Time- and dose-dependent responses of brain histamine to intracerebroventricular and intraperitoneal administrations of growth hormone-releasing factor (GRF1-44).

Cacabelos, Ramón; Yamatodani, Atsushi; Fukui, Hirokazu; Niigawa, Hisayoshi; Miyake, Akira; Watanabe, Takehiko; Nishimura, Tsuyoshi; Wada, Hiroshi

doi:10.1620/tjem.151.429

Cited by 5 publications

(6 citation statements)

References 38 publications

(28 reference statements)

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“…While some recent reports give support to the idea that HA may be involved in controlling the secretion of GH possibly by modifying the secretion of GRF and SS (Hall et al 1984), others denied it (Kakucska and Makara 1983; see Tuomisto and Mannisto 1985, for review). Nevertheless, what seems to be clear according to our own data is that GRF (Cacabelos et al 1987c) and SS play antagonistic roles on brain HA. In consequence, it is likely that HA somehow influences the STS following the criteria that we have previously established.…”

Section: Discussionmentioning

confidence: 60%

“…This effect seems to be opposite to that of GRF under similar experimental conditions (Cacabelos et al 1987c). Since SS contributes to multiple effects in the CNS (Reichlin 1983;Epelbaum 1986), its interaction with the histaminergic system may be multifactorial, affecting diverse central HA functions (Cacabelos 1984b;Wada et al 1985).…”

Section: Discussionmentioning

confidence: 80%

“…Hence, it is pertinent to investigate the effects of both GRF and SS on HA in the brain to clarify the interactions of HA with the STS. In this regard, we have first reported that GRF induces time-and dose-dependent responses in brain HA (Cacabelos et al 1987c), these responses being more specific in areas of the hypothalamo-hypophyseal system than in any other brain regions. However, the effect of SS on brain HA has never been reported.…”

mentioning

confidence: 99%

“…Moreover, to prove that HA is a modulator of the neuroendocrine system (Roberts and Calcutt 1983 ;Cacabelos 1984a, b), we suggest that this biogenic amine must fulfil some additional criteria : (a) the administration of its precursor, L-histidine, at a dose sufficient to increase the levels of endogenous HA in the brain, should induce specific changes in the neuroendocrine pathways modulated by HA ; (b) the administration of HA at a dose close to its physiological concentration in the hypothalamus should produce time-dependent changes in specific neuroendocrine substances ; (c) the administration of specific inhibitors of the synthesis of HA, such as alphafluoromethylhistidine (Kollonitsch et al 1978), should alter the normal functioning of the HA-modulated neuroendocrine pathways ; (d) the administration of those presumptive neuropeptides influenced by neuronal HA should modify the levels of hypothalamic HA in a time-and dose-related manner ; and (e) the manipulation of a given neuroendocrine axis should induce differential changes in the neurochemical dynamics of neuronal HA and its receptors. Some of these criteria were partially fulfilled by HA in the corticotropinergic , vasopressinergic (Cacabelos et al 1987d), gonadotropinergic (Cacabelos et al 1986), and somatotropinergic systems (Cacabelos et al 1987c). …”

mentioning

confidence: 99%

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Somatostatin-induced histamine response in the rat central nervous system.

Cacabelos

Niigawa

Nishimura

et al. 1987

Tohoku J. Exp. Med.

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Section: Discussionmentioning

confidence: 60%

Section: Discussionmentioning

confidence: 80%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Somatostatin-induced histamine response in the rat central nervous system.

Cacabelos

Niigawa

Nishimura

et al. 1987

Tohoku J. Exp. Med.

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“…Whereas intracerebroventricular (icv) GRF tended to increase the levels of HA in all areas of the hypothalamo-hypophyseal system, ip GRF reduced the levels of HA in the hypothalamus (17).…”

mentioning

confidence: 99%

Antagonistic Effects of Growth Hormone-Releasing Factor and Somatostatin on Brain Histamine*

Cacabelos

Niigawa²,

Yamatodani³

et al. 1988

Endocrinology

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Studies on the morphological distribution of histamine (HA)-secreting neurons and their hypothalamic projections suggest that HA may play a key role in regulating neuroendocrine functions, some of which have been recently elucidated. To investigate possible interactions between the somatotropinergic and histaminergic systems in the brain, the effects of GRF-44 [0.1-10 micrograms intracerebroventricular (icv)] and somatostatin (SS-14; 0.1-10 micrograms, icv) on HA in five different parts of the hypothalamo-hypophyseal system, and in the hippocampus and frontal cortex, were studied using a highly sensitive HPLC system for determination of HA. GRF-44 (1 microgram, icv) elicited significant (P less than 0.005) increases in the concentration of HA in the anterior hypothalamus, posterior hypothalamus, median eminence, adenohypophysis, neurohypophysis, frontal cortex, and, to a lesser extent, in the hippocampus, after a clear time-dependent pattern with maxima 15 min after injection. In contrast, SS-14 (1 microgram, icv) significantly (P less than 0.005) decreased the levels of HA in all areas studied, except in the neurohypophysis. The SS-induced HA levels reached minima 30 min after injection. The antagonistic effects of GRF-44 and SS-14 on the release of brain HA were dose dependent, showing an inverse linear correlation within the range 0.1-10 micrograms in the anterior hypothalamus (r = -0.59) and posterior hypothalamus (r = -0.75). Responses of HA to GRF-44 and SS-14 (range: 0.1-10 micrograms) also exhibited an inverse linear correlation in the median eminence (r = -0.90) and adenohypophysis (r = -0.58), while in the hippocampus and frontal cortex the antagonistic effects of GRF and SS displayed an inverse curvilinear correlation. SS-14 ED50 values ranged from 0.6 to 1.75 nmol with Emax of 0.65-6.10 nmol. GRF-44 ED50 values ranged from 0.02-0.3 nmol and the Emax values oscillated between 0.2 and 1.90 nmol in the regions studied. The greatest responses of HA to GRF-44 and SS-14 were obtained in the hypothalamo-hypophyseal system. Although brain HA is present in both the neuronal and the mast cell compartments, changes induced in the concentration of HA by centrally administered GRF-44 and SS-14 appear to occur mostly in the neuronal compartment. Therefore, it is likely that the somatotropinergic and histaminergic systems reciprocally interact at the central level to regulate still unknown neuroendocrine functions.

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