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Y 2 ‐receptor‐mediated selective inhibition of slow, inhibitory postsynaptic potential in submucous neurones of guinea‐pig caecum
Author(s) -
Cunningham Shauna M.C.,
Mihara Satoshi,
Lees Gordon M.
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb17075.x
Subject(s) - inhibitory postsynaptic potential , postsynaptic potential , caecum , guinea pig , submucous plexus , excitatory postsynaptic potential , neuroscience , biology , chemistry , anatomy , receptor , endocrinology , medicine , biochemistry , myenteric plexus , immunohistochemistry , immunology
1 The subtype of neuropeptide Y receptor mediating the selective inhibition of the slow inhibitory postsynaptic potential (i.p.s.p.) of submucous neurones in guinea‐pig caecum was investigated by use of conventional intracellular electrophysiological recording techniques. 2 Neuropeptide Y (NPY) (1‐300nM) was found to depress or abolish reversibly the slow i.p.s.p. evoked by focal stimulation of internodal fibre tracts. At low concentrations (1‐30nM), a reduction in the duration of the slow i.p.s.p. was often apparent before any inhibition of the amplitude of this synaptic potential. 3 These inhibitory effects of NPY were mimicked by peptide YY (PYY; 0.3–100 n m ), NPY13‐36 (1–300 n m ) and NPY22‐36 (10‐100nM); [Leu 31 , Pro 34 ]NPY ([Pro 34 ]NPY) and bovine pancreatic polypeptide (bPP) were without pre‐ or postsynaptic effects at concentrations of up to 300 n m . The IC 50 s.e. mean values for PYY, NPY, and NPY13‐36 were 2.7 ± 0.3, 7.8 ± 2.1 and 30 ± 4.8nM, respectively, and were significantly different from each other. Thus, the apparent rank order of potency was PYY>NPY>NPY13‐36>[Pro 34 ]NPY and bPP. 4 In concentrations of up to 300 n m , NPY and its analogues had no depressant effects on the active and passive properties of the impaled neurone and did not affect the amplitude or duration of either cholinergic fast synaptic potentials or non‐cholinergic, slow excitatory postsynaptic potentials (e.p.s.ps). Furthermore, none of these peptides altered the amplitude or time‐course of changes in membrane potential induced by focal application of acetylcholine or noradrenaline. 5 It is, therefore, concluded that the selective inhibition of the slow i.p.s.p. is mediated by Y 2 ‐receptors, located presynaptically on noradrenergic nerve terminals.