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      Evidence of interaction between fluoxetine and isosorbide dinitrate on neuroleptic-induced catalepsy in mice

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          Abstract

          Drugs which influence 5-HTergic mechanisms can modify neuroleptic-induced catalepsy (NC) in rodents, a phenomenon produced by striatal dopamine (DA) receptor blockade. Previous research also suggests a role for endogenous nitric oxide (NO) in the modulation of striatal DAergic neurotransmission; in addition, NO seems to play a role in the 5-HT reuptake mechanism. It is known that clomipramine potentiates NC in mice, but the reported effects of selective 5-HT reuptake inhibitors (SSRIs) in this model are rather contradictory. We then decided to re-address this issue, investigating the effect of fluoxetine (FX), an SSRI, on NC. In view of the ubiquitous role of NO as a central neuromodulator, we also studied the effect of isosorbide dinitrate (ID), a centrally active NO donor, and how both drugs interact to affect the phenomenon of NC. Catalepsy was induced in male albino mice with haloperidol (H; 1 mg/kg, ip) and measured at 30-min interval by means of a bar test. Drugs (FX, ID and FX + ID) or saline (controls) were injected ip 30 min before H, with each animal used only once. FX (5 mg/kg) significantly reduced NC, with maximal attenuation (about 74%) occurring at 150 min after H. ID (5 mg/kg) also inhibited NC (150 min: 62% attenuation). The combined drugs (FX + ID group), however, caused a great potentiation of NC (4.7-fold at its maximum, at 90 min). The effect observed with ID is compatible with the hypothesis that NO increases DA release in the striatum. The attenuation of NC observed with FX may be due to a preferential net effect on the raphe somatodendritic synapse, where inhibitory 5-HT1A autoreceptors are operative. The enhancement of NC caused by combined administration of FX and ID suggests the presence of a pharmacodynamic interaction, whose mechanism, still unclear, may be related to a decrease in striatal DA release

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          Most cited references16

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          Haloperidol-induced catalepsy is mediated by postsynaptic dopamine receptors.

          P Sanberg (1980)
          Antipsychotic or neuroleptic drugs, which block central dopamine receptors, produce a behavioural state in animals in which they fail to correct externally imposed postures. This is referred to as catalepsy. Previous lesion studies have shown that the dopamine receptors in the striatum are involved in this neuroleptic-induced catalepsy. Dopamine receptors, identified by the specific, high-affinity binding of the potent neuroleptic haloperiodol, have been shown to be equally distributed postsynaptically on striatal neurones and presynaptically on cortico-striatal terminals. Because the electrolytic lesioning studies have unavoidably damaged both pre- and postsynaptic striatal dopamine receptors, it is not known whether these two receptors are separately involved in neuroleptic-induced catalepsy. Using kainic acid and cortical ablation to destroy postsynaptic and presynaptic dopamine receptors, respectively, the present study demonstrates that the cataleptic effects of haloperidol are apparently mediated by dopamine receptors localised postsynaptically on striatal neurones.
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            The Biochemical Pathways of Nitric Oxide Formation from Nitrovasodilators

            M Feelisch (1991)
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              Extrapyramidal side effects and increased serum prolactin following fluoxetine, a new antidepressant

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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                bjmbr
                Brazilian Journal of Medical and Biological Research
                Braz J Med Biol Res
                Associação Brasileira de Divulgação Científica (Ribeirão Preto )
                1414-431X
                March 1998
                : 31
                : 3
                : 417-420
                Affiliations
                [1 ] Universidade Federal do Espírito Santo Brazil
                Article
                S0100-879X1998000300014
                10.1590/S0100-879X1998000300014
                ae1144be-7735-41e8-a0b5-2d88b4d1359c

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Brazil

                Self URI (journal page): http://www.scielo.br/scielo.php?script=sci_serial&pid=0100-879X&lng=en
                Categories
                BIOLOGY
                MEDICINE, RESEARCH & EXPERIMENTAL

                Medicine,General life sciences
                fluoxetine,isosorbide dinitrate,neuroleptic-induced catalepsy,nitric oxide,serotonin reuptake inhibitors,dopaminergic transmission

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