Perception and psychoses: The role of glutamatergic transmission within the nucleus accumbens septi

Gargiulo, Pascual Ángel; Gargiulo, A.

doi:10.1017/s0140525x04270182

Cited by 12 publications

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“…in animals, suggesting that a glutamatergic dysfunction within NAS is related to positive [2,21,[23][24][25]45] and negative [23,24,44] symptoms, and also, to working memory schizophrenic dysfunction [4]. These later findings are in accordance with the fact that NAS is considered today a switchboard for goaldirected behaviors [32].…”

supporting

confidence: 63%

Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi

López

Caif

Fraile

et al. 2013

Pharmacological Reports

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Abstract:Background: The effect of the agonism on g-aminobutyric acid (GABA) receptors was studied within medial prefrontal cortex (mPFC), amygdala (AMY) and ventral hipocampus (VH) in the plus-maze test in male rats bilaterally cannulated. These structures send glutamatergic projections to the nucleus accumbens septi (NAS), in which interaction and integration between these afferent pathways has been described. In a previous study of our group, blockade of glutamatergic transmission within NAS induced an anxiolytic like effect. Methods: Three rat groups received either saline or dipotassium chlorazepate (1 or 2 µg/1 µl solution) 15 min before testing. Time spent in the open arms (TSOA), time per entry (TPE), extreme arrivals (EA), open and closed arms entries (OAE, CAE) and relationship between open-and closed-arms quotient (OCAQ) were recorded. Results: In the AMY injected group TSOA, OAE and EA were increased by the higher doses of dipotassium chlorazepate (p < 0.01). In the mPFC, TPE was decreased by both doses (p < 0.05). Injection within ventral hippocampus (VH) decreased TSOA, OAE and OCAQ with lower doses (p < 0.05). When the three studied saline groups were compared, TSOA, OAE, EA and OCAQ were enhanced in the VH group when compared to mPFC and AMY (p < 0.001). Insertion of inner canula (p < 0.001, p < 0.01, p < 0.01) and saline injection showed an increasing significant difference (p < 0.001 in all cases) with the action of guide cannula alone within VH in TSOA, OAE and EA. Conclusion: We conclude that the injection of dipotassium chlorazepate has a differential effect depending of the brain area, leading to facilitatory and inhibitory effects on anxiety processing.

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supporting

confidence: 63%

Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi

López

Caif

Fraile

et al. 2013

Pharmacological Reports

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“…The circumstance that experimental alterations of Acc transmission mechanisms affected the visual discriminative performance of pigeons in a schi zophrenia-congruent manner (Acerbo et aI., 2002;Gm'giulo, 2003;Gargiulo et aI., 1998; Gm'giulo and Landa de Gargiulo, 2004) has suggested to us that the preparation could serve as a model to study the processes that might underlie the perceptuocognitive disturbances typical of schizophrenia (Conrad, 1966;Del Vecchio and Garg iulo, 1992;Silverstein et aI. , 2000).…”

mentioning

confidence: 99%

Cognitive effects of dopaminergic and glutamatergic blockade in nucleus accumbens in pigeons

Gargiulo

Acerbo

Krug

et al. 2005

Pharmacology Biochemistry and Behavior

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In earlier studies it was found that glutamatergic transmission within the nucleus accumbens septi is involved in the performance of a learned visual shape discrimination in pigeons. This study examines what effects several kinds of glutamate and dopamine antagonists have on the same task. Pigeons were trained with the relevant discrimination, bilaterally implanted with cannulas into the nucleus accumbens and tested after various transmission blockers had been administered intracerebrally. SCH-23390, a D1 dopamine antagonist, at the dose used, had no effect, and Spiperone, a D2-dopamine and 5HT2a-serotonine antagonist, significantly decreased the error repeat trials. CNQX, a non-NMDA glutamate receptor antagonist, and Cycloleucine, an antagonist of the glycine allosteric site of NMDA receptors, had no effect. CGS-19755, a selective competitive NMDA antagonist, significantly impaired performance by significantly decreasing the percent correct trials and increasing the error repeat trials. CPPG, a II/III metabotropic glutamate antagonist, remarkably improved performance. MMPG, a III/II metabotropic glutamate antagonist, at the dose used, did not have any significant effect. The preparation employed may be a useful animal model of perceptual disturbances in schizophrenia.

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“…Finally, cognitive symptoms, considered today as very relevant schizophrenic manifestation, were also modeled in our laboratory in both, punished [41] and not punished tests [42]. All evidences led to a glutamatergic neurotransmitter dysfunction within the nucleus accumbens septi (NAS) as a common fact (Table 1) [43]. We shall explain our evidence lines in this short review.…”

Section: Schizophrenic Symptoms: Our Translational Approachesmentioning

confidence: 89%

“…The perceptual disorders have been widely remarked by our team in the field of psychoses [43][44][45][46][47]. This topic has been recently taken as a central fact of this illness [48], since perceptual cognitive distortions are a core symptom of schizophrenic psychoses [37,49].…”

Section: Primary or Positive Symptoms: Perceptual Disordersmentioning

confidence: 99%

Glutamate and modeling of schizophrenia symptoms: Review of our Findings: 1990–2014

Gargiulo

2014

Pharmacological Reports

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In the early 90s, we studied the role of perception disturbances in schizophrenia in our first clinical approaches, using the Bender test in schizophrenic patients. Results were clear, showing a shape discrimination failure. Following this initial results, we reproduced nuclear symptoms of schizophrenia in animal models, showing that perceptual disturbances, acquisition disturbances, decrease in affective levels and working memory disturbances can be induced by specific N-methyl-D-aspartic acid (NMDA) glutamatergic blockade within the nucleus accumbens septi (NAS). We studied also another glutamatergic and dopaminergic drugs, finding that a decrease in glutamatergic transmission within NAS led to cognitive disturbances and affective flattening. An increase in glutamatergic transmission fully enhances cognition in the tasks used. Dopaminergic D-2 antagonists partially improved cognition. Our results link the proposed corticostriatal dysfunction with the thalamocortical disturbances underlying perceptual problems, but also influencing affective levels and cognitive variables. According to our translational findings, core schizophrenia symptoms may be translationally reproduced antagonizing NMDA receptors within NAS, and improved blocking the glutamate auto-receptor. Dopaminergic transmission appears to have a role in therapeutic but not in the early pathophysiology of schizophrenia.

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Perception and psychoses: The role of glutamatergic transmission within the nucleus accumbens septi

Cited by 12 publications

References 0 publications

Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi

Differential behavioral profile induced by the injection of dipotassium chlorazepate within brain areas that project to the nucleus accumbens septi

Cognitive effects of dopaminergic and glutamatergic blockade in nucleus accumbens in pigeons

Glutamate and modeling of schizophrenia symptoms: Review of our Findings: 1990–2014

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