{'fraction_non_alphanumeric': 0.021512838306731435, 'fraction_numerical': 0.008327550312283136, 'mean_word_length': 5.645161290322581, '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}}
[Serotonin receptor changes in depression: evidences and limitations].

Serotonin and serotonin receptors might be involved in the pathophysiology of depression. In the following, research data supporting the general hypothesis of adaptatives changes in density and functioning of serotonergic receptors in depression are review. Binding assays, platelet and neuroendocrine studies supports this theory. The density of 5-HT2A binding sites in postmortem brain tissue of depressed patients and suicide victims, as well as in platelets of drug-free depressed patients has been found to be increased by several authors. The reduce hormonal response to fenfluramine challenge test in depression appears to indicate a sub-normal functioning of 5-HT2A receptors, however studies evaluating physiologic platelet 5-HT2A receptor-mediated responses have produced conflicting results. On the other hand, neuroendocrine challenges tests with 5-HT1A agonists suggest that presynaptic and postsynaptic 5-HT1A receptors may be also desensitized in depression. To date, postmorten receptor 5-HT1A studies in suicide victims have not yielded consistent. Taken together, these findings provide support for hypotheses of amine receptor abnormalities in depression, and indicate the need for expanded studies of amine receptor density and function in depression. Nevertheless, the role of these changes in the pathophysiology of depression has not been proved.