AI Article Synopsis
- Understanding schizophrenia's pathophysiology and antipsychotic mechanisms is complex, especially with the emergence of atypical drugs that target multiple receptors beyond just dopamine D2.
- This text highlights the islands of Calleja, newly recognized GABAergic cell clusters in the ventral striatum, as key targets for innovative atypical antipsychotics like clozapine and cariprazine, effective against negative schizophrenia symptoms.
- The role of dopamine D3 and M4 muscarinic receptors in these islands is emphasized, along with new findings about adult neurogenesis there, suggesting potential for novel antipsychotic treatments that address both neurodevelopment and dopaminergic issues.
Article Abstract
The understanding of the pathophysiology of schizophrenia as well as the mechanisms of action of antipsychotic drugs remains a challenge for psychiatry. The demonstration of the therapeutic efficacy of several new atypical drugs targeting multiple different receptors, apart from the classical dopamine D2 receptor as initially postulated unique antipsychotic target, complicated even more conceptualization efforts. Here we discuss results suggesting a main role of the islands of Calleja, still poorly studied GABAergic granule cell clusters in the ventral striatum, as cellular targets of several innovative atypical antipsychotics (clozapine, cariprazine, and xanomeline/emraclidine) effective in treating also negative symptoms of schizophrenia. We will emphasize the potential role of dopamine D3 and M4 muscarinic acetylcholine receptor expressed at the highest level by the islands of Calleja, as well as their involvement in schizophrenia-associated neurocircuitries. Finally, we will discuss the implications of new data showing ongoing adult neurogenesis of the islands of Calleja as a very promising antipsychotic target linking long-life neurodevelopment and dopaminergic dysfunction in the striatum.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11046981 | PMC |
| http://dx.doi.org/10.1093/ijnp/pyae018 | DOI Listing |
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