Muscarinic Receptors in the Posterior Pituitary Gland

Tolliver, James M.; Taylor, Richard; Burt, David R.

doi:10.1159/000123126

Cited by 14 publications

(8 citation statements)

References 17 publications

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“…The observation that this effect is blocked by atropine is consistent with the recent demonstration of specific mus carinic receptors in the neurointermediate lobe of both sheep and rats [36], It also confirms the report by Gosbee and Lederis [13] that direct injection of acetylcholine or carbachol into the neurohypophysis of water-loaded rats in vivo was followed by an apparent increase in VP release. Carbachol is a cholinergic-like agent which has more mus carinic than nicotinic activity [22],…”

Section: Discussionsupporting

confidence: 91%

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The Compartmentalized Hypothalamo-Neurohypophysial System: Evidence for a NeurohypophysialAction of Acetylcholine on Vasopressin Release

Gregg¹

1985

Neuroendocrinology

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A portion of medial basal hypothalamus containing the supraoptic nuclei with the neurohypophysis attached was organ cultured. Hypothalamus and neurohypophysis were maintained in separate compartments, and the intact infundibular stalk passed through a hole in a fluid-tight barrier which separated the two compartments. After 24, 48 and 72 h in culture, vasopressin (VP) release from the neurohypophysis was measured during a control hour and again during an immediately subsequent test hour. Test hour VP release was expressed as a percentage of control hour release. Test substances were added to either the pituitary or the hypothalamus compartment. Acetylcholine stimulated pituitary VP release both when added to hypothalamus (10^–5M) and when added directly to neural lobe (10^–6 M and above). Acetylcholine 10^–5 M and no effect when isolated neural lobes (severed from hypothalamus to culture) were similarly tested. Hexamethonium blocked the stimulation of pituitary VP release evoked by addition of acetylcholine to hypothalamus. However, in pituitary, atropine prevented the stimulatory effect of acetylcholine. Atropine had no effect on VP release from severed neural lobes. These data show that high concentrations of acetylcholine can stimulate VP release from pituitary both by a hypothalamic action and also by a direct effect in neural lobe. Further, a nicotinic cholinergic receptor mediates the action of acetylcholine in hypothalamus whereas a muscarinic cholinergic receptor is involved in the direct pituitary response to acetylcholine. Intact axonal connections between hypothalamus and pituitary are required in order for acetylcholine to stimulate VP release in neurohypophysis.

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Section: Discussionsupporting

confidence: 91%

“…choline acetyltransferase [12,16,19] and acetylcholinesterase [39], respectively. Specific muscarinic cholinergic binding sites have also been demon strated in the neurointermediate lobe [36]. In contrast to re…”

mentioning

confidence: 99%

The Compartmentalized Hypothalamo-Neurohypophysial System: Evidence for a NeurohypophysialAction of Acetylcholine on Vasopressin Release

Gregg¹

1985

Neuroendocrinology

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“…Only autoradiographic studies on the intact gland combined with binding studies on isolated cells can fully resolve this problem. The only evidence to date for pituitary muscarinic receptors is that of quisnuclididinyl-benzilate binding sites in the neurointermediate lobe of the rat (Tolliver, Taylor & Burt, 1981;Gregg, 1985) and pirenzepine-sensitive secretory responses to ACh in the frog (Louiset et al 1989). To our knowledge there are no conclusive reports of ligand binding studies aimed at detecting either nicotinic or muscarinic receptors on either freshly dispersed or cultured cells.…”

Section: Cholinergic Excitation Of Central Originmentioning

confidence: 99%

Nicotinic acetylcholine receptors in porcine hypophyseal intermediate lobe cells.

Zhang

Feltz

1990

The Journal of Physiology

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3. ACh-evoked responses were blocked by d-tubocurarine (d-TC), hexamethonium and mecamylamine, but were insensitive to a-bungarotoxin. These characteristics define a neuronal type of nicotinic receptors.4. The whole-cell current induced by ACh showed a strong inward rectification with no outward current being obtained. This phenomenon was observed when the intracellular ion is either sodium or caesium, and even when Ca2+ and Mg2+ were totally removed from the intracellular medium.5. ACh-gated channels in intermediate lobe cells were cation selective and were permeable to Na+ and Cs+. In Ca2+-free extracellular solution, single-channel conductances were much larger (46 pS) than in the presence of 2 mM-Ca2+ (26 pS).6. The possibility of an excitatory cholinergic control of intermediate lobe cells is discussed.

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“…Earlier studies demonstrated the presence of specific QNB binding sites in anterior and posterior pituitary of rat and sheep [2,8,12,16,19]. When tissue homogenates were used in these experiments, it was found that the anterior pi tuitary bound approximately 2-3 times as much QN B as the posterior pituitary.…”

Section: Discussionmentioning

confidence: 88%

“…Direct effects could result from ACh traveling in the portal circulation from the median eminence to the pituitary or from ACh re leased from nerve endings in the pituitary. While ACh is present in the median eminence [9] and all lobes of the pitui tary [1], choline acetyltransferase (ChAT), a specific marker for cholinergic neurons [10], is localized in the median emi nence [3,9] [2,8,12,16,19], Most of these reports indicate that the anterior lobe contains more muscarinic receptors than the posterior pituitary. The present investigation utilized an autoradiographic technique to provide a more detailed lo calization of muscarinic receptors in the rat pituitary.…”

mentioning

confidence: 99%

Autoradiographic Localization of Quinuclidinyl Benzilate Binding to Rat Pituitary Gland

Hoover¹,

Hancock²

1983

Neuroendocrinology

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The location of muscarinic receptors in the rat pituitary gland was examined with an autoradiographic technique. Slides containing 10 or 20 μm horizontal sections of tissue were incubated in a solution of 1 nM[³H]quinuclidinyl benzilate (QNB) in phosphate-buffered saline to label muscarinic receptors. Autoradiograms were produced by placing the slides into X-ray cassettes with tritium-sensitive film and processing the film 8–10 weeks later. Minimal binding occurred when sections were incubated in 1 nM[³H]QNB plus 1 μMatropine. Highest specific binding of QNB was found in the anterior and intermediate lobes along their border with the pituitary cleft. Patches of high binding were also seen penetrating the intermediate lobe and at the border between the intermediate and neural lobes. The remainder of the intermediate lobe had background density of autoradiographic grains. Moderate density of specific binding was found throughout the anterior lobe. Low specific binding occurred in the neural lobe.

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Muscarinic Receptors in the Posterior Pituitary Gland

Cited by 14 publications

References 17 publications

The Compartmentalized Hypothalamo-Neurohypophysial System: Evidence for a NeurohypophysialAction of Acetylcholine on Vasopressin Release

The Compartmentalized Hypothalamo-Neurohypophysial System: Evidence for a NeurohypophysialAction of Acetylcholine on Vasopressin Release

Nicotinic acetylcholine receptors in porcine hypophyseal intermediate lobe cells.

Autoradiographic Localization of Quinuclidinyl Benzilate Binding to Rat Pituitary Gland

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