Opioid Receptors Undergo Axonal Flow

Young, W. Scott; Wamsley, James K.; Zarbin, M. A.; Kuhar, MJ

doi:10.1126/science.6158097

Cited by 243 publications

(40 citation statements)

References 20 publications

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“…Many of these receptors were characterized initially in the dorsal spinal cord (Yaksh, 1999), but some receptors that are synthesized in the cell body of dorsal root ganglia cells and transported centrally to reside presynaptically on primary afferent neurons also are transported peripherally can be demonstrated following ligation of the nerve and detection of an accumulation of receptors proximal and distal to the ligature. For example, -, ␦-, -opioid (Young et al, 1980;Laudron, 1984;Stein et al, 1990;Hassan et al, 1993), and cannabinoid receptors (Hohmann and Herkenham, 1999b) have been detected in this manner. Other inhibitory receptors, such as ␥-aminobutyric acid A (GABA A ) receptors , have been visualized directly on peripheral nerve profiles.…”

Section: Peripheral Pain Signalingmentioning

confidence: 95%

Topical and Peripherally Acting Analgesics

2003

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Section: Peripheral Pain Signalingmentioning

confidence: 95%

Topical and Peripherally Acting Analgesics

2003

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“…Thus, only adrenoceptors cause presynaptic inhibition in submucosal neurones. We cannot determine whether somatostatin or opiate receptors are present at presynaptic sites but there is ample evidence that many receptors, including opiate receptors, undergo axonal transport to nerve terminals in vagal and other peripheral nerves (Young, Wamsley, Zarbin & Kuhar, 1980). All submucosal neurones which show a postsynaptic response to noradrenaline (i.e.…”

Section: Expression Of Adrenroceptors At Presynaptic Sitesmentioning

confidence: 99%

Mechanisms underlying presynaptic inhibition through alpha 2‐adrenoceptors in guinea‐pig submucosal neurones.

Shen

Surprenant

1990

The Journal of Physiology

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Idazoxan and yohimbine competitively antagonized the action of noradrenaline with dissociation equilibrium constants of 20 and 30 nm respectively.3. In another series of experiments, noradrenaline and somatostatin were applied locally from a pipette so that they reached presynaptic terminals but not the cell bodies or axons of the presynaptic cell: noradrenaline inhibited EPSPs by 90 % in all neurones but somatostatin had no effect. When applied locally to the cell bodies giving rise to the presynaptic fibres, both agonists inhibited EPSPs in half the neurones by 40 %.4. When noradrenaline was applied locally to presynaptic terminals, the latency to onset of noradrenaline to inhibit EPSPs was 45-160 ms; cadmium applied similarly depressed EPSPs in 5-50 ms. 5. Pertussis toxin pre-treatment only partially blocked presynaptic inhibition caused by noradrenaline but abolished the reduction of EPSP amplitude by somatostatin.6. It is concluded that noradrenaline and somatostatin reduce the amplitude of the fast EPSP because they hyperpolarize cell bodies and prevent action potential initiation. Noradrenaline, but not somatostatin, has an additional action to inhibit acetylcholine release by acting at nerve terminal receptors.7. The presynaptic inhibitory action of noradrenaline results from activation of a2-adrenoceptors at nerve terminals but the mechanism(s) by which these presynaptic receptors act cannot be explained adequately by either activation of a potassium conductance and/or inhibition of a calcium conductance.MS 8372 20PHY 431

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“…Opioid receptors have been localized to sensory fibres of the vagus nerves (Atweh et al, 1978;Young et al, 1980). Selective destruction of unmyelinated afferent nerves by capsaicin leads to a reduction in opioid binding sites (Nagy et al, 1980;Laduron, 1984) suggesting that opioid receptors are present on a capsaicin-sensitive population of sensory nerves.…”

Section: Introductionmentioning

confidence: 99%

Opioid modulation of non‐cholinergic neural bronchoconstriction in guinea‐pig in vivo

Belvisi

Chung

Jackson

et al. 1988

British J Pharmacology

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1 Opioid receptors have been demonstrated on sensory fibres in the vagus nerve. Non-cholinergic (NC) neural bronchoconstriction in guinea-pig is due to release of neuropeptides from sensory nerve endings. We have therefore studied the effect of opioids on this NC bronchoconstriction in the anaesthetized guinea-pig. 2 Bilateral vagal stimulation (5 V, 5 ms, 10 Hz) caused reproducible bronchoconstriction in guineapigs which was reduced by atropine (1 mgkg 1), but the NC component was unaffected by hexamethonium (10 mg kg-1).3 NC bronchoconstriction was reduced by morphine in a dose-dependent manner (ED50= 132pgkg-1 with a maximal inhibition of 79 + 2.1% at 1 mgkg-1). Yohimbine (0.5 mgkg 1) did not alter the inhibitory effect of morphine (1 mg kg-1). 4 The inhibitory effect of morphine was completely reversed by naloxone (1 mg kg-1) which had no effect on NC bronchoconstriction. Propranolol (1 mg kg-1) significantly increased the NC bronchoconstrictor response but did not significantly alter the inhibition by morphine.5 The selective p-opioid receptor agonist Tyr-(D-Ala)-Gly-(N-Me-Phe)Glyol (DAGOL) was significantly more potent than morphine with an ED50 of 5.4pgkg-1 and complete inhibition at lOOgkg-. The 6-agonist Tyr4D-Pen)-Gly-Phe-D-Pen) (DPDPE) was less potent than DAGOL with an ED5o of 28pgkg-1 and a maximal inhibition of only 50 + 5% at lOOPgkg-. The Kreceptor agonist, U-50,488H had no inhibitory effect on the NC bronchoconstrictor response. 6 The bronchoconstrictor responses to exogenous substance P (25 pgkg-1) or acetylcholine (25 pg kg-1) were unaffected by morphine (500 pg kg-1). 7 We conclude that opioids inhibit the NC bronchoconstrictor response to vagal stimulation via an action on p-opioid receptors localized to sensory nerve endings in the airway.

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Opioid Receptors Undergo Axonal Flow

Cited by 243 publications

References 20 publications

Topical and Peripherally Acting Analgesics

Topical and Peripherally Acting Analgesics

Mechanisms underlying presynaptic inhibition through alpha 2‐adrenoceptors in guinea‐pig submucosal neurones.

Opioid modulation of non‐cholinergic neural bronchoconstriction in guinea‐pig in vivo

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