13 Thus, it is concluded that sensory information from the anterior two thirds of tongue may not be required for new taste recognition, but necessary for the development of sweet preferences, and its disruption result in the development of anhedonia. Development of anhedonia has been ascribed to dysfunction of the reward pathway, in which the nucleus accumbens plays a pivotal role.18 and 19 The nucleus accumbens core and shell receives a dense serotonergic innervation from the raphe nucleus,20 and chronically Natural Product Library stressed rats, a model of depression, showed a reduced serotonin response in the nucleus accumbens shell to cocaine.21 Also, it was suggested that mal-regulation of dopaminergic

activity in the nucleus accumbens by serotonin may be involved in a depressive phenotype.22 These reports together suggest a possible implication of serotonergic dysfunction in the nucleus accumbens, perhaps mal-regulating dopaminergic activity, in the pathophysiology of anhedonia. However, in this study, serotonin level in the nucleus accumbens was not significantly decreased even a month after the bilateral transections of the lingual and chorda tympani nerves. Thus, it is concluded that the pathophysiology of anhedonia that induced by the bilateral transections

of the lingual and chorda tympani nerves BTK inhibitor may not comprise a serotonergic dysfunction in the nucleus accumbens. In this study, Nx rats showed behavioural depressions with increased anxiety-like behaviours; i.e., ambulatory activities, centre zone activities and number of rearing were decreased, and rostral grooming increased, during the activity test; open arm stay was decreased during elevated plus maze test; immobility was increased during forced swim test per se. Dysfunction in the brain serotonin system is implicated in a variety of psychiatric disorders, including major depression23 and anxiety.24 Many studies have suggested that disrupted hippocampal

functions are implicated in depression-25 and anxiety-like behaviours,26 and that serotonin Isoconazole modulates the hippocampal function.27 In this study, the hippocampal serotonin level was markedly decreased in Nx rats compared to sham rats although its metabolite 5-HIAA levels did not differ between Nx and sham rats, suggesting that serotonergic neurotransmission in the hippocampus is decreased following the bilateral transections of the lingual and chorda tympani nerves. We have previously reported that in an animal model of early life stress experience, depression- and anxiety-like behaviours were accompanied by a decreased serotonin neurotransmission in the raphe–hippocampus axis,28 and improved depression-like behaviours were associated with an increased serotonergic activity in the raphe–hippocampus axis.