Action of morphine on the neuro‐effector transmission in the guinea‐pig ileum and in the mouse vas deferens.

The effects of Leu‐enkephalin, Met‐enkephalin and morphine on excitatory junction potentials (e.j.ps) and inhibitory junction potentials (i.j.ps) elicited by stimulation of efferent parasympathetic nerves were studied in cats and rabbits, anaesthetized and in vitro. Enkephalins (0.008 mg/kg in vivo and 10−6m in vitro) enhanced e.j.p. amplitude in rabbit proximal colon and decreased it in rabbit distal colon and in cat colon. Enkephalins decreased i.j.p. amplitude in all the three models. Morphine (0.2 mg/kg in vivo and 10−6m in vitro) had the same effects as enkephalins on e.j.ps. In contrast, morphine decreased i.j.p. amplitude in rabbit proximal and distal colon and increased it in cat colon. Enkephalins and morphine induced (especially in the cat) spike activity which was potentiated by atropine (0.1 mg/kg in vivo or 10−6m in vitro). All the effects of enkephalins and morphine were antagonized by naloxone (0.2 mg/kg in vivo or 10−6m in vitro). These results suggest that the facilitatory effects of enkephalins and morphine on e.j.ps of rabbit proximal colon are due to the absence of opiate receptors on the excitatory nerve pathway and to a removal of inhibition by blockade of the non‐adrenergic, non‐cholinergic inhibitory pathway. Enkephalinergic intramural neurones may modulate the activation of either excitatory or inhibitory pathways in intramural reflexes.

Section: Action Of Opiates On Emg Activitysupporting

confidence: 59%

Section: Discussionmentioning

confidence: 99%

Section: Action Of Opiates On Junction Potentialsmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Enkephalins and Morphine on Spontaneous Electrical Activity and on Junction Potentials Elicited by Parasympathetic Nerve Stimulation in Cat and Rabbit Colon

Bouvier

Gonella

1982

“…For example, found that naloxone antagonized the reduction in ij.ps caused by exogenous opioid agonists in the canine duodenum, but opioid receptor antagonists did not significantly affect ij.ps. Similar results have been reported from experiments on guinea-pig intestine; naloxone had no effect on resting membrane potential or on junction potentials (Ito & Tajima, 1980). These findings also suggest that the concentrations of opioids released by brief stimuli are too low to affect transmitter release.…”

Section: Discussionsupporting

confidence: 78%

Regulation of neural responses in the canine pyloric sphincter by opioids

Bayguinov

Sanders

1993

1 Regulation of excitatory and inhibitory junction potentials (ej.ps and ij.ps) by opioid peptides was studied in isolated muscle strips from the pyloric sphincter of the dog.2 Methionine enkephalin (MetEnk; 1010 to 10-6 M) and enkephalin (DADLE; 10-" to 10-' M), a 6-specific opioid agonist, inhibited ij.ps and ej.ps recorded from cells in the myenteric and submucosal regions of the circular muscle layer. These compounds had no effect on resting potential or slow wave activity suggesting that the effects on junction potentials were not due to direct effects on smooth muscle cells. 3 MetEnk and DADLE caused similar effects on junction potentials in preparations in which the myenteric plexus was removed, suggesting that opioids inhibit pre-junctional effects on nerve fibres within the muscularis externa. 4 Inhibition of junction potentials by MetEnk and DADLE was blocked by approximately the same extent by naloxone (106 M) and ICI 174,864 (106M), a 6-specific antagonist. 5 MetEnk and DADLE blocked a portion of the ij.p. that was sensitive to arginine analogues; after treatment with N0-nitro-L-arginine methyl ester (L-NAME, 10-4 M), MetEnk and DADLE had no further effect on i.j.ps. These data suggest that opioids regulate nitric oxide-dependent neurotransmission.6 Naloxone (10-6 M) alone had no effect on ij.ps elicited by short trains of electrical field stimuli. 7 Ij.p. amplitude was reduced after a period of conditioning stimulation (2 min, 30 Hz, 30 V). Naloxone blocked the post-stimulation inhibition. Repetitive stimulation at high frequencies (30 Hz) resulted in sustained hyperpolarization. Naloxone increased the amplitude of the hyperpolarization responses elicited by high frequency stimulation. 8 These results show that ej.ps and ij.ps in the canine pylorus are inhibited by opioids. A portion of the inhibitory effects appears to be mediated via 6 receptors. 9 Although pyloric muscles are richly innervated by nerves containing opioid peptides, brief trains of stimuli do not appear to release concentrations of opioids that are effective in regulating junction potentials. Higher frequency stimulation (or longer durations of stimulation) appear to be necessary to release concentrations of opioids that are effective in modulating the amplitude of junction potentials.

“…About 15 cm of the terminal ileum was dissected out, and the lumen flushed with Krebs solution. Strips of longitudinal muscle together with the myenteric plexus (about 10mm in length and 1.0-4.0 mm in width) and strips of circular mus-cle together with the myenteric plexus (about 10 mm in length and 1.0-4.0 mm in width) were prepared for recording by microelectrodes and the double sucrose gap method, according to the procedures described by Ito & Tajima (1980). Modified Krebs solution of the following ionic concentration was used (mM); Na+ 137.4, K+ 5.9, Mg2+ 1.2, Ca2+2.5, Cl-134.0, H2P04-1.2, HCO3-15.5 and glucose 11.5.…”

Section: Methodsmentioning

confidence: 99%

The Effects of Substance P on Smooth Muscle Cells and on Neuro‐effector Transmission in the Guinea‐pig Ileum

Fujisawa¹,

Ito²

1982

The effects of substance P (SP) on the membrane and contractile properties of the smooth muscle cell, or on neuro‐effector transmission in the guinea‐pig ileum were observed by means of microelectrodes, double sucrose gap and tension recording. SP (10−13‐10−10 M) induced a phasic contraction of longitudinal muscle strips, but did not change the muscle tone of circular muscle strips, in concentrations up to 10−8 M. SP (1010‐10‐8M) evoked three different membrane responses in longitudinal muscle cells: (i) bursts of spike discharges with no significant change in the membrane potential and input membrane resistance; (ii) bursts of spike discharges with a small but clear depolarization of the membrane and increase in the input membrane resistance; (iii) slow waves with no change in the membrane potential. In the circular muscle cells, low concentrations of SP (< 10−8M) did not affect the membrane potential or the spikes, but SP (10−7M) increased the spike discharges with no significant change in the membrane potential. SP (10−10M) reduced the threshold depolarization required for the generation of action potentials with no change in membrane potential of the longitudinal muscle cells. Pretreatment with atropine (5 × 10−6M), tetrodotoxin (TTX 10−6M) or baclofen (4.7 × 10−6M) had no effect on the excitatory actions of SP on the smooth muscle cells of longitudinal and circular muscle strips. Excitatory actions of SP on the membrane potential or spike activities of longitudinal muscle cells were preserved in NaCl but not in Ca‐deficient solution. SP (10−10‐10−9M) enhanced the amplitude of the excitatory junction potentials (e.j.ps) evoked by electrical field stimulation in longitudinal muscle cells with no change in the membrane potential and input resistance. SP (10−10‐10−9M), however, did not change the amplitude of inhibitory junction potentials (i.j.ps) recorded from the circular muscle cells. These results indicate that SP in relatively low concentrations acts on both smooth muscle cells and on excitatory neuro‐effector transmission in the longitudinal muscle; the main site of the action of SP is probably the muscle membrane.