Brain-Derived Neurotrophic Factor Promotes Differentiation of Striatal GABAergic Neurons

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood

“…[64][65][66][67][68] In interneurons SST, NPY and TAC1 are co-expressed to a great extent and SST/NPY expression can be induced by a BDNF/ TrkB-dependent mechanism. [69][70][71] While we observed a strong downregulation in the SST-NPY-TAC1 transcripts in both adult and embryonic BDNF-ablated mice, we found the expression of other GABA colocalizing neuropeptides and GABA-production enzymes unchanged. These data are in agreement with our recent findings that PV and GAD1 expression are not directly BDNF-dependent.…”

Amelioration of chronic neuropathic pain after partial nerve injury by adeno-associated viral (AAV) vector-mediated over-expression of BDNF in the rat spinal cord

“…BDNF has been demonstrated to directly rescue CNS GABA neurons and stimulate GABA neurotransmitter synthesis. [29][30][31][32] Exogenous BDNF has been seen to have a direct positive effect on both uninjured 33 and injured 34 serotonergic neurons in the brainstem, increasing 5HT synthesis and promoting regeneration of 5HT-axons, respectively. Transplants of BDNF-secreting cells in the subarachnoid space after nerve injury has been shown to restore the endogenous GABA system within 1 week after grafting.…”

“…4,5,[37][38][39][40] Whether such loss of GABA synthesis is due to excitotoxic cell death of GABA interneurons or temporary or permanent alterations in the neurotransmitter's synthesis, is not known, but neurotrophins such as BDNF may act directly to intervene in cell death and/or regulate GAD enzyme activity, as has been seen with BDNF and other GABA cells. [29][30][31][32] Assigning only a antinociceptive function for endogenous BDNF in neuropathy is difficult. Neurotrophic factors such as BDNF, and NT-3 play a significant role in the development, and perhaps maintenance, of the sensory neurons responsive to temperature and tactile pain, evidenced in neurotrophin-knockout mice.…”

Cellular Therapy and Induced Neuronal Replacement for Huntington's Disease

“…[101][102][103][104][105][106][107]. BDNF exerts its function by binding its high affinity TrkB receptor, either together with or apart from its low affinity p75 receptor.…”