Multiunit activity from the A9 and A10 areas in rats following chronic treatment with different neuroleptic drugs

Тодорова, Анна; Dimpfel, Wilfried

doi:10.1016/0924-977x(94)90298-4

Cited by 15 publications

(5 citation statements)

References 25 publications

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“…This reasoning has been successfully extended to newer antipsychotics (Meltzer et al , 2003). Interestingly, single‐unit in vivo recording from the A9 and A10 areas in rats has revealed two types of cells that responded differently to 3‐weeks repetitive dosing with haloperidol or clozapine (Todorova and Dimpfel, 1994). The putative non‐dopaminergic cells changing their activity in the presence of clozapine were speculated to be under the influence of 5‐HT.…”

Section: Discussionmentioning

confidence: 99%

Characterization of atypical antipsychotic drugs by a late decrease of striatal alpha1 spectral power in the electropharmacogram of freely moving rats

Dimpfel

2007

British J Pharmacology

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Background and purpose: Drug administration modifies the balance of neurotransmitter-controlled ion channel activity and consequently the firing pattern of local neuronal populations and intracerebral field potentials. Fast Fourier Transformation of these field potentials provides an electropharmacogram depicting drug-induced changes within defined frequency ranges. The present investigation was undertaken to investigate the difference between atypical and typical antipsychotic drugs. Experimental approach: Adult Fisher rats were implanted with 4 bipolar concentric steel electrodes using a stereotactic surgical procedure. Field potentials from four selected brain areas in freely moving rats were used to analyse the frequency content of the electropharmacogram after administration of 4 clinically used atypical antipsychotic drugs. Key results: Atypical antipsychotics exerted effects similar to those reported for typical antipsychotics, on the electropharmacogram during the first hour after administration, whereas clear differences emerged during the second and third hour after dosing. During the latter period, only atypical antipsychotic drugs produced a statistically significant decrease in alpha1 and beta1 spectral power, especially within the striatum, somewhat less in the cortex. Conclusions and implications: Previous studies have attributed alpha1 frequency changes to the influence of 5-hydroxytryptamine (5-HT) and the present data are consistent with additional binding of atypical drugs to 5-HT receptors. This implies that a change in the balance between dopaminergic and 5-hydroxytryptaminergic neurotransmission (activation of both) is likely to underlie the relative lack of extrapyramidal side effects characteristic of atypical antipsychotics and also for their higher efficacy in the treatment of mood and cognition deficits in schizophrenics.

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Section: Discussionmentioning

confidence: 99%

Characterization of atypical antipsychotic drugs by a late decrease of striatal alpha1 spectral power in the electropharmacogram of freely moving rats

Dimpfel

2007

British J Pharmacology

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“…Many research groups have provided data confirming antipsychotic drug-induced DA cell depolarization block (Skarsfeldt 1988, 1994; Henry et al 1992; Todorova and Dimpfel 1994; see Grace et al 1997 for review). In addition to electrophysiological data, several studies employing other techniques provided support for the ability of long-term antipsychotic drug treatment to induce depolarization block.…”

Section: Antipsychotic Drug Treatment and Da Cell Depolarization Blockmentioning

confidence: 99%

“…Thus, treatment with classical antipsychotics results in depolarization block of DA regions that project to motor-related structures, whereas the atypical antipsychotic drug clozapine induces depolarization block in mesolimbic/mesocortical DA cells located in the ventral tegmental area (Chiodo and Bunney 1983;White and Wang 1983) that project to the limbic system. Many research groups have provided data confirming antipsychotic drug-induced DA cell depolarization block (Skarsfeldt 1988(Skarsfeldt , 1994Henry et al 1992;Todorova and Dimpfel 1994;see Grace et al 1997 for review). In addition to electrophysiological data, several studies employing other techniques provided support for the ability of longterm antipsychotic drug treatment to induce depolarization block.…”

Section: Normal Schizophrenicmentioning

confidence: 99%

Dysfunctions in Multiple Interrelated Systems as the Neurobiological Bases of Schizophrenic Symptom Clusters

O’Donnell

Grace

1998

Schizophrenia Bulletin

177

115

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The absence of an animal model that accurately approximates schizophrenia limits current research into the pathophysiology of this disorder. Obviously, the cognitive disturbances associated with schizophrenia are difficult to evaluate in laboratory animals. Nonetheless, animal studies have provided insight into the anatomy and physiology of the brain systems that have been implicated in schizophrenia. These studies also suggest how brain systems may be involved in information processing in normal and pathological conditions. Thus, a careful assessment of the properties and functions of the brain regions suggested to be involved in schizophrenic symptoms has been a primary objective in several laboratories. In this review, we discuss the interactions among the brain regions implicated in schizophrenia-the ventral striatum, prefrontal cortex, hippocampus, and dopamine systems-and provide an integrative model linking altered function in these regions with specific clusters of symptoms of schizophrenia.Key words: Nucleus accumbens, hippocampus, prefrontal cortex, thalamus, dopamine, negative symptoms, positive symptoms, thought disorder. Schizophrenia Bulletin, 24(2):267-283,1998.Schizophrenia is a complex disorder characterized by a profound disturbance of cognitive functions. A major problem in the study of schizophrenia is the diversity of its symptoms, leading to the suggestion that schizophrenia is actually a cluster of diseases. An integrative clinical view was brought up by Liddle, who used factor analysis to segregate symptoms of schizophrenia into three clusters-reality distortion, psychomotor poverty, and disorganization (Liddle et al. 1992fc)-and proposed that dysfunctions in specific brain regions were involved in each cluster of symptoms (Liddle et al. 1992a). This interpretation is reinforced by a number of studies that implicate a variety of structures in the pathophysiology of schizophrenia. These structures include the prefrontal cortex (PFC), medial temporal lobe (including the hippocampus), ventral striatum, and mesolimbic dopamine (DA) system. In this review, we will link information regarding the physiological interactions among these systems with clinical investigations, in an attempt to analyze these symptom clusters from an anatomical perspective.

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“…Acute exposure to olanzapine or clozapine increases the number of spontaneously active dopaminergic neurons in A10 and reverses the acute inhibition of these neurons induced by d-amphetamine [54]. Todorova and Dimpfel [55] found that chronic haloperidol and clozapine exposure reduced the number of spontaneously active dopaminergic neurons in A10, while reductions in the number of spontaneously active dopaminergic neurons in A9 were observed only for haloperidol (see also ref. [56]).…”

Section: Non-human Animal Investigations Provide Neural Interpretatiomentioning

confidence: 99%

“…[56]). This basic pattern of reductions in the number of spontaneously active dopaminergic neurons in VTA, but not SNC, has been observed following chronic exposure to clozapine [55,57], sertindole [57], and olanzapine [58], as well as other putative antipsychotic agents [59]. In cortical targets of VTA neurons (e.g., frontal cortex) chronic haloperidol increases excitatory signaling, while clozapine reduces basal levels of glutamate [60] and exposure to olanzapine reduces firing rates [61].…”

Section: Non-human Animal Investigations Provide Neural Interpretatiomentioning

confidence: 99%

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

Abbott¹,

Jaramillo²,

Wilcox³

et al. 2013

Current Medicinal Chemistry

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The evidence that antipsychotics improve brain function and reduce symptoms in schizophrenia is unmistakable, but how antipsychotics change brain function is poorly understood, especially within neuronal systems. In this review, we investigated the hypothesized normalization of the functional magnetic resonance imaging (fMRI) blood oxygen level dependent signal in the context of antipsychotic treatment. First, we conducted a systematic PubMed search to identify eight fMRI investigations that met the following inclusion criteria: case-control, longitudinal design; pre-and post-treatment contrasts with a healthy comparison group; and antipsychotic-free or antipsychoticnaïve patients with schizophrenia at the start of the investigation. We hypothesized that aberrant activation patterns or connectivity between patients with schizophrenia and healthy comparisons at the first imaging assessment would no longer be apparent or "normalize" at the second imaging assessment. The included studies differed by analysis method and fMRI task but demonstrated normalization of fMRI activation or connectivity during the treatment interval. Second, we reviewed putative mechanisms from animal studies that support normalization of the BOLD signal in schizophrenia. We provided several neuronal-based interpretations of these changes of the BOLD signal that may be attributable to long-term antipsychotic administration.

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Multiunit activity from the A9 and A10 areas in rats following chronic treatment with different neuroleptic drugs

Cited by 15 publications

References 25 publications

Characterization of atypical antipsychotic drugs by a late decrease of striatal alpha1 spectral power in the electropharmacogram of freely moving rats

Characterization of atypical antipsychotic drugs by a late decrease of striatal alpha1 spectral power in the electropharmacogram of freely moving rats

Dysfunctions in Multiple Interrelated Systems as the Neurobiological Bases of Schizophrenic Symptom Clusters

Antipsychotic Drug Effects in Schizophrenia: A Review of Longitudinal fMRI Investigations and Neural Interpretations

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