Opposite Influences of Different Adrenoceptors on Baclofen‐Induced Antinociception in Mice

Sabetkasai, M; Doost-Mohammady, R.; Zarrindast, M.R.

doi:10.1111/j.1600-0773.1997.tb00276.x

Cited by 5 publications

(4 citation statements)

References 18 publications

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“…(1986a , b) studied different alpha‐1 and alpha‐2 adrenoceptor agonists and antagonists in rats and dogs and concluded that antinociception may be mediated by either alpha‐1 or alpha‐2 adrenoceptors whereas sedation is predominantly mediated by alpha‐2‐adrenoceptors. In another study with mice, however, alpha‐2 adrenoceptor stimulation increased, while alpha‐1‐adrenoceptor stimulation decreased baclofen‐induced antinociception ( Sabetkasai et al ., 1997 ). These two conclusions may appear to be contradictory as far as the role of alpha‐1‐adrenoceptors in antinociception is concerned but consideration should be given to the fact that different species, different drugs and different tests were used.…”

Section: Discussionmentioning

confidence: 97%

Correlation between serum concentrations following continuous intravenous infusion of dexmedetomidine or medetomidine in cats and their sedative and analgesic effects

Ansah

Raekallio

Vainio

2000

Vet Pharm & Therapeutics

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Dexmedetomidine (DEX) may have some therapeutic advantages over the racemate medetomidine (MED). Here we have examined how serum concentrations of DEX correlate with some of its anaesthetic effects. Cats (n = 6) were administered with a continuous stepwise intravenous (i.v.) infusion of DEX or MED on different occasions in a cross-over design. Maintenance infusion rates (mg/kg/min) used were: DEX = 0.25 (MED = 0.50); DEX = 1 (MED = 2) and DEX = 4 (MED = 8) for infusion steps 1, 2 and 3, respectively. Each maintenance infusion lasted at least 50 min and was preceded with a loading dose. There was no significant difference between serum DEX and 0.5 serum MED concentrations at any dose level nor was there a significant difference between serum DEX and the (entire) serum MED concentrations. There was no significant difference between DEX and MED for sedation, analgesia, muscular relaxation and heart and respiratory rates. For both DEX and MED, serum drug concentration and analgesia were dose-dependent and sedation increased until the end of infusion step 2 (dose level 2) and decreased at the end of step 3 (dose level 3). Muscular relaxation was not dose-dependent. We conclude that increasing the blood concentration of DEX or MED beyond a certain level decreases the level of sedation instead of increasing it even though analgesia increases. The rate at which DEX and MED are metabolized in cats may not be the same.

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Section: Discussionmentioning

confidence: 97%

Correlation between serum concentrations following continuous intravenous infusion of dexmedetomidine or medetomidine in cats and their sedative and analgesic effects

Ansah

Raekallio

Vainio

2000

Vet Pharm & Therapeutics

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“…However, given that there was no effect of propranolol when administered before the test of fear expression, which also depends on the LA, it appears that propranolol does not inactivate or disrupt the LA. One more explanation might be that propranolol attenuated footshock sensitivity, but in contrast to causing antinociception, propranolol has previously been shown to inhibit antinociception in the tail-flick test produced by systemic baclofen (Sabetkasai et al, 1997) or amygdala stimulation (Oliveira and Prado, 1998), and propranolol treatments that impair inhibitory avoidance retention are reported to have no effect on footshock sensitivity (Nielson et al, 1999). These findings suggest that the current effect on freezing during fear conditioning was not caused by reduced shock sensitivity.…”

Section: Discussionmentioning

confidence: 99%

Beta-Adrenergic Receptors in the Lateral Nucleus of the Amygdala Contribute to the Acquisition but Not the Consolidation of Auditory Fear Conditioning

Bush

Caparosa²,

Gekker

et al. 2010

Front. Behav. Neurosci.

105

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Beta-adrenergic receptors (βARs) have long been associated with fear disorders and with learning and memory. However, the contribution of these receptors to Pavlovian fear conditioning, a leading behavioral model for studying fear learning and memory, is still poorly understood. The aim of this study was to investigate the involvement of βAR activation in the acquisition, consolidation and expression of fear conditioning. We focused on manipulations of βARs in the lateral nucleus of the amygdala (LA) because of the well-established contribution of this area to fear conditioning. Specifically, we tested the effects of intra-LA microinfusions of the βAR antagonist, propranolol, on learning and memory for auditory Pavlovian fear conditioning in rats. Pre-training propranolol infusions disrupted the initial acquisition, short-term memory (STM), and long-term memory (LTM) for fear conditioning, but infusions immediately after training had no effect. Further, infusion of propranolol prior to testing fear responses did not affect fear memory expression. These findings indicate that amygdala βARs are important for the acquisition but not the consolidation of fear conditioning.

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“…The drug is known to interact with a variety of neurotransmitter systems. The noradrenergic (Sawynok 1983(Sawynok & 1987Sabetkasai et al 1997), dopaminergic (Zarrindast & Moghadampour 199 1) and adenosine systems (Sabetkasai & Zarrindast 1993) are known to influence baclofen antinociception. It has also been suggested that muscarinic mechanisms are involved in this response, as antinociception is reduced by the muscarinic receptor antagonists, atropine and scopolamine (Bartolini et al 1982;Kendall et al 1982;Tamayo et al 1988;Waught et al 1985) and increased by the choline esterase inhibitor, physostigmine (Tamayo et al 1988).…”

Section: Discussionmentioning

confidence: 99%

Baclofen‐Induced Antinociception and Nicotinic Receptor Mechanism(s)

Sabetkasai

Ahang

Shafaghi

et al. 1999

Pharmacology & Toxicology

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Abstract:In this study, the influences of nicotinic receptor agents on baclofen-induced antinociception in the tail-flick test have been studied. Intraperitoneal administration of baclofen (2.5, 5 and 10 mg/kg) to mice induced a dose-dependent antinociception in the tail-flick test. Subcutaneous injection of nicotine (0.5-2.5 mg/kg) also caused a dose-dependent antinociceptive response. Intracerebral (10 and 20 pg/mouse) but not intraperitoneal administration of hexamethonium (5 and 10 mg/kg) to mice decreased the response of both nicotine and baclofen. However, administration of the GABAB antagonist CGP 35348 (100 and 200 mglkg) decreased the response induced by baclofen but not by nicotine. It is concluded that at least part of the baclofen-induced antinociception may be mediated through a nicotinic mechanism.It is well-established that y-amino butyric acid (GABA) is an important inhibitory synaptic transmitter in the vertebrate central nervous system. GABA receptors in the brain have been classified as GABAA and GABAB (Bowery et ul. 1980(Bowery et ul. & 1981Hill & Bowery 1981). Whereas GABAA receptors are directly associated with C1-channels, the GABAs receptors seem to be G-protein coupled and linked to Ca' ' or K' channels (Bormann 1988). A third class of GABA binding site, the GAB& sites, resembles the GA-BAA receptor but is insensitive to bicuculline (Drew et al. 1984: Johnston 1996.Baclofen is a derivative of GABA (DeFeudis 1977; Johnston 1978) and the prototype GABAB agonist (Bowery 1982). The drug has major clinical use as an antispastic agent (Young & Delwaide 1981), reduces pain associated with spasticity (Pinto et al. 1972), and is useful in the treatment of trigeminal neuralgia (Fromm et al. 1984).In rodent studies, baclofen can produce antinociception in a variety of tests (Sawynok 1987; Zarrindast & Moghadampour 1991;Sabetkasai et al. 1999), but the mechanism by which this occurs is only partially understood. It has been shown that baclofen depresses the firing rate of dopamine neurones in the substantia nigra and in the ventral tegmental area (Olpe et al. 1977(Olpe et al. & 1978 electrophysiological studies have established that nicotine causes an excitation of neurones in the ventral tegmental area (Grenhoff et al. 1986;Mereu et al. 1987). Nicotinic receptor stimulation enhances the release of dopamine from the limbic system (Imperato et al. 1986) and striatal slices (Goodman 1974; Giorguieff et al. 1979).Nicotinic (Martin et al. 1983) and cholinergic (Iwamoto 1989; mechanisms have been suggested to be involved in the antinociception. However, whereas the role of monoamines in baclofen analgesia (Sawynok 1987) have been demonstrated, the role of nicotinic receptor mechanism(s) in baclofen antinociception has not been evaluated.In the present work, the effects of the nicotinic agents on baclofen-induced antinociception in the tail-flick test has been examined. Materials and MethodsAnimals. Male albino mice (25-30 g) were used in the experiments. Animals were housed in plastic cages in an an...

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Opposite Influences of Different Adrenoceptors on Baclofen‐Induced Antinociception in Mice

Cited by 5 publications

References 18 publications

Correlation between serum concentrations following continuous intravenous infusion of dexmedetomidine or medetomidine in cats and their sedative and analgesic effects

Correlation between serum concentrations following continuous intravenous infusion of dexmedetomidine or medetomidine in cats and their sedative and analgesic effects

Beta-Adrenergic Receptors in the Lateral Nucleus of the Amygdala Contribute to the Acquisition but Not the Consolidation of Auditory Fear Conditioning

Baclofen‐Induced Antinociception and Nicotinic Receptor Mechanism(s)

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