Functional evidence that acetylcholine release from Auerbach's plexus of guinea-pig ileum is modulated by α2A-adrenoceptor subtype

Blandizzi, Corrado; Dóda, M; Tarkovács, Gabor; Tacca, M. Del; Vizi, E.S.

doi:10.1016/0014-2999(91)90916-e

Cited by 27 publications

(11 citation statements)

References 9 publications

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“…1DMe is shown to reverse morphine-induced analgesia which was inhibited by naloxone in mouse (17) and rat (3). It is well known that norepinephrine inhibits the ACh release from the LMMP preparation of guinea pig ileum by activation of a2-receptors located on the presynaptic plasma membrane of cholinergic neurons (18). 1DMe did not affect the inhibitory effect of norepinephrine.…”

Section: Discussionmentioning

confidence: 78%

Effect of 1DMe, a Neuropeptide FF Analog, on Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum

Takeuchi

Fujita

Roumy

et al. 2001

Japanese Journal of Pharmacology

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ABSTRACT-Since neuropeptide FF (NPFF) is a putative neurotransmitter to exert anti-opioid activity, we examined the effects of [D-Tyr 1 , (NMe)Phe 3]neuropeptide FF (1DMe), a stable NPFF analog, on acetylcholine (ACh) release from a longitudinal muscle-myenteric plexus (LMMP) preparation of guinea pig ileum in which opioids were known to inhibit ACh release when muscarinic autoinhibition was not fully activated. In the presence of atropine, 1DMe increased spontaneous and electrical field stimulation (EFS)-evoked ACh release in a concentration-dependent manner. Naloxone also increased ACh release. The stimulatory effects of 1DMe and naloxone were not additive. In the absence of atropine, 1DMe did not affect ACh release. Morphine decreased spontaneous and EFS-evoked ACh release in the presence of 1 mM atropine. 1DMe as well as naloxone counteracted the inhibitory effects of morphine on EFS-evoked ACh release. The combination of 1DMe and naloxone was not more inhibitory than either drug alone. 1DMe had no appreciable effect on norepinephrine-induced inhibition of spontaneous and EFS-evoked ACh release. These results first demonstrated the effects of a NPFF analog on neurotransmitter release: 1DMe had a stimulatory effect on spontaneous and EFS-induced ACh release from the LMMP preparation of guinea pig ileum, probably by counteracting the inhibitory effect of endogenous opioids on ACh release.Keywords: Neuropeptide FF, Acetylcholine release, Morphine, Muscarinic autoinhibition, Myenteric plexusThe important role of an octapeptide neuropeptide FF (Phe-Leu-Phe-Gln-Pro-Gln-Arg-Phe-NH 2; NPFF) has been demonstrated in the central nervous system (1). NPFF exerts modulatory action on morphine-induced analgesia in rodents (2, 3). Namely, the intracerebroventricular administration of NPFF reverses morphine-induced analgesia in rats (1). NPFF antagonizes the modulation of Ca 2+ channels by mu-opioids in isolated rat spinal ganglion and dorsal raphe neurons (4, 5) and by nociceptin in rat dorsal raphe neurons (5). NPFF modulates the excitatory synaptic transmission through an interaction with presynaptic delta-opioid receptors in the pontine parabrachial nucleus in vitro (6). Although these results suggest that NPFF reverses the effect of morphine or endogenous opioids, the exact mechanism of the action of NPFF at the neuronal and cellular level remains unknown.It is well known that morphine has a marked inhibitory effect on the motility of the gastrointestinal tract in the human as well as experimental animals (7). The inhibitory effect of morphine is mainly due to reduction in acetylcholine (ACh) release from enteric cholinergic neurons (8, 9). In a previous report, we demonstrated that morphine inhibited ACh release from longitudinal muscle with myenteric plexus (LMMP) preparations of the guinea pig ileum when muscarinic autoinhibition was not fully activated (10). We also demonstrated that endogenous opioids are involved in the regulation of ACh release, because naloxone increases electrical field stimulation (EFS)-evoke...

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Section: Discussionmentioning

confidence: 78%

Effect of 1DMe, a Neuropeptide FF Analog, on Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum

Takeuchi

Fujita

Roumy

et al. 2001

Japanese Journal of Pharmacology

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“…These may largely correspond to postganglionic sympathetics originating in paraand prevertebral ganglia although intrinsic catecholaminergic enteric neurons were described in some regions of the gut (Furness and Costa 1974). a 2 -adrenoreceptors were found on cholinergic motor neurons of the ENS mediating inhibition of acetylcholine release and gastrointestinal transit in different species (Blandizzi et al 1991;Giaroni et al 1999b;Scheibner et al 2002). Human and rat vagal afferent neurons of nodose ganglia were described to possess b-adrenoceptors (Lawrence et al 1995).…”

Section: Close Contacts Of Vglut2-ir and Th/dbh-immunopositive Varicomentioning

confidence: 97%

Intraganglionic laminar endings and their relationships with neuronal and glial structures of myenteric ganglia in the esophagus of rat and mouse

Raab

Neuhuber

2000

Histochem Cell Biol

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Intraganglionic laminar endings (IGLEs) represent the only vagal mechanosensory terminals in the tunica muscularis of the esophagus and may be involved in local reflex control. We recently detected extensive though not complete colocalization of the vesicular glutamate transporter 2 (VGLUT2) with markers for IGLEs. To elucidate this colocalization mismatch, this study aimed at identifying markers for nitrergic, cholinergic, peptidergic, and adrenergic neurons and glial cells, which may colocalize with VGLUT2 outside of IGLEs. Confocal imaging revealed, besides substantial colocalization of VGLUT2 and substance P (SP), no other significant colocalizations of VGLUT2 and immunoreactivity for any of these markers within the same varicosities. However, we found close contacts of VGLUT2-positive structures to vesicular acetylcholine transporter, choline acetyltransferase, neuronal nitric oxide synthase, galanin, neuropeptide Y, and vasoactive intestinal peptide immunoreactive cell bodies and varicosities, as well as to glial cells. Neuronal perikarya were never positive for VGLUT2. Thus, VGLUT2 was almost exclusively found in IGLEs and may serve as a specific marker for them. In addition, many IGLEs also contained SP. The close contacts established by IGLEs to myenteric cell bodies, dendrites, and varicose fibers suggest that IGLEs modulate various types of enteric neurons and vice versa.

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“…Consequently, xylazine is added as an adjuvant. Work on the pharmacological effects of xylazine on guinea pig ileum has indicated that xylazine acts as an ␣2-adrenoceptor agonist ͑operating specifically at the ␣2 a subtype͒ which inhibits neurotensininduced release of acetylcholine ͑Blandizzi et al, 1991;Rakovska, 1993͒. Several researchers have suggested that the contralateral acoustic suppression effect produced by the efferents is mediated by cholinergic receptors of the MOC system ͑Puel and Rebillard, 1990;Kujawa et al, 1993͒.…”

Section: B Immediate Versus Delayed Effectsmentioning

confidence: 98%

Efferently mediated changes in the quadratic distortion product (f2−f1)

Chang

Norton

1997

The Journal of the Acoustical Society of America

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In this study, a preparation was developed which continuously monitored the f2−f1, 2 f1−f2, and 3f1−2 f2 distortion products in guinea pigs, in response to various contralateral and ipsilateral tones and broadband noise. A consistent decline over time in the quadratic distortion product, f2−f1, with continuous ipsilateral stimulation was observed, confirming previous findings by Kirk and Johnstone [Hearing Res. 67, 20–34 (1993)]. Broadband noise applied to the contralateral ear simultaneously increased both the magnitude and the rate of decline. This effect was shown for primaries across all frequencies tested (f2 from 2–16 kHz, f2/f1 ratio of 1.26), though a maximal effect was found for f2 of 4 kHz. Experiments using contralateral tones demonstrated a half-octave shift in the frequency specificity of this effect. A more “immediate” suppression effect on 2 f1−f2 (0.6 dB) was found in animals awakening from anesthesia, though this was even larger for f2−f1 (5.1 dB). Extended ipsilateral stimulation with contralateral noise results in completely diminishing f2−f1 to the noise floor. These findings suggest an adaptive process within the cochlea that may be modulated by efferent stimulation. A model relating the various even- and odd-order distortion products to outer hair cell receptor potentials is presented.

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Functional evidence that acetylcholine release from Auerbach's plexus of guinea-pig ileum is modulated by α2A-adrenoceptor subtype

Cited by 27 publications

References 9 publications

Effect of 1DMe, a Neuropeptide FF Analog, on Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum

Effect of 1DMe, a Neuropeptide FF Analog, on Acetylcholine Release From Myenteric Plexus of Guinea Pig Ileum

Intraganglionic laminar endings and their relationships with neuronal and glial structures of myenteric ganglia in the esophagus of rat and mouse

Efferently mediated changes in the quadratic distortion product (f2−f1)

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