{'fraction_non_alphanumeric': 0.026215644820295984, 'fraction_numerical': 0.008879492600422832, 'mean_word_length': 5.646067415730337, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Antidepressants and Atypical Neuroleptics Induce Fos‐like Immunoreactivity in the Central Extended Amygdala

On the basis of anatomical connections, it has been suggested that the extended amygdala plays an important role in neuropsychiatric disorders characterized by emotional and affective alterations.1,4 However, specific data showing the effect of drugs used in the therapy of these disorders are scarce. Induction of the early-gene c-fos is secondary to neuronal activation and is correlated to an increased function of specific areas in the CNS.8 Moreover, detection of the c-fos encoded protein Fos through Fos-like immunoreactivity (FLI) allows the study of the influence of drugs in small brain areas like those examined in this study. Using this methodology it was shown that antidepressant drugs increased FLI in specific limbic areas of the rat brain and that classical and atypical antipsychotics induced a different pattern of FLI in the striatum and prefrontal cortex which was predictive of their ability to induce extrapyramidal side effects (striatum) and to be effective on the negative symptoms of schizophrenia (prefrontal cortex).2,3,5–7,9 In order to evaluate the potential role of areas belonging to the extended amygdala in the effects of antidepressant and antipsychotic drugs, we have evaluated the induction of FLI in the rat central amygdaloid nucleus, sublenticular extended amygdala (SLEA), interstitial nucleus of posterior limb of the anterior commissure (IPAC) and the bed nucleus of stria terminalis (BST). As antidepressants, we utilized citalopram, which belongs to the class of serotonin reuptake inhibitors, and the tricyclic imipramine, which blocks the reuptake of both serotonin and noradrenaline. As antipsychotics, we used clozapine, which reduces the negative symptoms of schizophrenia, and haloperidol, which belongs to classical antipsychotics and which, differently from clozapine, induces extrapyramidal side effects. Two hr after treatments male Sprague-Dawley rats were anesthetized and then perfused transcardially with paraformaldehyde. Coronal brain sections, cut with a vibratome, were incubated for 48 hr with a Fos primary antibody (OA-11-824, CRB), at a dilution of 1:1,400. The reaction was visualized using biotinylated secondary antisera and by standard avidin-biotin horseradish-peroxidase technique.6