Slowly-developing depolarization of neurones in the guinea-pig inferior mesenteric ganglion following repetitive stimulation of the preganglionic nerves

Neild, T O

doi:10.1016/0006-8993(78)90457-2

Cited by 71 publications

(45 citation statements)

References 19 publications

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“…In this respect, there is evidence that in sympathetic neurones, two structurally unrelated peptides, luteinizing hormone-releasing hormone and angiotensin II suppress a voltagesensitive K+ current that is also inactivated by muscarine (Adams & Brown, 1980;Brown, Constanti & Marsh, 1980). The present finding that both an increase and decrease of membrane resistance can be elicited by substance P in neurones of the inferior mesenteric ganglia of the guinea-pig is important as these effects are analogous to the membrane resistance changes associated with the non-cholinergic depolarizing potential elicited by repetitive preganglionic stimulation in these neurones (Neild, 1978;Dun & Karczmar, 1979;Konishi et al 1979). This evidence, together with previous findings (Dun & Karczmar, 1979;Konishi et al 1979) provide further support for the hypothesis that substance P may be the transmitter mediating the non-cholinergic potential in sympathetic neurones of the guinea-pig.…”

Section: Discussionmentioning

confidence: 52%

Effects of substance P on neurones of the inferior mesenteric ganglia of the guinea‐pig

Dun

Minota

1981

The Journal of Physiology

110

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SUMMARY1. The membrane effects of substance P on neurones of isolated inferior mesenteric ganglia and the underlying ionic mechanisms were investigated by means of intracellular recording techniques.2. When applied to the neurones by superfusion, substance P (0 5 /M) caused a membrane depolarization; in a few neurones, the depolarization was preceded by a small hyperpolarization. Substance P effects were not altered in a low Ca2+/high Mg2+ solution or in a solution containing D-tubocurarine and atropine.3. When the membrane potential was clamped manually at the resting level between -50 and -60 mV, substance P caused, in about an equal number of neurones, a slight to moderate decrease and also increase of membrane resistance; a brief increase occurred prior to the decrease of membrane resistance.4. In neurones with high resting membrane potential (>-70 mV), substance P elicited a large depolarization accompanied by a marked increase in membrane resistance; the latter was probably due to anomalous rectification.5. Conditioning hyperpolarization of the membrane close to the level of EK increased and decreased substance P-induced depolarization in eleven and two neurones, respectively. 6. Substitution of external Na+ with an equimolar amount of either sucrose or Tris buffer markedly attenuated the depolarizing effect of substance P.7. The substance P-induced depolarization was diminished in a high K+ (10 mM) solution, and it could be augmented when membrane was hyperpolarized to EK. On the other hand, the effect of substance P was not appreciably affected in a low Clsolution. 8. It is concluded that substance P depolarizes the sympathetic neurones by increasing and decreasing membrane permeability to Na+ and K+, respectively, and that the concomitant membrane resistance change depends on interaction of GNa activation and GK inactivation.9. The possibility that substance P is the transmitter mediating the non-cholinergic slow excitatory potential elicited by repetitive preganglionic stimulation in the neurones of the inferior mesenteric ganglia is suggested.

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Section: Discussionmentioning

confidence: 52%

Effects of substance P on neurones of the inferior mesenteric ganglia of the guinea‐pig

Dun

Minota

1981

The Journal of Physiology

110

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“…Nishi & Koketsu (1968a) first discovered a slow, non-cholinergic synaptic potential in sympathetic ganglia of the frog and named it the late slow excitatory post-synaptic potential (late slow e.p.s.p.). Similar slow, non-cholinergic potentials have since been found in several autonomic ganglia, including superior cervical ganglia of dogs and cats (Alkadhi & McIssac, 1973;Dun, Nishi & Karczmar, 1978) and myenteric plexuses and inferior mesenteric ganglia of guinea-pigs (Katayama & North, 1978;Neild, 1978). Recent experiments indicate that these slow synaptic potentials may be mediated by peptides (Dun et al 1978;Katayama & North, 1978; Konishi, Tsunoo & Otsuka, 1979).…”

Section: Introductionmentioning

confidence: 67%

Peptidergic transmission in sympathetic ganglia of the frog.

Jan¹,

Jan²

1982

The Journal of Physiology

370

226

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SUMMARY1. A slow synaptic potential recorded in neurones of sympathetic ganglia of bullfrog, the late slow e.p.s.p., is probably mediated by a peptide resembling luteinizing hormone-releasing hormone (LHRH), because (1) a LHRH-like peptide is contained in preganglionic nerve terminals and is released upon nerve stimulation, (2) application of LHRH to ganglion cells mimics the effects of the natural transmitter for the late slow e.p.s.p., and (3) the pharmacological properties of LHRH and the natural transmitter for the late slow e.p.s.p. are similar.2. Neurones in frog sympathetic ganglia are also depolarized by substance P. The

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“…After perfusion with collagenase, the ganglia were perfused with Krebs-Ringer buffer containing ,l-alanine (1 mM), an inhibitor of glial cell GABA uptake (Schon & Kelly, 1975) and amino-oxyacetic acid (AOAA, 10 uM), an inhibitor of GABA breakdown (Neal & Starr, 1973 (Nield, 1978).…”

Section: Methodsmentioning

confidence: 99%

Enteric GABA‐containing nerves projecting to the guinea‐pig inferior mesenteric ganglion modulate acetylcholine release.

Parkman

Stapelfeldt

Williams

et al. 1993

The Journal of Physiology

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Slowly-developing depolarization of neurones in the guinea-pig inferior mesenteric ganglion following repetitive stimulation of the preganglionic nerves

Cited by 71 publications

References 19 publications

Effects of substance P on neurones of the inferior mesenteric ganglia of the guinea‐pig

Effects of substance P on neurones of the inferior mesenteric ganglia of the guinea‐pig

Peptidergic transmission in sympathetic ganglia of the frog.

Enteric GABA‐containing nerves projecting to the guinea‐pig inferior mesenteric ganglion modulate acetylcholine release.

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