Dopamine receptor‐mediated spinal antinociception in the normal and haloperidol pretreated rat: effects of sulpiride and SCH 23390

Barasi, S.; Ben-Sreti, M.M.; Clatworthy, Andrea L.; Duggal, K.N.; Gonzalez, J. P.; Robertson, James I.; Rooney, K. F.; Sewell, Robert David Edmund

doi:10.1111/j.1476-5381.1987.tb16820.x

Cited by 47 publications

(11 citation statements)

References 32 publications

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“…Such a depressant effect agrees with findings from previous behavioral studies [8,9,46] as well as intracellular and extracellular recordings in the dorsal horn and trigeminocervical complex [19,24,40,64,65]. In this study, we show, for the first time, that the efficacy of D2R in modulating spinal excitation to noxious input is enhanced after nerve injury.…”

Section: Enhanced D2r-mediated Modulation After Snl Involves Synapticsupporting

confidence: 92%

Synaptic upregulation and superadditive interaction of dopamine D2- and μ-opioid receptors after peripheral nerve injury

Aira¹,

Barrenetxea²,

Buesa³

et al. 2014

Pain

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A sound strategy for improving the clinical efficacy of opioids involves exploiting positive interactions with drugs directed at other targets in pain pathways. The current study investigated the role of dopamine receptor D2 (D2R) in modulation of spinal dorsal horn excitability to noxious input, and interactions therein with μ-opioid receptor (MOR) in an animal model of neuropathic pain induced by spinal nerve ligation (SNL). C-fiber-evoked field potentials in the spinal dorsal horn were depressed concentration dependently by spinal superfusion with the D2R agonist quinpirole both in nerve-injured and sham-operated (control) rats. However, quinpirole-induced depression was significant at 10 μmol/L after SNL but only at 100 μmol/L in control rats. This quinpirole effect was completely abolished by MOR antagonist CTOP at subclinical concentration (1 μmol/L) in nerve-injured rats, but was unaltered in sham-operated rats. Nine days after SNL, D2R was upregulated to both presynaptic and postsynaptic locations in dorsal horn neurons, as revealed by double confocal immunofluorescence stainings for synaptophysin and PSD-95. In addition, D2R/MOR co-localization was increased after SNL. Co-administration of 1 μmol/L quinpirole, insufficient per se to alter evoked potentials, dramatically enhanced inhibition of evoked potentials by MOR agonist DAMGO, reducing the IC50 value of DAMGO by 2 orders of magnitude. The present data provide evidence of profound functional and subcellular changes in D2R-mediated modulation of noxious input after nerve injury, including positive interactions with spinal MOR. These results suggest D2R co-stimulation as a potential avenue to improve MOR analgesia in sustained pain states involving peripheral nerve injury.

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Section: Enhanced D2r-mediated Modulation After Snl Involves Synapticsupporting

confidence: 92%

Synaptic upregulation and superadditive interaction of dopamine D2- and μ-opioid receptors after peripheral nerve injury

Aira¹,

Barrenetxea²,

Buesa³

et al. 2014

Pain

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“…Adult rats injected subcutaneously or intrathetically with apomorphine, LY 171555, or LY 141865 (the mixed enantiomer of LY 171555) typically show a decreased responsiveness to pain on footshock, tail-flick, and hot plate tasks: responses that can be antagonized by sulpiride and haloperidol (Barasi, Ben-Sreti, Clatworthy, Duggal, Gonzalez, Robertson, Rooney, & Sewell, 1987;Barasi & Duggal, 1985;Ben-Sreti, Gonzalez, & Sewell, 1983;Gonzales-Rios, Vlaiculescu, Ben Natan, Protais, & Costentin, 1986;Tricklebank, Hutson, & Curzon, 1984). Therefore, the purpose of the present experiment was to determine the antinociceptive and nociceptive properties of LY 171555 and sulpiride in 17-day-old rat pups.…”

Section: Methodsmentioning

confidence: 99%

Dopamine D‐2 receptor mediation of response suppression learning of young rats

McDougall

Nonneman

1989

Developmental Psychobiology

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In three experiments, the effects of augmenting or blocking dopamine (DA) D-2 receptor activity on the ontogeny of response suppression learning of preweanling rat pups were determined. In the initial experiment, rat pups were trained to traverse a straight alley for nipple attachment to an anesthetized dam. When footshock (0.2 mA, 0.5 sec) was made contingent on responding, younger (11- and 13-day-olds) rat pups were deficient to older (17- and 19-day-olds) pups at withholding punished responding. In the subsequent experiments, response suppression learning was assessed after injecting 11- and 17-day-old rat pups with the specific DA D-2 agonist, LY 171555 (0.005-, 0.01-, and 0.1-mg/kg, i.p.), or the specific DA D-2 antagonist, sulpiride (5.0-, 15.0-, and 50.0-mg/kg, i.p.). LY 171555 enhanced the punished responding of both the 11- and 17-day-old rat pups; whereas, sulpiride increased the punished responding of the 17-, but not the 11-day-olds. In four additional experiments, the effects of LY 171555 and sulpiride on the locomotor activity, nociception, and reinforcement processes of 17-day-old rat pups was assessed. Rat pups given LY 171555 (0.01 mg/kg, i.p.) exhibited enhanced locomotor activity and a trend towards hyperanalgesia using a hot plate task. Sulpiride (15.0 mg/kg, i.p.) completely antagonized LY 171555's activity enhancing effects and had hyperalgesic properties. In two experiments, sulpiride did not affect the nonpunished appetitive responding of the 17-day-olds; whereas, haloperidol-treated pups responded on fewer reinforced trials than did saline-treated pups. Therefore, these results indicate that the response suppression learning of 17-day-old rat pups is mediated, at least partially, by a DAD-2 receptor system, and that D-2 receptors are also involved in the locomotor activity and nociceptive responses of young rat pups.

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“…Initially the effects of DA on sensory processing of peripheral sensory information in the spinal cord were studied by measuring the latencies of several (spinal) reflexes, like the hot-plate and tail-flick reflexes, following application of DA and various DA agonists (Barasi et al, 1987;reviewed in Jensen, 1986) .…”

Section: Functional Considerationsmentioning

confidence: 99%

Distribution of dopamine immunoreactivity in the rat, cat, and monkey spinal cord

et al. 1996

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In the present study, the distribution of dopamine (DA) was identified light microscopically in all segments of the rat, cat, and monkey spinal cord by using immunocytochemistry with antibodies directed against dopamine. Only fibers and (presumed) terminals were found to be immunoreactive for DA. Strongest DA labeling was present in the sympathetic intermediolateral cell column (IML). Strong DA labeling, consisting of many varicose fibers, was found in all laminae of the dorsal horn, including the central canal area (region X), but with the exception of the substantia gelatinosa, which was only sparsely labeled, especially in rat and monkey. In the motoneuronal cell groups DA labeling was also strong and showed a fine granular appearance. The sexually dimorphic cremaster nucleus and Onuf's nucleus (or its homologue) showed a much stronger labeling than the surrounding somatic motoneurons. In the parasympathetic area at sacral levels, labeling was moderate. The remaining areas, like the intermediate zone (laminae VI-VIII), were only sparsely innervated. The dorsal nucleus (column of Clarke) showed the fewest DA fibers, as did the central cervical nucleus, suggesting that cerebellar projecting cells were avoided by the DA projection. In all species, the descending fibers were located mostly in the dorsolateral funiculus, but laminae I and III also contained many rostrocaudally oriented fibers. It is concluded that DA is widely distributed within the spinal cord, with few differences between species, emphasizing that DA plays an important role as one of the monoamines that influences sensory input as well as autonomic and motor output at the spinal level.

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Dopamine receptor‐mediated spinal antinociception in the normal and haloperidol pretreated rat: effects of sulpiride and SCH 23390

Cited by 47 publications

References 32 publications

Synaptic upregulation and superadditive interaction of dopamine D2- and μ-opioid receptors after peripheral nerve injury

Synaptic upregulation and superadditive interaction of dopamine D2- and μ-opioid receptors after peripheral nerve injury

Dopamine D‐2 receptor mediation of response suppression learning of young rats

Distribution of dopamine immunoreactivity in the rat, cat, and monkey spinal cord

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