Modulation of neurotransmitter release induced by brain-derived neurotrophic factor in rat brain striatal slices in vitro

Goggi, Julian; Pullar, Ian A.; Carney, Stephen; Bradford, H. F.

doi:10.1016/s0006-8993(02)02505-2

Cited by 108 publications

(75 citation statements)

References 44 publications

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“…BDNF can augment 5-HT signaling; in turn, 5-TH stimulates BDNF expression (Goggi et al, 2002;Juric et al, 2006;Mamounas et al, 2000;Mattson et al, 2004;Siuciak et al, 1996). However, we excluded the involvement of BDNF in the antidepressant effect of HG, change in the levels of neurotransmitters (5-HT and NE) is likely to be an important mechanism for HG as an antidepressant.…”

Section: Discussionmentioning

confidence: 96%

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Liang

Huang

Wang

et al. 2014

Pharmaceutical Biology

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Objective: This study compared the antidepressant ability of FAE with that of HG in mice and further investigated the antidepressant-like effects and potential mechanisms of HG in rats subjected to unpredictable chronic mild stress (UCMS). Materials and methods: Mice received FAE (50 mg/kg) and HG (20 mg/kg) once a day via intragastric administration (i.g.) for 3 weeks. The anxiolytic and antidepressant activities of FAE and HG were compared using elevated plus maze (EPM) and behavioral despair tests including tail suspension test (TST) and forced swimming test (FST), respectively. Antidepressant effects of HG (5 mg/kg) were assessed using the UCMS depressive rat model. Moreover, the levels of monoamine neurotransmitters and relevant gene expression in UCMS rats' hippocampi were determined through high-performance liquid chromatography with electrochemical detection and real-time polymerase chain reaction techniques. Results: The results of our preliminary screening test suggest that HG at 20 mg/kg, while not FAE at 50 mg/kg, significantly decreased the immobility in both TST and FST compared with the vehicle group when administered chronically; however, there were no significant differences observed between the HG and the FAE group. Chronic administration of HG failed to significantly reverse the altered crossing and rearing behavioral performance, time spent in the open arm and closed entries in the EPM, even if they showed an increased tendency, but HG significantly increased the percent of sucrose preference in the sucrose preference test (SPT) and decreased the immobility time in the FST. HG showed that significant increases of norepinephrine and serotonin levels and exhibited a tendency to increase the expression of 5-hydroxytryptamine (serotonin) 1A receptor mRNA, and to significantly decrease the expression of the mRNA for the serotonin transporter (5-HTT). However, there were no significant differences in the expression of the brain-derived neurotrophic factor. Conclusion: These findings confirm the antidepressant-like effects of HG in a behavioral despair test and UCMS rat model, which may be associated with monoamine neurotransmitters and 5-HTT mRNA expression.

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Section: Discussionmentioning

confidence: 96%

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Liang

Huang

Wang

et al. 2014

Pharmaceutical Biology

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“…Evidence suggests that BDNF can enhance serotoninergic transmission (44). The direct infusion of BDNF in the brain influences the survival and function of serotoninergic neurons by enhancing the release of serotonin.…”

Section: Discussionmentioning

confidence: 99%

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

et al. 2009

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Abstract. Cardiovascular disease (CVD) and depression are two of the most common human health problems. Patients with depression have an increased risk of developing cardiovascular disease and mortality after experiencing a cardiac event. Both diseases are complex disorders that are influenced by genetic and environmental factors. Brain-derived neurotrophic factor (BDNF) plays a critical role in regulating both vascular development and response to injury, and promotes survival, differentiation, and maintenance of neurons in the peripheral and nervous system. Evidence suggests that BDNF can enhance serotoninergic transmission. Serotonin modulates different brain functions and is known to regulate sleep, appetite, pain and inflammation. The aims of the present casecontrol study were to investigate the possible role of BDNF Val66Met, 5-HTTLPR and -1438 G/A polymorphisms in the development of coronary artery disease (CAD) in patients with and without depression. Regarding BDNF, our data suggest an involvement of the AA genotype in the pathogenesis of CAD in females and in the predisposition to CAD associated with depression. Furthermore, it could be argued that the GG genotype is protective against CAD in the female population and against CAD associated with depression. In our CAD population we also observed a significant increase in the L/L genotype and a decrease in the S/L genotype with respect to the controls. A higher frequency of the L allele, responsible for enhancing the efficiency of transcription, was found in CAD patients. These findings may be responsible for the increased capacity of platelet serotonin uptake previously observed in patients with CAD. Although no differences were found for genotype and allelic frequencies of the -1438 G/A polymorphism between the CAD patients and controls, we cannot exclude the possible role of this receptor in coronary artery disease.

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“…Infusion of BDNF into the brain enhances the expression of tryptophan hydroxylase (TpOH) (the ratelimiting enzyme in 5HT synthesis), upregulates 5-HT uptake and its activity-dependent release, and even modifies the firing patterns of serotonergic neurons in the raphe (Siuciak et al, , 1998Celada et al, 1996;Zhou et al, 2000;Goggi et al, 2002). In BDNF heterozygous mutant ( + /À) mice, levels of forebrain 5-HT, fiber densities of forebrain 5-HT neurons, as well as the 5-HT clearance rate, were significantly impaired (Lyons et al, 1999;Szapacs et al, 2004;Daws et al, 2007).…”

Section: Bdnf Regulation Of 5-ht Neuron Development and Functionsmentioning

confidence: 99%

Interaction between BDNF and Serotonin: Role in Mood Disorders

Martinowich

2007

Neuropsychopharmacol

686

458

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Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are two seemingly distinct signaling systems that play regulatory roles in many neuronal functions including survival, neurogenesis, and synaptic plasticity. A common feature of the two systems is their ability to regulate the development and plasticity of neural circuits involved in mood disorders such as depression and anxiety. BDNF promotes the survival and differentiation of 5-HT neurons. Conversely, administration of antidepressant selective serotonin reuptake inhibitors (SSRIs) enhances BDNF gene expression. There is also evidence for synergism between the two systems in affective behaviors and genetic epitasis between BDNF and the serotonin transporter genes.

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Modulation of neurotransmitter release induced by brain-derived neurotrophic factor in rat brain striatal slices in vitro

Cited by 108 publications

References 44 publications

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Involvement of norepinephrine and serotonin system in antidepressant-like effects of hederagenin in the rat model of unpredictable chronic mild stress-induced depression

Coronary artery disease and depression: Possible role of brain-derived neurotrophic factor and serotonin transporter gene polymorphisms

Interaction between BDNF and Serotonin: Role in Mood Disorders

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