determine whether this GLU-SRIF neuroendocrine interaction also operates in the in vivo adult rat.…”

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confidence: 97%

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Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Benyassi

Tapia‐Arancibia

Arancibia

1991

J Neuroendocrinology

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This study was designed to determine whether glutamate is able to stimulate somatostatin release from in vivo conscious animals when somatostatin release is monitored in unanaesthetized rats stereotaxically implanted with a push-pull cannula in the median eminence. One week after implantation, the median eminence was perfused with artificial cerebrospinal fluid alone or with the addition of either CGS 19755, an N-methyl-D-aspartate (NMDA) receptor antagonist M). The latter (which is able to cross the brain-blood barrier at large doses) was also peripherally administered (1 g/kg ip). Median eminence perfusate samples were collected every 15 min and somatostatin was measured by a sensitive radioimmunoassay. In rats receiving ip glutamate injection, somatostatin release from the median eminence was significantly increased (73.3+ 10.4 versus 24.8k6.2; P

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Section: Discussionsupporting

confidence: 66%

mentioning

confidence: 97%

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Benyassi

Tapia‐Arancibia

Arancibia

1991

J Neuroendocrinology

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“…A potential candidate for such a hypothalamic mediator is somatostatin, NMDA being an inhibitor of somatostatin release in vivo. However, since a stimulatory action of NMDA on the secretion of somatostatin in vitro has been reported [30], further experiments are needed in order to clarify the involvement of somatostatin in the modulation of NMDA-induced GH secretion.…”

Section: Discussionmentioning

confidence: 99%

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Pinilla

González²,

Tena‐Sempere³

et al. 1999

Neuroendocrinology

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Activation of N-methyl-D,L-aspartic acid (NMDA) receptors stimulates growth hormone (GH) secretion. The mechanisms involved in this action are still a matter of debate. Present experiments were carried out to assess specifically: (1) the age-related changes in NMDA effects; (2) the physiological role of NMDA in pulsatile GH secretion; (3) the hypothalamic and/or pituitary actions of NMDA, and (4) the influence of gonadal function on NMDA-induced GH release. NMDA (15 mg/kg i.p.) stimulated GH secretion in neonatal, prepubertal and adult males, this effect being blocked by MK-801, a selective antagonist of NMDA receptors. In adult males, pulsatile GH secretion was abolished after administration of MK-801 and AP-5, antagonists of NMDA receptors. The stimulatory effect of NMDA on GH release was exerted at the hypothalamic level, since in vitro GH secretion was slightly inhibited in the presence of NMDA (0.5 mM). The increase in GH release after NMDA treatment cannot be explained through an increase in GHRH release, as the NMDA effect persisted in animals pretreated with GHRH antiserum and in those neonatally injected with mono- sodium glutamate, a drug that destroys GHRH neurons. In addition, NMDA-induced GH secretion was independent of testicular function since it remained after orchidectomy, testosterone replacement as well as after permanent damage of testicular function by neonatal administration of estrogens (500 µg on day 1 of life). We conclude that NMDA receptors play a physiological role stimulating GH secretion through a hypothalamic mechanism that is, at least partially, not GHRH-dependent, and is not modulated by testicular secretion.

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“…Primary cultures were prepared by mechanoenzymatic dissociation of fetal (day 17) Sprague Dawley rat hypothalami, as previously described (22), with necessary modifications. Briefly, cells were plated in 35-, 22-, or 16-mm plastic culture dishes (Falcon, Lincoln Park, NJ) for immunocytochemical analysis or to measure RNA or somatostatin content, respectively.…”

Section: Hypothalamic Cell Culturesmentioning

confidence: 99%

“…Immunoreactive somatostatin was determined by a sensitive RIA (22), carried out in the same tube to minimize peptide loss. Binding curves were run in tubes containing 20 l of evaporated 1N acetic acid.…”

Section: Somatostatin Riamentioning

confidence: 99%

Brain-Derived Neurotrophic Factor and Neurotrophin-3 Enhance Somatostatin Gene Expression through a Likely Direct Effect on Hypothalamic Somatostatin Neurons

Rage

1999

Endocrinology

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Although neurotrophins (NTs) have been extensively studied as neuronal survival factors in some areas of the central nervous system, little is known about their function or cellular targets in the hypothalamus. To understand their functional significance and sites of action on hypothalamic neurons, we examined the effects of their cognate ligands on neuropeptide content and messenger RNA (mRNA) expression in somatostatin neurons present in fetal rat hypothalamic cultures. Treatments were performed in defined insulinfree medium between days 6 and 8 of culture, since the maximal effects of NTs on somatostatin content and mRNA expression were observed after 48-h incubations. Brain-derived neurotrophic factor and NT-3, but not nerve growth factor, induced a dose-dependent increase in somatostatin content, which was influenced by plating density. The same treatment increased somatostatin mRNA and immunostaining intensity of somatostatin neurons, but had no effect on the number of these labeled neurons. The increased levels of somatostatin (peptide and mRNA) induced by NTs were not blocked by tetrodotoxin or by glutamate receptor antagonists, suggesting that endogenous neurotransmitters (e.g. glutamate) were not involved in these effects. In contrast, the stimulatory effects were completely blocked by K-252a, an inhibitor of tyrosine kinase (Trk) receptors, whereas the less active analog K-252b was ineffective. Double-labeling studies demonstrated that both TrkB or TrkC receptors were located on somatostatin neurons. Our results show that, in rat hypothalamic cultures, brain-derived neurotrophic factor, and NT-3 have a potent stimulatory effect on peptide synthesis in somatostatinergic neurons, likely through direct activation of TrkB and TrkC receptors. (Endocrinology 140: 909 -916, 1999) T HE NEUROTROPHIN (NT) family, a group of structurally related neurotrophic factors, all expressed in neurons of the central nervous system, includes nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), NT-3, NT-4/5, and NT-6 (1-6). Their biological effects are mediated by high-affinity tyrosine kinase (Trk) receptors, although all bind to a low-affinity receptor (p75) (7). NGF binds to TrkA receptors, BDNF preferentially activates Trk B receptors, whereas NT-3 mainly interacts with TrkC receptors but also stimulates TrkB receptors. Trk receptor activation initiates differentiation and survival processes in selected neuronal populations (8).Within the hypothalamus, moderate levels of BDNF, low levels of NGF, and no NT-3 messenger RNA (mRNA) have been localized in adult or newborn rats (9 -15). It is noteworthy that, besides the hippocampus, the hypothalamus is the region where the highest levels of BDNF protein are found in adult rat brain (16,17). In situ hybridization studies have shown that, in adult rats, TrkB and TrkC mRNA are expressed in most cells of all hypothalamic nuclei, whereas TrkA mRNA is rarely detected in the hypothalamus (13, 18). In RT-PCR studies, we detected the expression of the three...

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Glutamate Stimulates Somatostatin Release from Diencephalic Neurons in Primary Culture*

Cited by 44 publications

References 37 publications

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Glutamate Peripherally Administered Exerts Somatostatin‐Releasing Action in the Conscious Rat

Gonadal and Age-Related Influences on NMDA-Induced Growth Hormone Secretion in Male Rats

Brain-Derived Neurotrophic Factor and Neurotrophin-3 Enhance Somatostatin Gene Expression through a Likely Direct Effect on Hypothalamic Somatostatin Neurons

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