Divergent Effects of Acute Depolarization on Somatostatin Release and Protein Synthesis in Cultured Fetal and Neonatal Rat Brain Cells

Frailes, Maria Teresa de los; Cacicedo, Lucinda; Lorenzo, María Jesús López; Sánchez‐Franco, Franco

doi:10.1111/j.1471-4159.1989.tb09176.x

Cited by 17 publications

(8 citation statements)

References 26 publications

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“…This inhibition was completely abolished with the blockade of SS with antiserum, thus indicating that the inhibitory effect was exerted by SS. This inhibition could be due to the fact that SS secretion by fetal hypothalamic cells in this in vitro model is 10 times greater than that of GHRH (11,14).…”

Section: Discussionmentioning

confidence: 95%

“…After 5 h of incubation, defined medium was replaced by Neurobasal medium. Experiments were performed after 15 days in vitro, which is when we have observed that high levels of SS secretion and the peak of GHRH secretion occur (11,14). Medium was changed every 3-4 days.…”

Section: Methodsmentioning

confidence: 99%

“…ronment, we established a model of coculture of pituitary and fetal hypothalamic cells, where interactions between the two cellular populations and certain treatments could be studied. To this end, hypothalamic cells from 17-day-old embryos were cultured for 15 days, the time at which we had observed the peak of GHRH and high levels of SS secretion (11,14).…”

Section: Igf-i and Igf-i-r Gene Expression In The Hypothalamus Of Agimentioning

confidence: 99%

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Insights into a role of GH secretagogues in reversing the age-related decline in the GH/IGF-I axis

Frutos¹,

Cacicedo²,

Fernández³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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Growth hormone (GH) secretion and serum insulin-like growth factor-I (IGF-I) decline with aging. This study addresses the role played by the hypothalamic regulators in the aging GH decline and investigates the mechanisms through which growth hormone secretagogues (GHS) activate GH secretion in the aging rats. Two groups of male Wistar rats were studied: young-adult (3 mo) and old (24 mo). Hypothalamic growth hormone-releasing hormone (GHRH) mRNA and immunoreactive (IR) GHRH dramatically decreased (P Ͻ 0.01 and P Ͻ 0.001) in the old rats, as did median eminence IR-GHRH. Decreases of hypothalamic IR-somatostatin (SS; P Ͻ 0.001) and SS mRNA (P Ͻ 0.01), and median eminence IR-SS were found in old rats as were GHS receptor and IGF-I mRNA (P Ͻ 0.01 and P Ͻ 0.05). Hypothalamic IGF-I receptor mRNA and protein were unmodified. Both young and old pituitary cells, cultured alone or cocultured with fetal hypothalamic cells, responded to ghrelin. Only in the presence of fetal hypothalamic cells did ghrelin elevate the age-related decrease of GH secretion to within normal adult range. In old rats, growth hormone-releasing peptide-6 returned the levels of GH and IGF-I secretion and liver IGF-I mRNA, and partially restored the lower pituitary IR-GH and GH mRNA levels to those of young untreated rats. These results suggest that the aging GH decline may result from decreased GHRH function rather than from increased SS action. The reduction of hypothalamic GHS-R gene expression might impair the action of ghrelin on GH release. The role of IGF-I is not altered. The aging GH/IGF-I axis decline could be rejuvenated by GHS treatment. growth hormone; ghrelin; growth hormone-releasing peptide-6; growth hormone secretagogue; aging; growth hormone decline GROWTH HORMONE (GH) secretion in humans and rats declines progressively with aging (17, 41) and results in lower serum insulin-like growth factor-I (IGF-I) levels.Early studies in elderly humans showed an age-associated attenuation of GH pulse amplitude and GH secretion in response to several stimuli, including insulin-induced hypoglycemia and arginine administration (32,43). Subsequent studies revealed a decrease in plasma IGF-I parallel to the decline in GH pulses (51). The studies in humans have been confirmed in experimental animals, and it is now evident that the decline in high-amplitude pulsatile GH release and plasma IGF-I concentrations is one of the best characterized events that occur with aging in humans and rats (61). Thus the aging rat is a model of relative or partial GH deficiency and consequently is suitable for studying the mechanisms of this alteration.GH has a broad range of actions and therefore its diminished secretion rate has clinical significance and may be responsible for the generalized catabolic state, functional alterations, cognitive impairment, and decreased neuroprotection associated with normal aging. In elderly adults, with or without GH defect, GH increases IGF-I, the lean-to-fat ratio, muscle strength, and skin thickness and reduces total body fat cont...

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Section: Discussionmentioning

confidence: 95%

Section: Methodsmentioning

confidence: 99%

Section: Igf-i and Igf-i-r Gene Expression In The Hypothalamus Of Agimentioning

confidence: 99%

See 1 more Smart Citation

Insights into a role of GH secretagogues in reversing the age-related decline in the GH/IGF-I axis

Frutos¹,

Cacicedo²,

Fernández³

et al. 2007

American Journal of Physiology-Endocrinology and Metabolism

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“…The preparation of primary long-term dispersed cell cultures from fetal rat cerebral cortices was carried out as previously de scribed [22], Briefly, on the 17th day of gestation fetal Wistar rats were removed from their mother under ether anesthesia via an ab dominal incision. Cortical regions of the brain were dissected in PBS.…”

Section: Cell Culturementioning

confidence: 99%

Thyroid Hormones Regulate Release and Content of Vasoactive Intestinal Peptide in Cultured Fetal Cerebral Cortical Cells

Lorenzo¹,

Sánchez‐Franco²,

Frailes³

et al. 1992

Neuroendocrinology

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The effects of thyroid hormones (TH) on brain immunoreactive-vasoactive intestinal peptide (IR-VIP) secretion and content in cultured fetal rat cortical cells were studied. Cerebral cortical cells were maintained as monolayer cultures for 14-18 days. T₃ or T₄ (10^–7M) caused a time-dependent decrease in total IR-VIP. Significant suppression was observed following treatment periods of 6 h or longer (24 and 48 h). Depending on the length of time cells had been deprived of TH prior to the addition of exogenous T₃ or T₄, these two thyroid hormones had different effects on IR-VIP accumulation. Both T₃ and T₄ caused a dose-dependent suppression or IR-VIP accumulation when there was no deprivation period or when it lasted 4 h. However, a biphasic effect was observed when cells were deprived of TH for 17 and 24 h: low doses of T3 or T₄ (from 10^–12 to 10^–10M) significantly increased (p < 0.05) total IR-VIP, while high T₃ or T₄ doses (10^–8 and 10^–7M) caused a significant decrease (p < 0.01). The TH action was furthermore shown to be reversible. After T₃ (10^–7M) removal and subsequent incubation in serum-free medium for 6, 24 and 48 h, T₃-treated and control cells exhibited similar levels of IR-VIP release and content. At this time, a new exposure to T₃ (10^–7M) again had a suppressive effect. These findings suggest that at this time of brain development, VIP release and content in cerebral cortical cells is affected by TH in a time- and dose-related manner, and furthermore this seems to be reversible.

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“…In this study, we sought to investigate the effect of GRF on SS regulation by fetal rat cerebral cortical and hypothalamic cells in culture, a system previously shown to be useful in the study of neuropeptide regulation [13,[15][16][17], In contrast with previous in vitro studies, where the interactions between neuropeptides were described on a pharmacological basis, in this work we have exam ined the possible physiological role of endogenous GRF in the control of locally produced SS by adding purified anti-GRF immunoglobulins G (IgG) to cultured neurons.…”

mentioning

confidence: 99%

Role of Locally Produced Growth Hormone-Releasing Factor in Somatostatin Regulation by Fetal Rat Brain Cells in Culture

Frailes¹,

Cacicedo²,

Fernandez³

et al. 1992

Neuroendocrinology

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To determine the possible physiological role of endogenous growth hormone-releasing factor (GRF) in the neuronal content and release of cerebral somatostatin (SS), we studied the effect of endogenous GRF blockade on the immunoreactive SS (IR-SS) content of cells and media in fetal rat cerebral cortical and hypothalamic cells in culture. Cells were cultured in minimum essential medium (MEM) with 10% fetal calf serum and 10% horse serum. After 7–10 days in vitro, media were replaced with MEM without sera containing anti-GRF immunoglobulins G (IgG) for 1, 5 or 24 h. Controls were incubated with equal amounts of IgG from normal rabbit serum (NRS). In another group of experiments, cells were incubated with GRF (10^–11 to 10^–7M) for 1 or 24 h. Long-term exposure (24 h) to anti-GRF IgG resulted in decreased media and intracellular IR-SS content, in both cerebral cortical and hypothalamic cells. 24 h treatment with GRF caused a dose-dependent increase in the IR-SS content of cells and media, the stimulatory action being abolished by the addition of anti-GRF to plates containing 10^–7M GRF. On the contrary, when cells were exposed to anti-GRF IgG for 1 h, IR-SS increased in the media as compared to the control group. Short-term incubation (1 h) with GRF (10^–9 to 10^–7M) resulted in a dose-dependent inhibition of IR-SS content in the cells and media. This inhibitory action was partially prevented by the addition of anti-GRF to plates containing 10^–7M GRF. Patterns of IR-SS cell and media content were qualitatively similar in both cerebral cortical and hypothalamic cells. In plates containing anti-GRF, the accumulation of IR-SS in the cells and media was lower than in the control groups (IgG from NRS) throughout the incubation time.

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Divergent Effects of Acute Depolarization on Somatostatin Release and Protein Synthesis in Cultured Fetal and Neonatal Rat Brain Cells

Cited by 17 publications

References 26 publications

Insights into a role of GH secretagogues in reversing the age-related decline in the GH/IGF-I axis

Insights into a role of GH secretagogues in reversing the age-related decline in the GH/IGF-I axis

Thyroid Hormones Regulate Release and Content of Vasoactive Intestinal Peptide in Cultured Fetal Cerebral Cortical Cells

Role of Locally Produced Growth Hormone-Releasing Factor in Somatostatin Regulation by Fetal Rat Brain Cells in Culture

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