Phosphinic acid analogues of GABA are antagonists at the GABAB receptor in the rat anococcygeus

Hills, Judith M.; Sellers, Andrew J.; Mistry, Jayshree; Broekman, Marianne; Howson, William

doi:10.1111/j.1476-5381.1991.tb12121.x

Cited by 28 publications

(12 citation statements)

References 6 publications

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“…preloaded with 3H-noradrenaline, the electrically evoked tritium overflow repre sents quasi-physiological noradrenaline re lease [6], The inhibitory effect of R-(-)-baclofen on the electrically evoked tritium over flow was attenuated by CGP 35348. The ap parent pA2 value (4.94) is almost identical to that obtained in our previous study [6] for the interaction of CGP 35348 with GABA itself (4.76); it resembles the pA2 values reported for the GABAb receptor in the rat anococcygeus muscle (5.38 [13]) and in the rat vas deferens (5.0 [14]). …”

Section: Pithed Ratssupporting

confidence: 73%

“…another GABAb receptor antagonist [ 15], used in our previous study [8], In an in vitro study on the rat anococcygeus muscle, a simi lar difference between the potencies of both GABAr receptor antagonists was found [13]. Thus, the present study shows that CGP 35348 is suitable for the characterization of GABAb receptors both in vitro (including the newly characterized GABAb receptor in the pig retina) and in situ.…”

Section: Pithed Ratsmentioning

confidence: 81%

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CGP 35348 Blocks Noradrenaline- Release-Inhibiting GABAB Receptors in the Pig Retina, Rat Vena cava and Pithed Rat Vasculature

1993

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In superfused pig retina discs, preincubated with ³H-nor-adrenaline, the electrically (3 Hz) evoked tritium overflow was inhibited by γ-aminobutyric acid (GABA) and the GABA_Breceptor agonist R-(–)-baclofen but was not affected by the GABA_A receptor agonist 3-amino-1-propanesulphonic acid. The effect of GABA was counteracted by the GABA_B receptor antagonist CGP 35348 [P-(3-aminopropyl)-P-diethoxyme-thylphosphinic acid] but was not influenced by the GABA_Areceptor antagonist SR 95531 [2-(3-carboxypropyl)-3-amino-6-paramethoxyphenylpyridazinium bromide]. Furthermore, CGP 35348 antagonized the inhibitory effect of R-(–)-baclofen on the electrically (0.66 Hz) evoked tritium overflow in superfused rat vena cava segments, preincubated with ³H-noradrenaline, and on the electrically (0.5 Hz) induced rise in diastolic blood pressure in pithed rats. The present results suggest that GABA is capable of inhibiting noradrenaline release (most likely from vascular sympathetic nerve endings) in the pig retina via GABA_B receptors and that CGP 35348 is a valuable tool for the characterization of GABA_B receptors in vitro and in situ.

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Section: Pithed Ratssupporting

confidence: 73%

Section: Pithed Ratsmentioning

confidence: 81%

CGP 35348 Blocks Noradrenaline- Release-Inhibiting GABAB Receptors in the Pig Retina, Rat Vena cava and Pithed Rat Vasculature

1993

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“…Bicuculline and CGP35348 are generally regarded as selective antagonists for GABA A and GABA B receptors, respectively [15,17,23] see [16] for review}. All drugs were dissolved in phosphate buffered saline (PBS).…”

Section: Methodsmentioning

confidence: 99%

Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord

Tambeli

Levine

Gear

2009

Pain

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The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR-5, mu-opioid, GABA-A, and GABA-B), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABA-B and mu-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR-5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABA-B agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the mu-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors.

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“…However, some phosphinic analogs of GABA itself are highly effective in GABA, binding and as agonists in functional tests. [268][269][270][271][272][273] This may be because the phosphinic acidic head more closely resembles the carboxylic group of GABA and baclofen than is found in the tetrahedral sulfonic or the dibasic phosphonic analogs. Since the parent phosphinic analog (3-APPiA; Fig.…”

Section: A Gaba-receptor Agonistsmentioning

confidence: 99%

GABA agonists and antagonists

Kerr

Ong

1992

Medicinal Research Reviews

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Phosphinic acid analogues of GABA are antagonists at the GABA_B receptor in the rat anococcygeus

Cited by 28 publications

References 6 publications

CGP 35348 Blocks Noradrenaline- Release-Inhibiting GABA<sub>B</sub> Receptors in the Pig Retina, Rat Vena cava and Pithed Rat Vasculature

CGP 35348 Blocks Noradrenaline- Release-Inhibiting GABA<sub>B</sub> Receptors in the Pig Retina, Rat Vena cava and Pithed Rat Vasculature

Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord

GABA agonists and antagonists

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