Effect of gabapentin-like compounds on development and maintenance of morphine-induced conditioned place preference

Andrews, Nick; Loomis, Sally; Blake, Robert W.; Ferrigan, Leanne; Singh, Lakhbir; McKnight, A.T.

doi:10.1007/s002130100839

Cited by 64 publications

(47 citation statements)

References 19 publications

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“…The opioid consumption was found to be reduced in several pain states when gabapentin was co-administered clinically (Table 2). On the other hand, gabapentin might also be helpful in reducing the dependence and tolerance of opioids, as suggested by animal studies (49,50). It seems that gabapentin is relatively a pretty safe drug in terms of its tolerable effective doses with minor unwanted or side effects clinically (Table 2).…”

Section: -2 Clinical Studiesmentioning

confidence: 99%

Mechanisms of the Antinociceptive Action of Gabapentin

2006

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Abstract. Gabapentin, a γ-aminobutyric acid (GABA) analogue anticonvulsant, is also an effective analgesic agent in neuropathic and inflammatory, but not acute, pain systemically and intrathecally. Other clinical indications such as anxiety, bipolar disorder, and hot flashes have also been proposed. Since gabapentin was developed, several hypotheses had been proposed for its action mechanisms. They include selectively activating the heterodimeric GABA B receptors consisting of GABA B1a and GABA B2 subunits, selectively enhancing the NMDA current at GABAergic interneurons, or blocking AMPA-receptor-mediated transmission in the spinal cord, binding to the L-α-amino acid transporter, activating ATP-sensitive K + channels, activating hyperpolarization-activated cation channels, and modulating Ca 2+ current by selectively binding to the specific binding site of [3 H]gabapentin, the α 2 δ subunit of voltage-dependent Ca 2+ channels. Different mechanisms might be involved in different therapeutic actions of gabapentin. In this review, we summarized the recent progress in the findings proposed for the antinociceptive action mechanisms of gabapentin and suggest that the α 2 δ subunit of spinal N-type Ca 2+ channels is very likely the analgesic action target of gabapentin.

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Section: -2 Clinical Studiesmentioning

confidence: 99%

Mechanisms of the Antinociceptive Action of Gabapentin

2006

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“…26 Pregabalin may also provide benefits to morphine analgesia without the danger of enhanced dependence liability. 27 The present study was the first presenting data regarding the use of pregabalin added to morphine in advanced cancer pain. It was preferred to use a flexible approach in dosing pregabalin, avoiding a rigid protocol, to better reproduce the clinical setting and to extrapolate this information in clinical practice.…”

Section: Discussionmentioning

confidence: 88%

The Effects of Low Doses of Pregabalin on Morphine Analgesia in Advanced Cancer Patients

Mercadante

Porzio

Aielli

et al. 2013

The Clinical Journal of Pain

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Objectives: The aim of this study was to evaluate the opioid response in patients receiving morphine and pregabalin, independently from the presumed pain mechanisms, in comparison with patients receiving morphine treatment only.Methods: A multicenter prospective randomized controlled study was carried out in a sample of 70 advanced cancer patients with pain requiring strong opioids. Thirty-five patients (group MO) were randomized to receive sustained-release morphine using initial doses of 60 mg/day. Thirty-five patients (group MO-PR) were randomized to start the same morphine doses and pregabalin in increasing doses, starting with 25 mg/day up to 150 mg/day in one week. The following data were also recorded before starting the treatments (T0) and then at week intervals for four weeks (W1-4): age, gender, primary cancer and known metastases, pain causes and mechanisms, symptoms associated with opioid therapy, pain intensity, Brief Pain Inventory (BPI), morphine doses and escalation indexes (OEIs), and quality of life.Results: Forty-eight patients completed the study, twenty-eight and sixteen patients in group MO and MO-PR, respectively. Twenty patients were females, the mean age was 65.5 (±10.3), and the mean Karnofsky status was 66.0 (±18.9). No differences between groups were found in age (P = 0.839), Karnofsky status (P = 0.741), opioid doses as well as escalation indexes (OEI mg, P = 0.260, and OEI%, P = 0.270). No differences between the two groups were found in quality of life and all BPI items. Conclusion:The use of low doses of pregabalin added to morphine therapy in advanced cancer patients does not seem to provide advantageous analgesic effects, despite limitations of the present study due to the number of drop-outs.

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“…Gabapentin is a clinically effective anticonvulsant (Czapinski et al 2005) and blocked PTZinduced tonic convulsions in rats (Dalby and Nielsen 1997). It impaired rotarod performance (Field et al 1997) and prevented the development of morphine-induced conditioned place preference (Andrews et al 2001). Gabapentin and tiagabine share anticonvulsant properties and the ability to increase synaptic GABA, although it is clear that gabapentin has additional effects at calcium channels.…”

Section: Discussionmentioning

confidence: 98%