Effect of JTP-2942, a novel thyrotropin-releasing hormone analogue, on pentobarbital-induced anesthesia in rats

Matsushita, Mutsuyoshi; Yonemori, Fumihiko; Hamada, Atsushi; Toide, Katsuo; Iwata, Kunio

doi:10.1016/0014-2999(95)00034-i

Cited by 16 publications

(9 citation statements)

References 10 publications

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“…For instance, replacement of the pyroglutamyl moiety of TRH by a cyclopentanone structure showed increased potency and longer duration of action on the CNS compared to TRH [45][46][47][48]. This compound (3) (Fig.…”

Section: Pyroglutamic Acidmentioning

confidence: 99%

Thyrotropin-Releasing Hormone Analogs

Colson

Gershengorn²

2006

MRMC

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Thyrotropin releasing hormone (TRH: pyroglutamic acid-histidine-prolineamide) regulates the activity of cells in the anterior pituitary and within the central and peripheral nervous systems. TRH, which has been the subject of much research over the past three decades, exerts its effects by acting through class A G-protein coupled receptors. The recent discovery of a second receptor subtype has generated an interest in the discovery of receptor subtype-selective TRH analogs. In this review, we describe advances in the development of TRH analogs and in the understanding of their mechanism of interaction with TRH receptors. We also describe the recent breakthrough in the identification of analogs that bind selectively at TRH-R2.

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Section: Pyroglutamic Acidmentioning

confidence: 99%

Thyrotropin-Releasing Hormone Analogs

Colson

Gershengorn²

2006

MRMC

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“…Antagonist effects of TRH were seen on anaesthesia produced by ketamine and by ethanol. Earlier reports have demonstrated antagonism of both ethanol and pentobarbitone (Breese et al ., 1974; French et al ., 1993; Matsushita et al ., 1995), but no effect was seen with pentobarbitone in the present study. The earlier reports, however, all used ‘sleeping time’ to measure the potency of the effects of the anaesthetics so only high doses of anaesthetics, which produced loss of righting reflex in all animals, were used.…”

Section: Discussionmentioning

confidence: 99%

“…There have been a small number of studies reporting antagonism of general anaesthesia with various drugs but no systematic investigation has been made and usually only one or two anaesthetics have been studied. Compounds which have been reported to antagonize anaesthesia are 4‐aminopyridine (4‐AP), against ethanol and ketamine (Agostin et al ., 1980; Sellin & Laakso, 1987), and thyrotropin releasing hormone (TRH) against ethanol and pentobarbitone (Breese et al ., 1974; French et al ., 1993; Matsushita et al ., 1995). Anticholinesterase agents have also been shown to have some effects (Livingston & Waterman, 1978; Leeuwin et al ., 1984).…”

Section: Introductionmentioning

confidence: 99%

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Investigations into pharmacological antagonism of general anaesthesia

Little

Clark

Watson

2000

British J Pharmacology

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1 The eects of convulsant drugs, and of thyrotropin releasing hormone (TRH), were examined on the general anaesthetic actions of ketamine, ethanol, pentobarbitone and propofol in mice. The aim was to investigate the possibility of selective antagonism, which, if seen, would provide information about the mechanism of the anaesthesia. 2 The general anaesthetic eects of ketamine were unaected by bicuculline; antagonism was seen with 4-aminopyridine and signi®cant potentiation with 300 mg kg 71 NMDLA (N-methyl-DLaspartate). The calcium agonist, Bay K 8644, potentiated the anaesthesia produced by ketamine and antagonism of such anaesthesia was seen with TRH. 3 A small, but signi®cant, antagonism of the general anaesthesia produced by ethanol was seen with bicuculline, and a small, signi®cant, potentiation with 4-aminopyridine. There was an antagonist eect of TRH, but no eect of NMDLA. 4 Potentiation of the anaesthetic eects of pentobarbitone was seen with NMDLA and with 4-aminopyridine and the lower dose of bicuculline (2.7 mg kg 71) also caused potentiation. There was no signi®cant change in the ED 50 value for pentobarbitone anaesthesia with TRH. 5 Bicuculline did not alter the anaesthetic actions of propofol, while potentiation was seen with NMDLA and 4-aminopyridine. TRH had no signi®cant eect on propofol anaesthetic, but Bay K 8644 at 1 mg kg 71 signi®cantly potentiated the anaesthesia. 6 These results suggest that potentiation of GABA A transmission or inhibition of NMDA receptor-mediated transmission do not appear to play a major role in the production of general anaesthesia by the agents used.

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“…JTP‐2942 ( N α ‐[(1 S ,2 R )‐2‐methyl‐4‐oxocyclopentylcarbonyl]‐ L ‐histidyl‐ L ‐prolinamide monohydrate 2,3 ) is a novel thyrotropin‐ releasing hormone (TRH) analogue in which the pyroglutamyl residue is replaced with methyl‐oxocyclopentane. It has a more potent and longer‐lasting antagonistic effect against reserpine‐induced hypothermia compared with TRH, 4,5 it has an antagonistic effect against pentobarbital‐induced anaesthesia, 2 it activates electroencephalography 6 and has an acetylcholine‐releasing action 3 . It was previously reported in a rat focal ischaemic model that JTP‐2942 improved neurological deficits and memory and learning disturbances when administered for a duration of 8 weeks begining 1 week after middle cerebral artery occlusion 1 .…”

Section: Introductionmentioning

confidence: 99%

Delayed Administration Of Jtp‐2942, A Novel Thyrotropin‐Releasing Hormone Analogue, Improves Cerebral Blood Flow And Metabolism In Rat Postischaemic Brain

Katsumata

Katayama

Yonemori

et al. 2001

Clin Exp Pharma Physio

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1. The aim of the present study was to examine the central nervous system action of JTP-2942, a novel thyrotropin-releasing hormone (TRH) analogue, from the point of view of cerebral blood flow (CBF) and metabolism in the postischaemic brain. 2. Left middle cerebral artery ischaemia was induced for 90 min followed by reperfusion. 3. Animals were separated into four groups: (i) low-dose (0.003 mg/kg) JTP-2942; (ii) high-dose (0.03 mg/kg) JTP-2942; (iii) cystidine diphosphate choline (500 mg/kg); and (iv) saline. The test drug or saline was administered intravenously 1 week after ischaemia. 4. Local CBF and local cerebral glucose utilization were measured autoradiographically, adjacent sections were stained with haematoxylin-eosin and infarction size was measured. 5. JTP-2942 ameliorated the reduction of local CBF and glucose utilization except in the ischaemic core. In particular, the higher dose (0.03 mg/kg) of JTP-2942 significantly increased local CBF and glucose utilization not only in peri-infarcted areas, but also in distal and contralateral areas. 6. These results suggest that JTP-2942 treatment may be beneficial for improving cerebral circulation and metabolism in the postischaemic brain.

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Effect of JTP-2942, a novel thyrotropin-releasing hormone analogue, on pentobarbital-induced anesthesia in rats

Cited by 16 publications

References 10 publications

Thyrotropin-Releasing Hormone Analogs

Thyrotropin-Releasing Hormone Analogs

Investigations into pharmacological antagonism of general anaesthesia

Delayed Administration Of Jtp‐2942, A Novel Thyrotropin‐Releasing Hormone Analogue, Improves Cerebral Blood Flow And Metabolism In Rat Postischaemic Brain

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