Alterations of Thalamic Activity in Schizophrenia and in Response to Antipsychotic Drugs Studies in the Legacy of Seymour S. Kety

Cohen, Bruce M.; Yurgelun‐Todd, Deborah

doi:10.1016/s0893-133x(01)00277-9

Cited by 11 publications

(7 citation statements)

References 57 publications

(52 reference statements)

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“…There is evidence from post mortem and in vivo imaging studies of abnormalities of nucleus accumbens, thalamus, and amygdala in individuals with psychotic disorders (Stevens 1973;Tamminga et al 1992;Bogerts 1993;Andreasen et al 1994;Buchsbaum et al 1996;Nelson et al 1998;Lawrie et al 1999;McCarley et al 1999;Gur et al 2000;Byne et al 2001;Ende et al 2001). There is also preliminary evidence in human subjects that, as in laboratory animals, these regions may respond to antipsychotic drugs (Lewis et al 1992;Bartlett et al 1994Bartlett et al , 1998Yurgelun-Todd et al 2000;Cohen and Yurgelun-Todd 2001). Thus the findings presented here are consistent with a larger body of data suggesting that cells of the nucleus accumbens, midline thalamus and Fig.…”

Section: Discussionmentioning

confidence: 99%

Cells in midline thalamus, central amygdala, and nucleus accumbens responding specifically to antipsychotic drugs

Cohen

Cherkerzian

et al. 2003

Psychopharmacology

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Typical and atypical antipsychotic drugs shared a distinctive pattern of robust activation of cells in nucleus accumbens, central medial thalamus, and central amygdala. Antipsychotic drug-induced activation of amygdala was shared by lorazepam, but activation of thalamus and nucleus accumbens was much greater following antipsychotic drugs than following lorazepam. The pattern of activated cells may be relevant to the therapeutic actions of antipsychotic drugs.

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Section: Discussionmentioning

confidence: 99%

Cells in midline thalamus, central amygdala, and nucleus accumbens responding specifically to antipsychotic drugs

Cohen

Cherkerzian

et al. 2003

Psychopharmacology

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“…Antipsychotic drugs are all potent antimanic agents and all induce activation of similar populations of cells in the NAc (Cohen et al, 1998), regions that may be responsible for mediating many of the symptoms of bipolar disorder. While these studies were performed in rats, similar regional effects of antipsychotic drugs may occur in human subjects (Cohen and Yurgelun-Todd, 2001). Double-label immunohistochemistry identified the cells responding to antimanic/antipsychotic drugs as dynorphinergic/GABAergic neurons (Ma et al, 2003), implying that antipsychotic drugs may increase dynorphin release, leading to an antimanic or mood-lowering effect.…”

Section: Kor Agonistsmentioning

confidence: 99%

Kappa-opioid ligands in the study and treatment of mood disorders

Carlezon

Béguin

Knoll

et al. 2009

Pharmacology & Therapeutics

135

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The biological basis of mood is not understood. Most research on mood and affective states has focused on the roles of brain systems containing monoamines (e.g., dopamine, norepinephrine, serotonin). However, it is becoming clear that endogenous opioid systems in the brain may also be involved in regulation of mood. In this review, we focus on the potential utility of kappa-opioid receptor (KOR) ligands in the study and treatment of psychiatric disorders. Research from our group and others suggests that KOR antagonists might be useful for depression, KOR agonists might be useful for mania, and KOR partial agonists might be useful for mood stabilization. Currently available agents have some unfavorable properties that might be addressed through medicinal chemistry. The development of KOR-selective agents with improved drug-like characteristics would facilitate preclinical and clinical studies designed to evaluate the possibility that KORs are a feasible target for new medications.

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“…Again, the fact that the thalamus volumes were not different between typicals and atypicals groups would support that both classes of drugs may affect this region, but to a different extent. For example, differences between the effects of typical and atypical drugs have been described in thalamic GABA-mediated neural transmission (Sakai et al, 2001), monoamine metabolism (Kikumoto et al, 1993), in thalamic cerebral blood volume (Cohen and Yurgelun-Todd, 2001), and in the expression of the protein Fos, which is a marker of cellular activation (Cohen et al, 2003). It is possible that the limbic selectivity of D2/D3 receptor occupancy of atypical antipsychotics is reflected on different effects on thalamus.…”

Section: Proposed Effects Of Typical and Atypical Antipsychotics On Bmentioning

confidence: 99%

Different Effects of Typical and Atypical Antipsychotics on Grey Matter in First Episode Psychosis: the ÆSOP Study

Dazzan

Morgan

Orr

et al. 2005

Neuropsychopharmacol

248

160

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Typical antipsychotic drugs act on the dopaminergic system, blocking the dopamine type 2 (D2) receptors. Atypical antipsychotics have lower affinity and occupancy for the dopaminergic receptors, and a high degree of occupancy of the serotoninergic receptors 5-HT2A. Whether these different pharmacological actions produce different effects on brain structure remains unclear. We explored the effects of different types of antipsychotic treatment on brain structure in an epidemiologically based, nonrandomized sample of patients at the first psychotic episode. Subjects were recruited as part of a large epidemiological study (AESOP: aetiology and ethnicity in schizophrenia and other psychoses). We evaluated 22 drug-free patients, 32 on treatment with typical antipsychotics and 30 with atypical antipsychotics. We used high-resolution MRI and voxel-based methods of image analysis. The MRI analysis suggested that both typical and atypical antipsychotics are associated with brain changes. However, typicals seem to affect more extensively the basal ganglia (enlargement of the putamen) and cortical areas (reductions of lobulus paracentralis, anterior cingulate gyrus, superior and medial frontal gyri, superior and middle temporal gyri, insula, and precuneus), while atypical antipsychotics seem particularly associated with enlargement of the thalami. These changes are likely to reflect the effect of antipsychotics on the brain, as there were no differences in duration of illness, total symptoms scores, and length of treatment among the groups. In conclusion, we would like to suggest that even after short-term treatment, typical and atypical antipsychotics may affect brain structure differently.

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Alterations of Thalamic Activity in Schizophrenia and in Response to Antipsychotic Drugs Studies in the Legacy of Seymour S. Kety

Cited by 11 publications

References 57 publications

Cells in midline thalamus, central amygdala, and nucleus accumbens responding specifically to antipsychotic drugs

Cells in midline thalamus, central amygdala, and nucleus accumbens responding specifically to antipsychotic drugs

Kappa-opioid ligands in the study and treatment of mood disorders

Different Effects of Typical and Atypical Antipsychotics on Grey Matter in First Episode Psychosis: the ÆSOP Study

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