Some behavioural effects of risperidone in rats: comparison with haloperidol

Nowakowska, Elżbieta; Chodera, A; Kus, Krzysztof; Rybakowski, Janusz

doi:10.1016/s0924-977x(99)00021-8

Cited by 24 publications

(17 citation statements)

References 19 publications

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“…27, NO. 4 Nicotine-Antipsychotic Interactions and Memory 539 ing a working memory task (Honey et al 1999;Nowakowska et al 1999). In the current nicotine-risperidone experiment, acute risperidone administration in isolation did not induce a significant change in memory performance in rats on the radial-arm maze.…”

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Nicotine Interactions with Haloperidol, Clozapine and Risperidone and Working Memory Function in Rats

Addy

Levin

2002

Neuropsychopharmacology

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Nicotine has been shown in a variety (Buccafusco et al. 1996;Levin 1992;Levin et al. 1996b;Levin and Simon 1998). In particular, nicotine has been shown to improve working memory performance. In previous work, acute and chronic nicotine administration led to working memory improvements in rats tested on the radial-arm maze. In chronic administration studies, these effects persisted for at least two weeks after drug administration ended. The nicotinic antagonist, mecamylamine, blocked the memory improvements of both chronic and acute nicotine administration (Levin et al. 1993;Levin and Russell 1992). Nicotinic systems play an important role in the neural basis of memory function.Nicotinic systems interact with a variety of other neural systems, which may be important in the neural basis of memory function. Activation of nicotinic receptors leads to the downstream release of many neurotransmitters including acetylcholine, dopamine (DA), NO . 4 Nicotine-Antipsychotic Interactions and Memory 535 norepinephrine, serotonin, and glutamate (Wonnacott et al. 1989). DA in particular has been shown to be important for memory function (Levin 1988). Several studies have examined the role of DA in memory function as well as the interactive effects of nicotine and DA. Previous work in our laboratory has illustrated the importance of DA in cognitive function by showing that both nicotinic and DA antagonists cause working memory deficits in rats tested on the radial arm maze. Nicotinic and DA agonists, on the other hand, induced working memory improvements in rats (Levin and Eisner 1994;Levin et al. 1990;Levin and Rose 1992; McGurk et al. 1989a,b). In addition, nicotine and nicotinic agonists have been shown to increase DA release in the striatum and the nucleus accumbens (Brazell et al. 1990;el-Bizri and Clarke 1994;Grady et al. 1992). Thus, the data illustrate that nicotinic and DA interactions are important for memory function (Levin et al. 1996a). However, the mechanisms of these interactions and their effects on memory are still unclear (Levin et al. 1996a).The aim of the current study was to further explore the memory effects of interactions between the nicotinic and DA systems. While our previous studies involved the use of selective DA receptor drugs, this study employed the use of three antipsychotic medications: haloperidol, clozapine and risperidone. Many previous studies have explored DA effects on memory by looking at the memory effects of antipsychotic medications, which often act as DA antagonists at specific DA receptors. Haloperidol, a typical antipsychotic, is characterized by its antagonistic binding at the D 2 DA receptors. Clozapine, an atypical antipsychotic, binds to the D 4 DA receptor subtype 10 times as strongly as it binds to D 2 receptors. It also differs from haloperidol in that it shows a high affinity for 5-HT 2 sites and a much lower affinity for D 2 sites in the cerebral cortex and striatum (Matsubara et al. 1993). Risperidone, another atypical antipsychotic, also has a higher affinity for th...

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Nicotine Interactions with Haloperidol, Clozapine and Risperidone and Working Memory Function in Rats

Addy

Levin

2002

Neuropsychopharmacology

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“…Carbamazepine (CBZ), a drug useful in treating partial and complex seizures, is effective in treating posttraumatic stress disorder [13,17,32] and panic disorder [13,17,33,34] . Several studies on animals also emphasize the anxiolytic [35][36][37] and anticonflict [38] effects of acute or chronic administration of CBZ. The anxiolytic properties of CBZ may derive from the preventive effect it has upon the release of excitatory neurotransmitters through the blockade of voltage-gated sodium channels, from its influence on glutamatergic neurotransmission (via NMDA receptors [13] ) or via the GABA receptor mechanism [13,39,40] .…”

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Role of Ventral Hippocampal GABA<sub>A</sub> and NMDA Receptors in the Anxiolytic Effect of Carbamazepine in Rats Using the Elevated Plus Maze Test

Rezvanfard¹,

Zarrindast²,

Bina³

2009

Pharmacology

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Background: The successful use of antiepileptic drugs to treat a wide range of nonepileptic disorders led us to evaluate the potential efficacy of carbamazepine (CBZ) in anxiety disorders. Anxiety may be related to the imbalance between γ-aminobutyric acid (GABA) and glutamate neurotransmitters, systems that are also involved in the CBZ effects. We investigated the role of these systems in the ventral hippocampus (VH) and their interactions with the CBZ effect on anxiety-like behavior in rats using the elevated plus maze. Methods: Animals received GABAergic and NMDA agents in a volume of 1 μl/rat, which was injected into the VH (0.5 μl for each side) 60 min after receiving systemic administration of CBZ. The test sessions took place 10 min later. Results: The systemic administration of CBZ increased the percentage of open arm time (%OAT) at the dose of 40 mg/kg, which is representative of an anxiolytic response. Intra-VH injection of the GABA_A receptor agonist muscimol (0.25–1 μg/rat) in the absence or presence of an ineffective dose of CBZ (30 mg/kg) did not show any significant changes in the parameters of anxiety-like behavior. The administration of GABA_A receptor antagonist bicuculline by itself decreased %OAT at a dose of 1 μg/rat, indicating possible anxiogenic effect. The antagonist (0.75 and 1 μg/rat) also decreased CBZ response. A microinjection of NMDA (0.125 and 0.25 μg/rat) decreased %OAT, which was reversed by the administration of CBZ (40 mg/kg). This indicates interaction between the two drugs. However, the NMDA receptor antagonist DAP-5 (1 μg/rat) significantly increased %OAT, but combined with the lower dose of CBZ (30 mg/kg), it did not trigger any response on anxiety-like parameters. Conclusion: Both GABAergic and NMDA systems in the VH play a role in modulation of anxiety-like behavior of rats. The anxiolytic-like effects of CBZ seem to be mediated, at least in part, through an interaction with GABA_A and NMDA systems in the VH.

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“…Again, such effects would not be expected to underlie deficits in water maze performance. It should be noted that risperidone has been observed to have anxiolytic effects in other rodent studies (Nowakowska et al, 1999).…”

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confidence: 99%

Protracted effects of chronic oral haloperidol and risperidone on nerve growth factor, cholinergic neurons, and spatial reference learning in rats

et al. 2007

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The primary therapeutic agents used for schizophrenia, antipsychotic drugs, ameliorate psychotic symptoms; however, their chronic effects on cognition (or the physiologic processes of the brain that support cognition) are largely unknown. The purpose of this rodent study was to extend our previous work on this subject by investigating persistent effects (i.e., during a 14 day drug-free washout period) of chronic treatment (i.e., ranging from 45 days to six months) with a representative first and second generation antipsychotic. Drug effects on learning and memory and important neurobiological substrates of memory, the neurotrophin, nerve growth factor (NGF) and its receptors, and certain components of the basal forebrain cholinergic system were investigated. Behavioral effects of oral haloperidol (2.0 mg/kg/day), or risperidone (2.5 mg/kg/day) were assessed in an open field, a water maze task, and a radial arm maze procedure and neurochemical effects in brain tissue were subsequently measured by enzyme linked immunosorbant assays (ELISAs). The results indicated that both antipsychotics produced time-dependent and protracted deficits in the performance of a water maze procedure when compared to vehicle-treated controls, while neither drug was associated with significant alterations in radial arm maze performance. Interestingly, haloperidol, but not risperidone, was detectible in the rodent brain in appreciable levels for up to two weeks after drug discontinuation. Both antipsychotics were also associated with reduced levels of NGF protein in the basal forebrain and prefrontal cortex and significant (or nearly significant) decreases in phosphoTrkA protein and the vesicular acetylcholine transporter (depending on the brain region analyzed). Neither antipsychotic markedly affected TrkA or p75 NTR levels. These data indicate that chronic treatment with either haloperidol or risperidone may be associated with protracted negative effects

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Some behavioural effects of risperidone in rats: comparison with haloperidol

Cited by 24 publications

References 19 publications

Nicotine Interactions with Haloperidol, Clozapine and Risperidone and Working Memory Function in Rats

Nicotine Interactions with Haloperidol, Clozapine and Risperidone and Working Memory Function in Rats

Role of Ventral Hippocampal GABA<sub>A</sub> and NMDA Receptors in the Anxiolytic Effect of Carbamazepine in Rats Using the Elevated Plus Maze Test

Protracted effects of chronic oral haloperidol and risperidone on nerve growth factor, cholinergic neurons, and spatial reference learning in rats

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