Research reportDevelopmental expression of brain derived neurotrophic factor mRNA by neurons of fetal and adult monkey prefrontal cortex
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Perisynaptic astrocytes as a potential target for novel antidepressant drugs
2021, Journal of Pharmacological SciencesCitation Excerpt :Of note, other studies have also shown that brain BDNF levels may be increased by glutamatergic activation,28–30 suggesting an interaction between BDNF and glutamate in synaptic signaling. In addition, evidence of the regulatory action of glutamate-induced BDNF on neuronal connectivity was first demonstrated in the prefrontal cortex of primates.31 The role of these cellular mechanisms in depression has been investigated by researchers over the last few years, and many studies have reported evidence that links glutamatergic activity, BDNF expression, and synaptic connectivity.32
Pre- and postsynaptic twists in BDNF secretion and action in synaptic plasticity
2014, NeuropharmacologyCitation Excerpt :Consequently, the presence of BDNF mRNA in rodents correlates very well with the site of synthesis of BDNF protein in specific tissues and cells (Conner et al., 1997). The mRNA for BDNF is widely distributed throughout the central nervous system (CNS) of rat and mice, including brain regions like the hippocampal formation (Conner et al., 1997; Connor and Dragunow, 1998; Ernfors et al., 1990; Hofer et al., 1990; Phillips et al., 1990; Schmidt-Kastner et al., 1996; Son and Winzer-Serhan, 2009; Wetmore et al., 1990, 1991), cerebral cortex (Conner et al., 1997; Hofer et al., 1990; Huntley et al., 1992; Phillips et al., 1990; Schmidt-Kastner et al., 1996; Timmusk et al., 1993; Wetmore et al., 1990, 1991), thalamus (Conner et al., 1997; Hofer et al., 1990; Schmidt-Kastner et al., 1996; Timmusk et al., 1993), hypothalamus (Conner et al., 1997; Hofer et al., 1990; Liao et al., 2012), olfactory bulb (Conner et al., 1997; Hofer et al., 1990; Phillips et al., 1990), amygdala (Conner et al., 1997; Phillips et al., 1990; Schmidt-Kastner et al., 1996; Wetmore et al., 1991), cerebellar granule cell layer (Hofer et al., 1990; Vazquez-Sanroman et al., 2013; Wetmore et al., 1990) and spinal cord (Conner et al., 1997; Hofer et al., 1990; Luo et al., 2001). In the hippocampus a similar distribution of BDNF mRNA was described for rodents and primates (Phillips et al., 1990).
Sensitized activation of Fos and brain-derived neurotrophic factor in the medial prefrontal cortex and ventral tegmental area accompanies behavioral sensitization to amphetamine
2011, NeuropharmacologyCitation Excerpt :As such, it is likely that after repeated amphetamine, BDNF-containing mPFC neurons preferentially, but not exclusively, innervate the VTA. Because BDNF is only present in prefrontal pyramidal neurons during adulthood (Huntley et al., 1992), we infer that the observed increase in mPFC BDNF after amphetamine occurred exclusively in glutamate-containing projection neurons, and not GABA-containing interneurons. Consistent with this, the VTA receives more glutamatergic innervation from the PFC than any other region (Geisler et al., 2007).
Higher BDNF concentrations in the hippocampus and cortex of an aggressive mouse strain
2009, Behavioural Brain ResearchChapter 15 Persistent neural activity in the prefrontal cortex: A mechanism by which BDNF regulates working memory?
2008, Progress in Brain ResearchCitation Excerpt :As working memory dysfunction is central to the pathology of schizophrenia, we specifically note that expression of BDNF and TrkB is significantly reduced in the dorsolateral PFC of schizophrenic patients (Weickert et al., 2003, 2005; Hashimoto et al., 2005). In monkeys, BDNF mRNA is highly expressed in large pyramidal neurons of layers III and IV throughout the PFC of fetal and adult monkeys (Huntley et al., 1992). Correspondingly, full-length TrkB receptor immunoreactivity is also expressed in pyramidal cells of layers II, III, V, and VI, and is developmentally regulated (Hayashi et al., 2000).
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Present address: Department of Neurobiology, Box 1065, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.
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Present address: Department of Neuroscience, University of Virginia, School of Medicine, Box 230 Medical Center, Charlottesville, VA 22908, USA.
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Present address:Department of Biochemistry and Molecular Biology, Mayo Clinic, Jacksonville, FL 3224, USA.