Drugs online research references
Neurosci Lett. 1994 Jul 4;175(1-2):161-5.
Muscarinic acetylcholine receptors on an identified motor neurone in the cockroach, Periplaneta americana.
Bai D, Sattelle DB.
AFRC Laboratory of Molecular Signalling, Department of Zoology, University of Cambridge, UK.
Muscarinic acetylcholine receptors (mAChRs) on the cell body of the fast coxal depressor motor neurone (Df) in the metathoracic ganglion of the cockroach Periplaneta americana were investigated using electrophysiological methods. Muscarinic agonists, arecoline and oxotremorine, induced dose-dependent depolarizations on motor neurone Df. McN-A-343, a vertebrate mAChR M1 subtype-selective agonist, failed to induce any responses when tested on the same neurone at concentrations of up to 1.0 x 10(-4) M. The order of effectiveness of a series of muscarinic antagonists on the mAChRs of motor neurone Df is as follows: scopolamine > atropine > pirenzepine. 4-DAMP (1.0 x 10(-5) M) had only a weak blocking effect and AF-DX 116 (1.0 x 10(-5) M) was completely inactive. The pharmacological profile of muscarinic responses on motor neurone Df reveals a novel type of insect mAChR.
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J Neurophysiol. 1993 Jun;69(6):1821-36.
Muscarinic acetylcholine receptors modulate the excitability of an identified insect motoneuron.
Trimmer BA, Weeks JC.
Department of Biology, University of Oregon, Eugene 97403.
1. With the use of an isolated, perfused ganglion preparation from the tobacco hornworm, Manduca sexta, we have examined the responses of an identified proleg retractor motoneuron (designated PPR) to trains of stimuli delivered to sensory branches of the ventral nerve (VN). 2. Trains of stimuli (50 Hz, 100 ms to 5 s) delivered to the proleg sensory nerve, VNA, caused PPR to depolarize and initiate a bout of spiking activity that outlasted the stimulus. A fast component of this response was due to monosynaptic input from planta hair sensory neurons, acting on nicotinic acetylcholine receptors (nAChRs). The fast response to VNA stimulation was abolished when the ganglion was treated with the nicotinic antagonist, mecamylamine, leaving a slow, long-lasting depolarization of PPR, which we have called the slow excitatory postsynaptic potential (sEPSP). 3. A sEPSP could be evoked by stimulation of all the major subbranches of VNA ipsilateral to PPR's cell body. Small sEPSPs were also evoked by stimulation of all but one of the major contralateral subbranches of VNA. 4. During a sEPSP the spike threshold of PPR became more negative. This increase in excitability was not correlated with changes in membrane potential measured at the cell body, and there was no detectable change in input resistance. We conclude that the spike-threshold change reflects either a depolarization electrically remote from the cell body, or a change in PPR's spike initiation properties that are not reflected in the membrane potential. 5. Both the sEPSP and the associated change in PPR's spike threshold were blocked by several muscarinic antagonists. Scopolamine was effective at concentrations > 2 x 10(-7) M, atropine at concentrations > 1 x 10(-6) M, and pirenzepine at 5 x 10(-5) M. 4-Diphenylacetoxy-N-methylpiperidine (4-DAMP), methoctramine, hexahydrosiladifenidol, and AF-DX 116 were all poor antagonists. 6. Bath application of the muscarinic agonist oxotremorine-M (oxo-M) at concentrations > 3 x 10(-7) M increased the spontaneous spiking activity of PPR and other proleg motoneurons. In PPR, this increased activity was accompanied by a small depolarization and a more negative spike threshold, both of which were inhibited by 1 x 10(-7) M scopolamine. 7. At concentrations > 6 x 10(-8) M, bath-applied oxo-M depolarized PPR even when spike activity in the ganglion was blocked with tetrodotoxin. During such spike blockage, pressure ejection of brief puffs of oxo-M into the neuropil evoked a long-lasting depolarization of PPR that resembled the sEPSP.(ABSTRACT TRUNCATED AT 400 WORDS)
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Acta Physiol Scand. 1986 Jul;127(3):335-42.
Presynaptic inhibition of acetylcholine release.
Aas P, Fonnum F.
High potassium (51 mM) has been shown to evoke release of acetylcholine ([3H]ACh and endogenous ACh) from cholinergic nerves in rat bronchial smooth muscle. The release of [3H]ACh was reduced by 85% when the Ca2+ concentration was changed from 2 to 0.1 mM. The veratridine-induced release was completely inhibited by tetrodotoxin, but tetrodotoxin did not reduce the potassium-evoked release. The muscarinic agonist, oxotremorine, reduced the potassium stimulated release of [3H]ACh, without affecting the basal release. In contrast, scopolamine substantially potentiated the potassium-evoked release. Adenosine had a dual effect in the rat bronchi. Adenosine inhibited the potassium-evoked release of [3H]ACh and this presynaptic effect of adenosine was antagonized by 8-phenyltheophylline. Adenosine also induced contraction of the bronchial smooth muscle and there was potentiation by adenosine of the ACh-induced contraction. The results indicate that cholinergic nerve terminals in the rat bronchi possess muscarinic receptors which inhibit the release of ACh. Adenosine may have analogous effects, e.g. presynaptic inhibition of transmitter release in addition to postsynaptic enhancement of bronchial smooth muscle contraction.
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