Nitric oxide synthase inhibition attenuates signs of ethanol withdrawal in rats

Uzbay, I.T.; Erden, Bekir Faruk; Tapanyigit, E.Ebru; Kayaalp, S. O.

doi:10.1016/s0024-3205(97)00922-3

Cited by 97 publications

(50 citation statements)

References 31 publications

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“…Similarly, the anxiolytic effect of ethanol was increased by the intrahippocampal microinjection of the preferential neuronal NOS (nNOS) inhibitor 7-nitroindazole (7-NI) and blocked by a similar injection of a cGMP analogue or NO donors (Ferreira et al 1999). Conversely, symptoms of ethanol withdrawal can be attenuated by the inhibition of NO dependent pathways (Uzbay et al 1997;Adams and Cicero 1998), but are accentuated by the enhancement of NO generation (Uzbay and Oglesby 2001).…”

Section: Introductionmentioning

confidence: 99%

Influence of drugs acting on nitric oxide-dependent pathways on ethanol tolerance in rats

Wazlawik

Morato

2003

Psychopharmacology

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The present results suggest that activation or inhibition of NO-dependent pathways increases or blocks rapid tolerance, respectively. These results give additional support to the hypothesis that brain NO plays a role in the development of tolerance to ethanol, but it remains to be confirmed if the same basic cellular mechanisms are also applicable to tolerance to other behavioural and/or physiological effects of this drug.

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Section: Introductionmentioning

confidence: 99%

Influence of drugs acting on nitric oxide-dependent pathways on ethanol tolerance in rats

Wazlawik

Morato

2003

Psychopharmacology

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“…For example, agmatine selectively inhibits nitric oxide synthase (Galea et al 1996), an enzyme converting L-arginine to nitric oxide, and the NMDA subclass of glutamate receptor channels (Yang and Reis 1999) in rat brain. Several reports indicated that an important role of NMDA receptors and nitric oxide in development of the opioid (Trujillo and Akil 1991;Adams et al 1993;Thorat et al 1994;Vaupel et al 1997) and ethanol (Rossetti and Carboni 1995;Adams et al 1995;Kotlinska and Liljequist 1996;Uzbay et al 1997) physical dependence. Agmatine also attenuates naloxone-induced morphine withdrawal signs in morphine-dependent mice (Aricioglu-Kartal and Uzbay 1997) and many signs of ethanol withdrawal syndrome in ethanol-dependent rats (Uzbay et al 2000).…”

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confidence: 99%

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

Yeşilyurt

Uzbay

2001

Neuropsychopharmacology

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The effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and a combination of agmatine and morphine on tail-flick test have been investigated in mice. Adult maleSwiss-Webster mice were used in the study. Agmatine (10, 20 and 40 mg/kg) Agmatine is a cationic amine formed by decarboxylation of arginine by the enzyme arginine decarboxylase (Tabor and Tabor 1984). It is a biological active substance (Lortie et al. 1996) and binds with high affinity to both imidazoline and ␣ 2 -adrenergic receptors of all subclasses (Li et al. 1994;Piletz et al. 1995;Regunathan and Reis 1996;Reis and Regunathan 1998a). Recently, it has been suggested that agmatine meets many criteria for a neurotransmitter in brain. It is synthesised, stored, and released in brain; is contained in neurones and axon terminals; interacts with cell-specific receptors; and elicits biological actions within the central nervous system (Reis and Regunathan 1998a,b). Thus, results of some recent studies indicate the modulatory effects of agmatine in central nervous system. For example, agmatine selectively inhibits nitric oxide synthase (Galea et al. 1996), an enzyme converting L-arginine to nitric oxide, and the NMDA subclass of glutamate receptor channels (Yang and Reis 1999) in rat brain. Several reports indicated that an important role of NMDA receptors and nitric oxide in development of the opioid (Trujillo and Akil 1991;Adams et al. 1993;Thorat et al. 1994;Vaupel et al. 1997) et al. 2000). The drugs that have selective agonistic activity on imidazoline/ ␣ 2 -adrenergic receptors such as clonidine, xylazine, and moxonidine produce antinociceptive responses in rodents (Paalzow 1974;Browning et al. 1982;Ossipov et al. 1989;Fairbanks et al. 2000). The role of adrenoceptors, particularly the ␣ 2 subtype, in the potentiation of opioid-induced analgesia is also well known (Wigdor and Wilcox 1987;Dambisya et al. 1991). In the light of these reports, it would be expected that agmatine, another agent binding imidazoline/ ␣ 2 -receptors, should also have antinociceptive activity. Thus, some recent studies indicate modulatory effects of agmatine on opioid analgesia in mice (Kolesnikov et al. 1996;Fairbanks and Wilcox 1997) and rats (Horváth et al. 1999). It was reported that intrathecal administration of agmatine potentiated morphine-induced ␦ -opioid receptor-mediated analgesia ninefold without affecting pain thresholds and chronic administration prevented 1 -opioid receptor-mediated tolerance in mice (Kolesnikov et al. 1996;Bradley and Headley 1997). However, the mechanisms of these effects remain to be fully understood. It is not certain whether these effects are mediated by ␣ 2 -adrenergic or imidazoline receptors. On the other hand, there are limited studies investigating the antinociceptive effect of peripheral agmatine administration in rodents.The main objective of the present study was to investigate the possible effects of agmatine and an agmatinemorphine combination on nociception by using the tai...

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“…Opiate abstinence signs, like nicotine abstinence signs, have been alleviated by NOS inhibitors (Adams et al 1993;Cappendijk et al 1993;Kimes et al 1993Kimes et al ,1994Kolesnikov et al 1993;Majeed et al 1994;Thorat et al 1994;Vaupel et al 1995;Bhargava and Thorat 1996;Dambisya and Lee 1996;Leza et al 1996). Ethanol, like nicotine, induces release of endogenous opioid peptides (Herz 1997), and ethanol abstinence signs have also been alleviated by NOS inhibitors (Adams et al 1995;Uzbay et al 1997). These observations suggest that common mechanisms (endogenous opioid release, alteration of NO synthesis) may at least partially underlie physical dependence on a wide range of habit-forming drugs.…”

Section: Discussionmentioning

confidence: 99%

The nitric oxide synthesis inhibitor nitro- L -arginine ( L -NNA) attenuates nicotine abstinence syndrome in the rat

Malin¹,

Lake²,

Shenoi³

et al. 1998

Psychopharmacology

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Nitric oxide synthesis contributes to opiate tolerance and dependence. Nicotine dependence and abstinence syndrome in the rat appear to involve opiate mechanisms. Therefore, it was postulated that nitric oxide synthase (NOS) activity might be essential for the expression of nicotine abstinence syndrome. Twenty-one rats were rendered dependent by SC infusion of 9 mg/kg per day nicotine tartrate via Alzet osmotic minipump. Rats were pretreated SC with vehicle alone, or with 18 or 30 mg/kg of the NOS inhibitor L-NNA (nitro-L-arginine). Thirty minutes later, rats were challenged by 1 mg/kg of the nicotinic antagonist mecamylamine SC and observed for 30 additional minutes. Rats pretreated with vehicle displayed a total of 68.7+/-8.0 mecamylamine-precipitated abstinence signs (mean+/-SEM), while those receiving 18 or 30 mg/kg L-NNA had 12.7+/-2.0 and 5.1+/-1.7 signs, respectively. All three groups differed significantly from one another according to Dunn's post-hoc procedure. Rats pretreated with L-NNA combined with an excess of the NOS substrate L-arginine had significantly more mecamylamine-precipitated abstinence signs than rats receiving L-NNA combined with D-arginine. Also, D-NNA, which does not selectively bind to NOS, was significantly less effective than L-NNA in preventing mecamylamine-precipitated abstinence syndrome. Additional studies determined the effect of L-NNA on spontaneous nicotine abstinence syndrome. Rats were assessed for abstinence signs at 17 and 20 h after termination of nicotine infusion. They received injections of 9, 18, or 30 mg/kg L-NNA SC or vehicle alone immediately before the 20-h observation; all rats were observed for 30 min. Signs at 20 h (post-injection) as a percentage of signs at 17 h (pre-injection) declined significantly as a function of L-NNA dose. Once again, this effect was attenuated significantly more by co-administration of L-arginine than by D-arginine. The overall pattern of results suggests that nitric oxide synthesis is critical to the expression of nicotine abstinence syndrome.

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Nitric oxide synthase inhibition attenuates signs of ethanol withdrawal in rats

Cited by 97 publications

References 31 publications

Influence of drugs acting on nitric oxide-dependent pathways on ethanol tolerance in rats

Influence of drugs acting on nitric oxide-dependent pathways on ethanol tolerance in rats

Agmatine Potentiates the Analgesic Effect of Morphine by an α2-Adrenoceptor-Mediated Mechanism in Mice

The nitric oxide synthesis inhibitor nitro- L -arginine ( L -NNA) attenuates nicotine abstinence syndrome in the rat

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