Neurons for whole-body energy balance and the development of obesity.AcknowledgmentsWe thank Drs. Streamson Chua and Derek Huffman for critical comments 
on the manuscript, Catherine Waddell for technical support and Dr. Sukamar Vijayaraghavan for the generous gift of the Chat-tauGFP transgenic line.ConclusionBoth nicotinic and muscarinic cholinergic signaling pathways have been implicated in ingestive behavior [16,17,19]. Hypothalamic cholinergic neurons are found in the DMH, which receives information on environmental temperature as well as nutrient status [9,10] and relays this information to other hypothalamic nuclei, including the PVN, LH, SCN, and ARC [33,34]. TheAuthor ContributionsConceived and designed the experiments: YHJ. Performed the experiments: FG JHJ. Analyzed the data: FG. Contributed reagents/materials/ analysis tools: FG DAT. Wrote the paper: YHJ LWR.
It has been proposed the loudness dependence of auditory evoked potentials (LDAEP) is a reliable indicator of central serotonin system Docosahexaenoyl ethanolamide activity in humans [1,2]. The LDAEP reflects the change in the auditory evoked N1/P2 component evoked by an Lecirelin site increase in stimulus intensity and has been found to be inversely associated with central nervous system serotonergic activity [3], such that a weak LDAEP reflects high serotonergic neurotransmission, and vice versa [4]. From these findings it has been proposed that the LDAEP is a biological marker of central serotonergic activity in major depressive disorder and other psychiatric diseases [1,5,6]. In other words, a significant correlation has been found between a strong LDAEP ?indicating low serotonergic function ?and a favorable response to selective serotonin reuptake inhibitors (SSRIs) in patients with major depressive disorder or generalized anxiety disorder [7,8,9,10,11,12]. Brain-derived neurotrophic factor (BDNF) is known to play a role in neuronal survival and plasticity and to be required for proper development and survival of dopaminergic, GABAergic,cholinergic, and serotonergic neurons [13]. It was found that BDNF increases both the serotonin levels and turnover of serotonin [14]. Chronic antidepressant drug therapy up-regulates the expression of BDNF and its receptor and increases neurogenesis in the adult rat hippocampus [15,16,17]. There is also evidence that acute treatment rapidly activates TrkB (tropomyosin-related kinase B) receptors, which are related to BDNF [18]. This effect is not observed in serotonin-depleted mice, which points to the crucial role of serotonin in increasing the actions of BDNF on its receptor [18]. Low serum BDNF levels are reportedly associated with a strong LDAEP as a reflection of low central serotonergic activity [19]. Recently, another study found an association between BDNF single-nucleotide polymorphisms (SNPs; rs6265-rs2030324rs1491850) and the LDAEP as an indicator of central nervous serotonergic activity, as revealed in both haplotype and singlemarker analyses in German descendents [20]. The haplotype analysis revealed that the LDAEP was stronger in carriers of the G(Val)-C-T [rs6265(Val66Met)-rs2030324-rs1491850] haplotype within the BDNF gene than in other haplotype carriers [20]. From this it was suggested that subjects with the BDNF haplotypeBDNF Gene and LDAEPG(Val)-C-T are characterized by low serotonergic activity and possibly by low serum BDNF levels [20]. The aim of this study was thus to determine the association between genetic polymorphisms of BDNF and the LDAEP in a hea.Neurons for whole-body energy balance and the development of obesity.AcknowledgmentsWe thank Drs. Streamson Chua and Derek Huffman for critical comments on the manuscript, Catherine Waddell for technical support and Dr. Sukamar Vijayaraghavan for the generous gift of the Chat-tauGFP transgenic line.ConclusionBoth nicotinic and muscarinic cholinergic signaling pathways have been implicated in ingestive behavior [16,17,19]. Hypothalamic cholinergic neurons are found in the DMH, which receives information on environmental temperature as well as nutrient status [9,10] and relays this information to other hypothalamic nuclei, including the PVN, LH, SCN, and ARC [33,34]. TheAuthor ContributionsConceived and designed the experiments: YHJ. Performed the experiments: FG JHJ. Analyzed the data: FG. Contributed reagents/materials/ analysis tools: FG DAT. Wrote the paper: YHJ LWR.
It has been proposed the loudness dependence of auditory evoked potentials (LDAEP) is a reliable indicator of central serotonin system activity in humans [1,2]. The LDAEP reflects the change in the auditory evoked N1/P2 component evoked by an increase in stimulus intensity and has been found to be inversely associated with central nervous system serotonergic activity [3], such that a weak LDAEP reflects high serotonergic neurotransmission, and vice versa [4]. From these findings it has been proposed that the LDAEP is a biological marker of central serotonergic activity in major depressive disorder and other psychiatric diseases [1,5,6]. In other words, a significant correlation has been found between a strong LDAEP ?indicating low serotonergic function ?and a favorable response to selective 
serotonin reuptake inhibitors (SSRIs) in patients with major depressive disorder or generalized anxiety disorder [7,8,9,10,11,12]. Brain-derived neurotrophic factor (BDNF) is known to play a role in neuronal survival and plasticity and to be required for proper development and survival of dopaminergic, GABAergic,cholinergic, and serotonergic neurons [13]. It was found that BDNF increases both the serotonin levels and turnover of serotonin [14]. Chronic antidepressant drug therapy up-regulates the expression of BDNF and its receptor and increases neurogenesis in the adult rat hippocampus [15,16,17]. There is also evidence that acute treatment rapidly activates TrkB (tropomyosin-related kinase B) receptors, which are related to BDNF [18]. This effect is not observed in serotonin-depleted mice, which points to the crucial role of serotonin in increasing the actions of BDNF on its receptor [18]. Low serum BDNF levels are reportedly associated with a strong LDAEP as a reflection of low central serotonergic activity [19]. Recently, another study found an association between BDNF single-nucleotide polymorphisms (SNPs; rs6265-rs2030324rs1491850) and the LDAEP as an indicator of central nervous serotonergic activity, as revealed in both haplotype and singlemarker analyses in German descendents [20]. The haplotype analysis revealed that the LDAEP was stronger in carriers of the G(Val)-C-T [rs6265(Val66Met)-rs2030324-rs1491850] haplotype within the BDNF gene than in other haplotype carriers [20]. From this it was suggested that subjects with the BDNF haplotypeBDNF Gene and LDAEPG(Val)-C-T are characterized by low serotonergic activity and possibly by low serum BDNF levels [20]. The aim of this study was thus to determine the association between genetic polymorphisms of BDNF and the LDAEP in a hea.