Transcultural aspects of somatic symptoms in the context of depressive disorders.

Somatic symptoms are a common presentation of mental disorders or psychological distress worldwide, and may often coexist with depressive and anxiety symptoms, thus accounting for what might be the most frequent psychiatric syndrome in primary care. Indeed, physical symptoms accompanying the clinical presentations of a variety of mental disorders may be considered as universal 'idioms of distress' that may vary across cultures, depending on attitudes and explanations embedded in each one of them. These variations in symptom presentations are the result of various interacting factors that ultimately determine how individuals identify and classify bodily sensations, perceive illness, and seek medical attention. This chapter examines the impact of culture on the experiencing of somatic symptoms, based on an inclusive review of the topic from ethnic, nosological, clinical and social perspectives. Particular attention is paid to the association of somatic symptoms with mood symptoms, since depressive disorders appear to be the most common, costly and disabling psychiatric entities worldwide. The review shows that racial/ethnic variations in somatic symptoms in the context of depression are common, and seem to be related to depression severity. Sociocultural factors, particularly stigma, may influence the unique emphasis placed on somatic symptoms within depression, and may account for some racial/ethnic differences in somatic symptom reporting.

Regulated release of BDNF by cortical oligodendrocytes is mediated through metabotropic glutamate receptors and the PLC pathway.

A number of studies suggest that OLGs (oligodendrocytes), the myelinating cells of the central nervous system, are also a source of trophic molecules, such as neurotrophins that may influence survival of proximate neurons. What is less clear is how the release of these molecules may be regulated. The present study investigated the effects of BDNF (brain-derived neurotrophic factor) derived from cortical OLGs on proximate neurons, as well as regulatory mechanisms mediating BDNF release. Initial work determined that BDNF derived from cortical OLGs increased the numbers of VGLUT1 (vesicular glutamate transporter 1)-positive glutamatergic cortical neurons. Furthermore, glutamate acting through metabotropic, and not AMPA/kainate or NMDA (N-methyl-d-aspartate), receptors increased BDNF release. The PLC (phospholipase C) pathway is a key mediator of metabotropic actions to release BDNF in astrocytes and neurons. Treatment of OLGs with the PLC activator m-3M3FBS [N-(3-trifluoromethylphenyl)-2,4,6-trimethylbenzenesulfonamide] induced robust release of BDNF. Moreover, release elicited by the metabotropic receptor agonist ACPD [trans-(1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid] was inhibited by the PLC antagonist U73122, the IP3 (inositol triphosphate 3) receptor inhibitor 2-APB (2-aminoethoxydiphenylborane) and the intracellular calcium chelator BAPTA/AM [1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetra-acetic acid tetrakis(acetoxymethyl ester)]. Taken together, these results suggest that OLG lineage cells release BDNF, a molecule trophic for proximate neurons. BDNF release is regulated by glutamate acting through mGluRs (metabotropic glutamate receptors) and the PLC pathway. Thus glutamate and BDNF may be molecules that support neuron-OLG interactions in the cortex.