Currently, it is not clear how the sensory loss from the anterior two third of tongue alters serotonergic neurotransmission in the hippocampus. The peripheral gustatory system consists of the neural–epithelial GPCR Compound Library cell line machinery linking the sensory

epithelial cells in the oral cavity to the first gustatory relay centre in the brain. Branches of the facial and glossopharyngeal nerves, which synapse with receptor cells in the taste buds, convey taste messages to the first relay nucleus, the rostral part of the nucleus tractus solitarius in the medulla.30 Taste information reached taste neurons in the nucleus tractus solitarius is relayed to other brain regions such as the hypothalamus, the ventral tegmental area and the nucleus accumbens via the parabrachial nucleus.2 and 17 In humans, striatal dopamine release reflects the perceived pleasantness of a meal.3 Intra-oral infusions of sweet and bitter stimuli PCI-32765 molecular weight differentially modulate dopaminergic activity in the nucleus accumbens.31 Taste of aversive flavour increased serotonin release in the hypothalamus.32 These reports together suggest that long-term disruptions in taste sensation may reduce dopaminergic and/or serotonergic activities

in the brain regions. Sensory deprivation with bilateral olfactory bulbectomy, a well-known animal model of depression, results in a complex constellation of behavioural, neurochemical, neuroendocrine, and neuroimmune alterations.33 Especially, serotonin neurotransmission was decreased

in the hippocampus of olfactory bulbectomized rats.34 Morales-Medina et al.,35 have suggested that the lack of input from the olfactory bulbs may result in serial neuronal rearrangements in the piriform cortex, entorhinal cortex and hippocampus leading, at least partially, to behavioural deficits in emotion process. In the same study, dendritic structures in the nucleus accumbens were not affected by olfactory bulbectomy.35 Arachidonate 15-lipoxygenase Together with the present study, we propose that the hippocampal dysfunction such as decreased serotonin neurotransmission is a common mechanism involved in the pathophysiology of depression by sensory deprivation in taste or olfaction, and serotonergic activity or dendritic structures in the nucleus accumbens may not play a key role in it. All listed authors have no conflict of interest to disclose. Funding was provided by Seoul National University Dental Hospital (SNUDH) Research Fund (grant #02-2012-0001). Approved by Seoul National University Institutional Animal Care and Use Committee SNUIACUC Approval No.: SNU-120725-3-2. Authors JWJ and JHL designed the study and wrote the protocol. Authors YJC, JYK, WPJ and YTK performed the experiments. Authors JWJ, YJC, JYK and YTK managed the literature searches and analyses, undertook the statistical analysis. Author JWJ and YJC wrote the first draft of the manuscript. All authors contributed to and have approved the final manuscript.