Release of [3H]acetylcholine from rat hippocampal slices: Effect of septal lesion and of graded concentrations of muscarinic agonists and antagonists

Szerb, John C.; Hadházy, P.; Dudar, J.D.

doi:10.1016/0006-8993(77)90995-7

Cited by 114 publications

(22 citation statements)

References 13 publications

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“…Our results therefore suggest that the ACh released from presynaptic nerves significantly inhibits further release of ACh. A similar effect has been described in the central nervous system using potassium evoked ACh release (Szerb, Hadhazy & Dudar, 1977) although this was not seen in more refined electrophysiological studies (Valentino & Dingledine, 1981). The results also imply that ACh released from presynaptic nerves acts on terminals of fibres which release another transmitter which causes the slow e.p.s.p., probably substance P. This finding is therefore closely analogous to that by Lundberg, Anggard, Emson, Fahrenkroug & Hokfelt (1981) that VIP released by repetitive stimulation of post-ganglionic parasympathetic fibres is greatly increased by atropine, suggesting inhibition by concomitantly released ACh.…”

Section: Discussionsupporting

confidence: 77%

Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Morita¹,

North²,

Tokimasa³

1982

The Journal of Physiology

105

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SUMMARY1. The effect of oxotremorine (300 pM to 30 nM) on synaptic transmission in isolated myenteric ganglia of guinea-pig ileum was investigated with intracellular recording techniques.2. These low concentrations ofoxotremorine had no effect on the resting membrane potentials or on the membrane conductance.3. Oxotremorine reduced the amplitude of the fast excitatory post-synaptic potential (e.p.s.p.) but did not reduce the amplitude of nicotinic responses to ionophoretic application of acetylcholine (ACh). This effect of oxotremorine on the fast e.p.s.p. was dose-dependent; the amplitude was reduced by about 45 % by 30 nM-oxotremorine.4. Non-cholinergic slow e.p.s.p.s evoked by repetitive presynaptic nerve stimulation were reduced in amplitude by oxotremorine.5. Hyoscine or atropine (1 nM) completely antagonized both these effects of oxotremorine (30 nM).6. Muscarinic antagonists alone increased the amplitude of second and subsequent fast e.p.s.p.s when these were evoked at intervals of 1 s, and increased the amplitude and duration of the slow e.p.s.p. evoked by repetitive presynaptic nerve stimulation.7. The results indicate that muscarinic receptor activation inhibits the release of the transmitters which mediate both the fast and the slow e.p.s.p.s and that this can occur with physiologically released ACh during repetitive presynaptic nerve activity.

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Section: Discussionsupporting

confidence: 77%

Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Morita¹,

North²,

Tokimasa³

1982

The Journal of Physiology

105

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“…refs. 26 and 27) exerted at autoreceptors on the terminals of septal afferents (28). As shown here, muscarinic antagonists produce substantial release in vivo, whereas muscarinic agonists inhibit both basal and evoked release by 30-40% (28).…”

Section: Discussionmentioning

confidence: 57%

“…The galanin-produced inhibition of the evoked release of AcCho is as potent as the muscarinic feedback inhibition. In vivo, galanin fully blocked the scopolamine-enhanced release, which was most due to disinhibition of the muscarinic feedback by antagonist (26)(27)(28). A basic difference between the inhibitory actions of muscarinic agonists and galanin seems to be that the former are also potent in altering basal AcCho outflow, whereas galanin seems to inhibit only the evoked release and in our …”

Section: Discussionmentioning

confidence: 88%

Galanin inhibits acetylcholine release in the ventral hippocampus of the rat: histochemical, autoradiographic, in vivo, and in vitro studies.

Fisone

Consolo

et al. 1987

Proc. Natl. Acad. Sci. U.S.A.

286

158

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A high density of galanin binding sites was found by using 1251-labeled galanin, iodinated by chloramine-T, followed by autoradiography in the ventral, but not in the dorsal, hippocampus of the rat. Lesions of the runbria and of the septum caused disappearance of a major population of these binding sites, suggesting that a large proportion of them is localized on cholinergic nerve terminals of septal afferents. Amersham. Scopolamine hydrobromide was purchased from Aldrich; physostigmine sulfate was from Sigma. All the other chemicals used were of analytical grade. Galanin antiserum was purchased from Peninsula Laboratories (San Carlos, CA). Secondary antisera were purchased from Boehringer Mannheim (Stockholm).Surgical Procedures. Four rats were anesthetized with chloral hydrate. Lesions of the dorsal hippocampal afferents were performed by the use of a retractable knife. The knife was lowered into the brain (coordinates in relation to bregma: AP, -1.4; ML, 3.0; DV, -4.0), and the blade was pushed out to the midline and retracted through the brain.Immunohistochemical, Histochemical, and Autoradiographic Analyses. Two rats were perfused through the ascending aorta with a picric acid/formalin mixture (14) for 6 min. The brains were postfixed in the same fixative, rinsed, and sectioned on a cryostat. Sections were incubated overnight at 4°C with galanin antiserum (1:400 dilution), rinsed, incubated with fluorescein isothiocyanate-conjugated secondary antibody (1:40 dilution) at 37°C for 30 min (15), rinsed, mounted, and examined with a fluorescence microscope. Some sections were processed for demonstration of AcChoE, either by the method of Karnovsky and Roots (16) or by immunohistochemistry using rabbit polyclonal antibody to AcChoE (17). For the autoradiographic analysis of 1251_ labeled galanin binding sites, the procedure of Young and Kuhar (18) was used. Briefly, pig galanin was iodinated with Na[1251] by the chloramine-T method and purified on an ion-exchange column. Rats were perfused with ice-cold Tyrode's solution, and the brain was sectioned on a cryostat, followed by incubation with 1251I-labeled galanin for 45 min at room temperature. Sections were rinsed, dried by a stream of cold air, exposed to formalin vapors, and covered by tritiumsensitive film (Ultrofilm, LKB, Stockholm). For control of nonspecific binding, unlabeled galanin (1 ,uM) was added to the incubation medium.In Vivo Experiments. In the in vivo release experiments, a thin dialysis fiber was implanted, essentially as described by Ungerstedt (19) and Benveniste et al. (20), in the hippocampi of anesthetized rats. A looped dialysis probe was implanted vertically into the ventral hippocampus of one side, while a straight dialysis probe was inserted through both dorsal hippocampi. The day after implantation, the dialysis tube was Abbreviations: AcCho, acetylcholine; AcChoE, acetylcholinesterase. §To whom reprint requests should be addressed. 7339The publication costs of this article were defrayed in part by page charge payment. This a...

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“…It should be borne in mind that the dopamine receptor within the striatum is known to be heterogeneous (Nagy et al 1978;Schwarcz et al 1978) while the muscarinic receptor also exists in pre-and postsynaptic regions (Szerb et al 1977;Aguilar et al 1979). The effect of various heavy metals upon the muscarinic has been previously reported (Aronstam and Eldefrawi 1979) and mercuric chloride was found to be much more effective in vitro than lead nitrate.…”

Section: Discussionmentioning

confidence: 95%

The inhibition of cerebral high affinity receptor sites by lead and mercury compounds

Bondy

Agrawal

1980

Arch Toxicol

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Abstract. The effect of various concentrations of several lead and mercury compounds upon various high affinity receptor sites within discrete brain regions has been measured. The specific binding of radioactive spiroperidol and quinuclidinyl benzilate to striatal and cortical membranes respectively, was much more severely inhibited in the presence of tri-n-butyl lead acetate than by lead acetate. This suggested that the hydrophobic organic lead derivative was able to interfere with receptor structure more readily than the lead acetate. On the other hand mercuric chloride was more effective in blocking these two neurotransmitter receptor sites than was the organic methylmercuric chloride. This implied that sulfhydryl groups may be within, or proximal to the allosteric binding site. The relative ineffectiveness of all heavy metal compounds studied in blocking the glycine, GABA or the diazepam receptors indicated that the mechanism of binding may not be similar with different receptor proteins. Since micromolar concentrations of some lead and mercury compounds suffice to severely inhibit neurotransmitter binding sites, such a direct interference with postsynaptic events may in part account for the neurological consequences of heavy metal poisoning.

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Release of [3H]acetylcholine from rat hippocampal slices: Effect of septal lesion and of graded concentrations of muscarinic agonists and antagonists

Cited by 114 publications

References 13 publications

Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea‐pig ileum.

Galanin inhibits acetylcholine release in the ventral hippocampus of the rat: histochemical, autoradiographic, in vivo, and in vitro studies.

The inhibition of cerebral high affinity receptor sites by lead and mercury compounds

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