Autoradiographic localisation of benzodiazepine receptors in the rat pituitary gland

Brown, ChloëL.; Martin, Ian L.

doi:10.1016/0014-2999(84)90584-3

Cited by 34 publications

(18 citation statements)

References 4 publications

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“…Autoradiographic studies have revealed that dis crete areas exhibit a very high density of peripheral-type benzodiazepine sites within the CNS, e.g. olfactory bulb, pineal and pars nervosa of the pituitary [9,14,22], The posttransectional increase in the density of this binding site over the pars nervosa is consistent with previous suggestions [14], that is localized to pituicytes. Interestingly, an increase in peripheral-type benzodiazepine binding sites accompan ies kainic acid-induced gliosis in the striatum [26].…”

Section: Discussionsupporting

confidence: 78%

“…The peripheral-type benzodiazepine binding sites were labelled using a method described by Brown and Martin [9]. Each pituitary section was incubated for I h at 4°C with 250 pi of 2.0 nAf ['H|-Ro5-4864 in isotonic Tris buffer(50 mAf Tris, 190 mAf sucrose) pH 7.4.…”

Section: [3hjro5-4864mentioning

confidence: 99%

“…These [3H]-ligands were chosen because they bind to re ceptors which have been reported to regulate oxytocin or vasopressin release [21 ], or because high levels of binding to the pars nervosa have been reported [9,28]. This report con centrates on the pars nervosa, although for comparison and completeness data are included on the ligand binding site densities in the pars intermedia and pars distalis.…”

mentioning

confidence: 99%

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Autoradiographic Localization of Peripheral Benzodiazepine, Dihydroalprenolol and Arginine Vasopressin Binding Sites in the Pituitaries of Control, Stalk Transected and Brattleboro Rats

Sj¹,

Mr²,

Gp³

1986

Neuroendocrinology

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The autoradiographic distribution of [³H]arginine vasopressin, [³H]spiperone, [³H]GABA, [³H]dihydroalprenolol and the peripheral-type benzodiazepine ligand [³H]Ro5-4864 were examined in the rat pituitary before and after pituitary stalk transection. Stalk transection produced dramatic changes in the cellular architecture of the pars nervosa. Glial fibrillary acidic protein, an astrocyte marker reported in pituicytes, increased after stalk transection, whereas neurofilament, a marker for neuronal innervation, was lost. These structural changes demonstrated a successful stalk transection, permitting interpretation of changes in the densities of several [³H]-ligands over the three lobes. [³H]Ro5-4864 binding was markedly increased, suggesting that this site was located on the pituicytes. Conversely [³H]spiperone and [³H]arginine vasopressin binding density over the pars nervosa decreased. In the mutant diabetes insipidus rat (Brattleboro), which lacks pituitary vasopressin, [³H]arginine vasopressin binding was undetectable in the pars nervosa. [³H]dihydroalprenolol and [³H]GABA binding sites were unchanged by the lesion. These results are discussed in terms of the occurrence of functional acceptors on pituicytes and their possible role in neurohydrophyseal secretions.

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Section: Discussionsupporting

confidence: 78%

Section: [3hjro5-4864mentioning

confidence: 99%

mentioning

confidence: 99%

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Autoradiographic Localization of Peripheral Benzodiazepine, Dihydroalprenolol and Arginine Vasopressin Binding Sites in the Pituitaries of Control, Stalk Transected and Brattleboro Rats

Sj¹,

Mr²,

Gp³

1986

Neuroendocrinology

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“…The release of hormones from the anterior pituitary gland is controlled at the level of a gland by various neuro peptides as well as by several classical neurotransmitters such as dopamine [ 1 ], noradrenaline [2] and GABA [3][4][5][6][7], but not by excitatory amino acids [8], Receptor-binding studies have suggested the coexistence of both GABAr and GABAa [5,9] receptors, and the presence of benzodi azepine-binding sites [10,11] in the anterior pituitary gland. Electrophysiological studies on the GABAa recep tor in anterior pituitary cells are rare because of the small size and heterogeneity of the cell population.…”

Section: Introductionmentioning

confidence: 99%

Electrophysiological Characterization of GABA<sub>A</sub> Receptors in Anterior Pituitary Cells of Newborn Rats

Zemková¹,

Vanĕcek²,

Krůšek³

1995

Neuroendocrinology

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The γ-aminobutric acid (GABA)-ergic communication between the CNS and the anterior pituitary gland has been documented in numerous histochemical and biochemical studies but electrophysiological studies characterizing the GABA_A receptor in the anterior pituitary are still lacking. In the present report we studied the GABA-induced current responses in cultured cells from the anterior pituitary gland of 6- to 10-day-old rats using the patch-clamp technique in the whole cell configuration. Fast application of GABA (100 µM) induced membrane currents in 90% of cells in 2-day-old cultures. The EC₅₀ for GABA was 22.9 µM and the Hill coefficient was 1.8. The responses to GABA (10 µM) were inhibited by bicuculline (2 µM) to 14%, by picrotoxin (5 µM) to 21% and by zinc (10 µM) to 33%. Inhibition to 56% was observed with 6 µM strychnine. The GABA responses were sensitive to diazepam and pentobarbital. Half-maximal potentiation of responses to GABA (10 µM) was found with 1.0 µM diazepam and with 14.4 µM pentobarbital. The maximal potentiation of GABA responses was 222% for diazepam and 195% for pentobarbital. Pentobarbital (100 µM) did not induce any response in anterior pituitary cells in the absence of GABA. The application of GABA at concentrations 10 µM or higher, induced membrane currents that desensitized. Desensitization proceeded as a biexponential process with estimated fast and slow time constants which decreased with concentration. The responses to GABA (300 µM) desensitized to 93% with time constants of 1.4 and 5.3 s. Half-maximal desensitization was found with 13.4 µM GABA. The recovery of GABA responses from desensitization proceeded as a single-exponential process. Responses induced by 300 µM GABA, resensitized with a time constant of 20.8 s. We conclude that anterior pituitary cells possess GABA_A receptors which exhibit the same pharmacological characteristics and desensitization kinetics but lower sensitivity to GABA as compared to those present in CNS neurones.

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“…It is, however, also possible that chlordiaz¬ epoxide attenuates GH release by other mechanisms, since Gershengorn et al (1988) demonstrated that benzodiazepines could modulate voltage-sensitive cal¬ cium channels in GH3 pituitary cells at sites distinct from TRH receptors. Central-type benzodiazepinespecific receptors are present in the rat pituitary gland (Anderson & Mitchell, 1984;Brown & Martin, 1984) and may directly mediate chlordiazepoxide action. Benzodiazepine and/or TRH-binding sites in extrapituitary tissues, particularly the brain (Marangos et al 1982;Young & Kuhar, 1980) are also likely to participate in the regulation of GH secretion in vivo.…”

Section: Benzodiazepines In Vivomentioning

confidence: 99%

Benzodiazepine antagonism of thyrotrophin-releasing hormone receptors: biphasic actions on growth hormone secretion in domestic fowl

Harvey

1993

Journal of Endocrinology

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Benzodiazepines are pharmacological agents widely used for their anxiolytic and anticonvulsant properties. However, as these drugs are known to antagonize the binding and action of thyrotrophin-releasing hormone (TRH) in pituitary tissue, the possibility that they may modulate GH secretion was investigated in domestic fowl, in which TRH is a GH-releasing factor. Chlordiazepoxide (an antagonist of central-type benzodiazepine receptors) had no significant effect on the basal release of GH from incubated chicken pituitary glands, but at concentrations > 10 mumol/l chlordiazepoxide suppressed somatotroph responsiveness and sensitivity to TRH stimulation. At this concentration, chlordiazepoxide competitively displaced the binding of [3H]3-methyl-histidine2-TRH ([3H]MeTRH) to chicken pituitary membranes. The prior incubation of pituitary glands with chlordiazepoxide had no significant effect on the number of [3H]MeTRH-binding sites, which were also unaffected by the administration of chlordiazepoxide in vivo. However, contrary to its effects in vitro, chlordiazepoxide reduced basal GH secretion in vivo, whilst potentiating the GH response to systemic TRH challenge. These results demonstrate benzodiazepine antagonism of TRH-binding sites in domestic fowl and a biphasic modulation of GH secretion, which may be mediated through opposing actions at pituitary and central sites.

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Autoradiographic localisation of benzodiazepine receptors in the rat pituitary gland

Cited by 34 publications

References 4 publications

Autoradiographic Localization of Peripheral Benzodiazepine, Dihydroalprenolol and Arginine Vasopressin Binding Sites in the Pituitaries of Control, Stalk Transected and Brattleboro Rats

Autoradiographic Localization of Peripheral Benzodiazepine, Dihydroalprenolol and Arginine Vasopressin Binding Sites in the Pituitaries of Control, Stalk Transected and Brattleboro Rats

Electrophysiological Characterization of GABA<sub>A</sub> Receptors in Anterior Pituitary Cells of Newborn Rats

Benzodiazepine antagonism of thyrotrophin-releasing hormone receptors: biphasic actions on growth hormone secretion in domestic fowl

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