Interactions of Phospholipids and Free Fatty Acids with Antidepressant Recognition Binding Sites in Rat Brain

Stockert, Marta; Zieher, Luis Marı́a; Medina, Jorge H.

doi:10.1007/978-1-4615-3426-6_29

Cited by 6 publications

(2 citation statements)

References 15 publications

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“…204 8) Whereas chronic morphine exposure may retard nerve regeneration and induce permanent neurological deficits, 81,238 activity of PLA2 appears critical for the induction and maintenance of nerve regeneration (see text for references). 9) The inhibitory effects of glucocorticosteroids, 239 ketamine, [240][241][242] phenytoin, 243 and imipramine, 244 upon PLA2 activity, together with potentiation of imipramine binding to synaptosomal membranes by PLA2 245,246 may, in some part, contribute to the reported efficacy of these drugs in managing neuropathic pains.…”

Section: ) Consistent With the Above Observationsmentioning

confidence: 99%

“…With the discovery that PLA2 may be a messenger of the CCK B receptor, there arise new targets for attenuating the effects of CCK upon opioid analgesia. It is interesting to note that the inhibitory effects of glucocorticosteroids, 239 ketamine, [240][241][242] phenytoin 243 and imipramine 244 on PLA2 activity, together with the potentiation of imipramine binding to synaptosomal membranes by PLA2, 245,246 may, in some part, contribute to the reported efficacy of these drugs in managing neuropathic pains (refer to key points previously listed under 'PLA2: an anti-opioid messenger of the CCK B receptor? ').…”

Section: Buprenorphinementioning

confidence: 99%

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Signal transduction in neuropathic pain, with special emphasis on the analgesic role of opioids - Part II: Moving basic science towards a new pharmacotherapy

McCormack¹

1999

Pain Reviews

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In the first part of this three-part article I explored the notion that pharmacological intervention, aimed at eliminating abnormal sensations such as hyperalgesia or paraesthesia arising as a direct result of nerve injury, activates adaptive responses that ensure adequacy of neurotransmission, regardless of whether such transmission ultimately evokes normal or abnormal sensations. Thus, by their nature, such adaptive responses will act to oppose and surmount any drug-induced intervention designed to diminish pain through attenuation of signal conduction. A corollary of this hypothesis is that even the most sophisticated novel pharmacological entities, when used to block the pain signal, represent substrates for evoking a repertoire of failsafe mechanisms that have evolved throughout a history of challenge and response. In Part II, I explore in greater depth how activation of these responses may explain why the treatment of neuropathic pains, particularly with opioids, can be so frustrating. Opioid analgesia and cholecystokinin CCK as an anti-analgesic peptide Numerous reports have indicated that CCK antagonizes opioid antinociceptive effects. Indeed, administered by peripheral or central (intracerebroventricular (i.c.v.), intrathecal (i.t.)) routes, CCK can reduce morphine-, PL017-or ohmefentanyl-(two selective µ-agonists), and β-endorphininduced analgesia, as well as the morphineinduced depression of the nociceptive flexion reflex in rats. 19-27 In the mouse tail-flick test, CCK attenuates the analgesic effects of morphine. 28 In addition, in the same species, CCK administered i.t. antagonizes the inhibition of tail flick by i.c.v. β-endorphin. 29 Furthermore, the inhibitory effect of morphine and [D-Ala 2-Me)Phe 4-Glyol 5 ] enkephalin (DAMGO) on C-fibre-evoked activity of rat spinal nociceptive neurones can be reduced by CCK. 30-33 Thus, from these data, it can be concluded that CCK has the pharmacological property of reducing the antinociceptive effects of endogenous opioids.

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