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      Involvement of calcium in pain and antinociception

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          Abstract

          Calcium ions are widely recognized to play a fundamental role in the regulation of several biological processes. Transient changes in cytoplasmic calcium ion concentration represent a key step for neurotransmitter release and the modulation of cell membrane excitability. Evidence has accumulated for the involvement of calcium ions also in nociception and antinociception, including the analgesic effects produced by opioids. The combination of opioids with drugs able to interfere with calcium ion functions in neurons has been pointed out as a useful alternative for safer clinical pain management. Alternatively, drugs that reduce the flux of calcium ions into neurons have been indicated as analgesic alternatives to opioids. This article reviews the manners by which calcium ions penetrate cell membranes and the changes in these mechanisms caused by opioids and calcium antagonists regarding nociceptive and antinociceptive events.

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          II - Prostaglandin hyperalgesia: the peripheral analgesic activity of morphine, enkephalins and opioid antagonists.

          Sérgio Ferreira, Meire Nakamura (1979)
          Morphine, enkephalins, nalorphine, naloxone and pentazocine are shown to have a peripheral analgesic effect. In our modification of the Randall-Selitto test these substances were 50--100 times more potent than a standard local anaesthetic, lidocaine. At this peripheral site, naloxone did not antagonize the effect of morphine. Morphine had a marked analgesic effect on the hyperalgesia induced by PGE2 and PGI2, BaCl2, Ca2+ ionophore A23187, isoprenaline but not on that induced by dibutyryl cyclic AMP. It was suggested that the peripheral analgesic effect of morphine is due to an inhibition of adenylate-cyclase activity.
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            Role of voltage-dependent calcium channel subtypes in experimental tactile allodynia.

            S Chaplan, T L Yaksh, J Pogrel (1994)
            Peripheral nerve lesions can result in exaggerated pain responses to low intensity mechanical stimuli (tactile allodynia). In the present work, the pharmacology of voltage-dependent calcium channels (VDCCs) involved in the transmission of neuropathic pain was characterized by examining the effects of antagonists specific to the N-, L- and P-type VDCCs, as well as an antagonist at a non-L-, non-N-type site. Drugs were administered via chronic lumbar intrathecal, i.v. or regional nerve block catheters implanted in rats with tactile allodynia induced by tight ligation of the left fifth and sixth lumbar spinal nerves. Intrathecally delivered N-type VDCC (omega-conopeptides SNX239, SNX159 and SNX111) produced dose-dependent blockade of tactile allodynia. Intrathecal L-type (diltiazem, verapamil and nimodipine), non-N-, non-L-type (omega-conopeptide SNX230) and P-type (omega-agatoxin IVA) VDCC antagonists had no effect on pain behavior at the highest doses examined. No VDCC antagonist suppressed paw withdrawal when administered i.v. SNX239, although effective when administered intrathecally, was without effect when applied regionally to the injured portion of the nerve. These results emphasize the importance of N-type, but not L- or P- type, VDCCs in the spinal cord on systems mediating persistent tactile allodynia after nerve injury.
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              Selective N-type neuronal voltage-sensitive calcium channel blocker, SNX-111, produces spinal antinociception in rat models of acute, persistent and neuropathic pain.

              M Pettus, S Bowersox, T Gadbois … (1996)
              Male Sprague-Dawley rats were used to evaluate the antinociceptive properties of the selective N-type voltage-sensitive calcium channel (VSCC) blocker, SNX-111, when the compound is administered spinally by either bolus injection or continuous, constant-rate infusion into the subarachnoid space. SNX-111 produced significant, dose-dependent antinociceptive effects by suppressing both the acute (phase 1: ED50, 14 ng/hr) and tonic (phase 2: ED50, 0.82 ng/hr) phases of the formalin test when it was infused for 72 hr immediately before testing. Phase 2 nociceptive responses were suppressed by bolus injections of 100 ng SNX-111. SNX-111 was approximately 1000-fold more potent than morphine in blocking phase 2 responses when the compounds were administered by intrathecal bolus injection. In rats with an experimentally induced painful peripheral neuropathy, intrathecal bolus injections of 30 to 300 ng SNX-111 blocked mechanical allodynia in a dose-dependent manner. Subacute administration of SNX-111 (1, 10 and 100 ng/hr) by continuous intrathecal infusion produced a reversible blockade of mechanical allodynia without apparent development of tolerance. These results show that: 1) selective N-type VSCC blockers are potent and efficacious antinociceptive agents when they are administered by the spinal route; 2) selective N-type VSCC blockers are effective in rat models of acute, persistent and neuropathic pain; and 3) N-type VSCCs play a significant role in the spinal processing of noxious somatosensory input.
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                Author and article information

                Journal
                Journal ID (publisher-id): bjmbr
                Title: Brazilian Journal of Medical and Biological Research
                Abbreviated Title: Braz J Med Biol Res
                Publisher: Associação Brasileira de Divulgação Científica (Ribeirão Preto, SP, Brazil )
                ISSN (Print): 0100-879X
                ISSN (Electronic): 1414-431X
                Publication date (Print and electronic): April 2001
                Volume: 34
                Issue: 4
                Pages: 449-461
                Affiliations
                [01] Ribeirão Preto SP orgnameUniversidade de São Paulo orgdiv1Faculdade de Medicina de Ribeirão Preto orgdiv2Departamento de Farmacologia Brasil
                Article
                Publisher ID: S0100-879X2001000400003 Publisher ID: S0100-879X(01)03400403
                DOI: 10.1590/S0100-879X2001000400003
                PubMed ID: 11285455
                SO-VID: 6e8c790b-905b-430f-96ef-0b3c2dfa3550
                License:

                This work is licensed under a Creative Commons Attribution 4.0 International License.

                History
                Date accepted : 06 February 2001
                Date received : 05 December 2000
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 60, Pages: 13
                Product

                SciELO Brazil

                Categories
                Subject: Review

                Keywords: calcium antagonists,antinociception,analgesia,calcium ions,opioids
                Data availability:
                Keywords: calcium antagonists, antinociception, analgesia, calcium ions, opioids

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