Neuronal and subcellular localization of acetylcholine in the posterior pituitary of the rabbit

Lederis, K.; Livingston, A.

doi:10.1113/jphysiol.1970.sp009203

Cited by 26 publications

(7 citation statements)

References 21 publications

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“…These receptors, when activated, could facilitate VP release by in creasing the amount of calcium which enters the terminals in response to an action potential. The report that acetyl choline is primarily found in non-neurosecretory nerve terminals in the pituitary [20] is consistent with this hypo thesis, and axo-axonic synapses have been reported in neu rohypophysis [2]. Alternatively, acetylcholine could act presynaptically to inhibit release of an inhibitory substance such as dopamine.…”

Section: Discussionsupporting

confidence: 59%

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: 59%

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

Gregg¹

1985

Neuroendocrinology

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“…Thus, acetylcholine (ACh) has been reported in the neuro hypophysis of rabbits, oxen and rats [19], where it appears by subcellular fractionation to be localized to vesicles of nerve terminals [20]. Acetylcholinesterase (AChE) has been found similarly in glands of cats [17], rabbits [19], and cattle [18], where it appears histochemically to be localized to pars intermedia parenchymal cells in the rat and in addition in certain pituicytes of the posterior pituitary in cat and rabbit [36, 37], Another group [7] additionally found AChE reac tion product over some nerve terminals in pars intermedia.…”

Section: Abstract the Characteristics Of Atropine-sensitive Binding mentioning

confidence: 99%

Muscarinic Receptors in the Posterior Pituitary Gland

Tolliver¹,

Taylor²,

Burt³

1981

Neuroendocrinology

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The characteristics of atropine-sensitive binding of l-[³H]-quinuclidinyl benzilate ([³H]-QNB) to membrane re-suspensions of sheep posterior pituitary indicate that the binding sites represent muscarinic cholinergic receptors. Scat-chard plots of 6 saturation experiments showed a single class of binding sites, with an equilibrium dissociation constant of 16 ± 2 pM and a density equivalent to 1.8 ± 0.2 pmol/g wet weight of tissue. Kinetic analysis of 2 association and 3 dissociation curves yielded mean association and dissociation rate constants of 3.9 × 10⁸M^–1 min^–1 and 4.3 × 10^–3 min^–1, respectively. The binding had a detailed pharmacology for 12 drugs consistent with muscarinic receptor identification. In rat neurointermediate lobes, superior cervical ganglionectomy had no demonstrable effect on [³H]-QNB binding. The location(s) and functional role(s) of neurohypophyseal muscarinic receptors remain to be elucidated.

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“…Lederis & Livingston (1970) found that isolated neurohypophysial nerve-endings could be obtained at the same density of sucrose as isolated elementary granules, and to attempt to study the functional aspects of uptake or metabolism of a particle without establishing whether it was enclosed in a cell membrane could lead to erroneous conclusions.…”

Section: Discussionmentioning

confidence: 97%

“…They measured vasopressin and protein in this fraction and found that the hormone activity was low, but they did not measure acetylcholine in the gradient fractions. Lederis & Livingston (1968 examined small vesicles prepared from rabbit neurohypophysis in a way similar to that described by Bindler et al (1967), namely osmotic disruption of a preparation of neurosecretory nerve-endings followed by density gradient centrifugation, and found that 63 % of the acetylcholine in the gradient was localized in the small-vesicle fraction whilst the pituitary hormones were divided between the supernatant (36%) and elementary-granule fractions (36 %). Electron microscopy of these fractions confirmed that the acetylcholine-rich fraction consisted of small vesicles of 20-70 nm diameter and that the hormone-rich particulate fraction consisted mainly of elementary granules and occasional mito¬ chondria.…”

Section: Small Vesiclesmentioning

confidence: 97%