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Switching antipsychotics is more and more common in our clinical practice. Several reasons can explain this observation. We have more and more antipsychotics available on the market with different receptor binding profiles and also different tolerability issues. Usually, the reasons of the switch are the following: insufficient efficacy or problems of tolerance (weight gain, metabolic disorders, extrapyramidal symptoms, hyperprolactinemia, sedation, sexual dysfunction). So that the switch takes place without complications, it is essential for the clinician to have full knowledge of both the receptor binding profiles of the antipsychotics in question and their half-life. The clinician has to expect a dopaminergic rebound when the introduced antipsychotic has a lesser affinity for the dopaminergic D2 receptor than that which is withdrawn or if it is a partial agonist with a particularly long half-life. On the other hand, a histaminergic or cholinergic rebound can be expected if the new antipsychotic has a lesser affinity for these two receptors. In all these scenarios, a "plateau" switch will often be recommended. Now, if a faster switch is imperative, various medication strategies exist to try to decrease the impact of the rebound effects., (Copyright © 2013 L’Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

A hallmark of the host response to Plasmodium parasite is an inflammatory reaction characterized by elevated histaminemia levels. Since histamine, which acts through four different receptors and which synthesis is under the control of the histidine decarboxylase (HDC), is endowed with pro-inflammatory and immunosuppressive activities, we hypothesized that this vaso-active amine may participe to malaria pathogenesis. Combining genetic and pharmacologic approaches by using H1R(-/-), H2R(-/-), H3R(-/-), HDC(-/-) mice and H1R, H2R-, and H3R-antagonists, respectively, we found that cerebral malaria-associated pathogenetic processes such as blood brain barrier disruption, and T lymphocyte sequestration to cerebral vascular endothelium in mice were associated with histamine production. The identification of this novel inflammatory pathway and its implication in Plasmodium infection may lead to novel strategies to manipulate the anti-Plasmodium immune response and may provide new therapeutic tools to alleviate malaria disease.

Rhinitis affects about 10% of the global population. Whatever is the cause of the rhinitis, allergic or not, the physio-pathology is the same, with intervention of mediators as the origin of the nervous stimulation of the epithelium and mucosae. This innervation is threefold: parasympathetic (ACH), sympathetic (Nor ADR), non-adrenergic, non cholinergic system: neuropeptides: VIP. Rhinitis is therefore linked with imbalance of these systems. Treatment of rhinitis must be composed not only of anti H1 which are effective against secretions and sneezes, but also the anti-inflammatory steroids, which are effective against inflammation. Cromoglycate, ketotifen... should be obligatory as membrane stabilizers.

Histamine is considered as a neurotransmitter, since it is present in hypothalamus and pituitary gland. It has been reported to stimulate prolactin (PRL) release in rats and humans; it seems to be involved in the control of LH release in rats. But cimetidine, an H2 antagonist also induces PRL release in humans. To investigate the relationship between the PRL secretion and possible histaminergic pathways, the response of PRL and LH was studied for 180 minutes in 10 normal subjects (5 men, 5 women) after H1 antagonist (diphenhydramine 50 mg iv), H2 antagonist (cimetidine 300 mg iv) and placebo. Diphenhydramine and placebo injection resulted in a decrease of PRL from 0800 until 11.00 hours, suggesting a spontaneous diurnal variation. Cimetidine induced a short but significant rise of PRL before a similar diurnal secretory pattern. LH levels were unaffected by H1 and H2 antagonists. These data suggest that PRL and LH secretion in humans is unresponsive to H1 histaminergic pathways. The specific action of cimetidine remains to be defined.