Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

Jia, Yousheng; Gall, Christine M.; Lynch, Gary

doi:10.1523/jneurosci.3310-10.2010

Cited by 103 publications

(80 citation statements)

References 43 publications

(50 reference statements)

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“…Furthermore, MARK induces hippocampus granular cells to produce continuous long-term potentiation (LTP) (Kobayashi et al 2006), which is currently recognized as the neural basis for learning and memory. The influences of BDNF on learning and memory are mainly due to the regulatory effects of BDNF on LTP (Jia et al 2010). In our study, BDNF expression in the PND7 newborn rats in the M group was significantly lower than the N group, which suggests that the relative thyroid hormone deficiency in female rats with marginal iodine deficiency has a negative impact on BDNF and can further influence the brain development of offspring.…”

Section: Discussionmentioning

confidence: 52%

Maternal marginal iodine deficiency affects the expression of relative proteins during brain development in rat offspring

Liu¹,

Zhang²,

Li³

et al. 2013

Journal of Endocrinology

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Marginal iodine deficiency is a major health problem in pregnant women, but its impact on nerve and intelligence development in offspring has been rarely reported. Our study aimed to investigate the effects of maternal marginal iodine deficiency on nerve and cognitive development in offspring and the related mechanisms. Marginal iodine-deficient rats were given 3 mg iodine per day, while normal control rats were given 4 mg iodine daily. Western blot was used to detect the amounts of brain-derived neurotropic factor (BDNF) and early growth response protein 1 (EGR1) in the hippocampus of each group. Immunohistochemistry was used to measure c-jun and c-fos expression in the hippocampal CA1 region. Finally, the water maze method was used to measure spatial performance. Free thyroxine (FT 4 ) levels in marginal iodine-deficient rats decreased by about 30%. Seven days after birth, EGR1 and BDNF protein levels significantly decreased in the hippocampus of marginal iodine deficiency rats compared with the normal control group. In addition, c-jun and c-fos expression in the hippocampus of 40-day-old rats was decreased in marginal iodine-deficient rats, compared with control. The spatial learning and memory ability of 40-day-old marginal iodine-deficient rats had a downward trend compared with the normal control group. FT 4 significantly decreased after pregnancy in rats with marginal iodine deficiency, affecting the expression of related proteins in the brain of offspring.

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Section: Discussionmentioning

confidence: 52%

Maternal marginal iodine deficiency affects the expression of relative proteins during brain development in rat offspring

Liu¹,

Zhang²,

Li³

et al. 2013

Journal of Endocrinology

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“…This shift in iSPNs could reflect a homeostatic adaptation to a reduction in the strength or number of glutamatergic synapses following TrkB deletion. Consistent with this conjecture, BDNF and TrkB signal- ing enhanced LTP induction at glutamatergic synapses on striatal SPNs (42) and, thus, their downregulation in HD would be expected to impair LTP (43,44), as described in other regions (45,46). This could prevent cortical neurons from effectively activating iSPNs to suppress unwanted activity.…”

Section: Hd Pathogenesis Is Rooted In Network Dysfunctionmentioning

confidence: 53%

Brain networks in Huntington disease

Eidelberg¹,

Surmeier²

2011

J. Clin. Invest.

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Recent studies have focused on understanding the neural mechanisms underlying the emergence of clinical signs and symptoms in early stage Huntington disease (HD). Although cell-based assays have focused on cell autonomous effects of mutant huntingtin, animal HD models have revealed alterations in the function of neuronal networks, particularly those linking the cerebral cortex and striatum. These findings are complemented by metabolic imaging studies of disease progression in premanifest subjects. Quantifying metabolic progression at the systems level may identify network biomarkers to aid in the objective assessment of new disease-modifying therapies and identify new regions that merit mechanistic study in HD models. Neuropathology in Huntington diseaseHuntington disease (HD) is caused by expansion of a CAG repeat in the huntingtin (Htt) gene. Expansion of the repeat length beyond 35 CAGs significantly elevates disease risk (1). The Htt gene is ubiquitously expressed in the brain with relative enrichment in cortical pyramidal neurons projecting to the striatum but relatively low levels in striatal projection neurons (2, 3).Although there are clear effects in the cerebral cortex and hippocampus, the most pronounced neuropathology in HD is found in the striatum (4, 5). The striatum is a key component of the basal ganglia, an interconnected set of subcortical nuclei involved in the regulation of how to act (and not act) in particular contexts (6). The striatum is composed primarily of GABAergic projection neurons with dendrites that are heavily studded with spines. These spiny projection neurons (SPNs) can be subdivided into two major classes on the basis of their axonal projection, dendritic size, and physiology as well as their expression of dopamine receptors and releasable peptides (7,8). SPNs that project to the external segment of the globus pallidus (GPe) form what is called the indirect SPN (iSPN) pathway because they indirectly control the nuclei that interface between the basal ganglia and the rest of the brain. SPNs that project to the internal segment of the globus pallidus (GPi) and substantia nigra pars reticulata form the direct SPN (dSPN) pathway. iSPNs are smaller and more excitable than dSPNs (Figure 1 and ref. 9); this difference is very likely to reflect a tonic negative modulation of iSPNs by dopamine acting at D 2 receptors. In contrast, dSPNs are positively modulated by D 1 receptors that appear to only be activated by transient elevations in dopamine release produced by bursts of action potentials in dopaminergic neurons (10).iSPNs and dSPNs are generally thought to play complementary roles in movement control and action selection. Both SPN populations have a rich, highly convergent synaptic connectivity with glutamatergic neurons distributed throughout much of the cerebral cortex (11). Both populations also have rich connectivity with glutamatergic neurons in the thalamus (12). A broad array of experimental evidence supports the proposition that iSPNs help to suppress cortical selection of...

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“…Previous studies have shown that theta-burst stimulation induces the release of endogenous BDNF from mossy fibers, as well as Schaffer collaterals onto the dendrites of CA3 and CA1 pyramidal neurons, respectively, and this mediates long-lasting changes in potentiation or depression (3,48,6,49). Moreover, a recent study demonstrated that release of BDNF from cortical axons onto dendrites of medium spiny neurons in the dorsal striatum induced postsynaptic LTP (50). It is conceivable that dendritically derived BDNF-TrkB endosomes have a role in these pathways.…”

Section: Discussionmentioning

confidence: 96%

Neurotrophin-mediated dendrite-to-nucleus signaling revealed by microfluidic compartmentalization of dendrites

Cohen

Bas‐Orth

Kim

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

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Signaling from dendritic synapses to the nucleus regulates important aspects of neuronal function, including synaptic plasticity. The neurotrophin brain-derived neurotrophic factor (BDNF) can induce long-lasting strengthening of synapses in vivo and this effect is dependent on transcription. However, the mechanism of signaling to the nucleus is not well understood. Here we describe a microfluidic culture device to investigate dendrite-to-nucleus signaling. Using these microfluidic devices, we demonstrate that BDNF can act directly on dendrites to elicit an anterograde signal that induces transcription of the immediate early genes, Arc and c-Fos. Induction of Arc is dependent on dendrite-and cell body-derived calcium, whereas induction of c-Fos is calcium-independent. In contrast to retrograde neurotrophin-mediated axon-to-nucleus signaling, which is MEK5-dependent, BDNF-mediated anterograde dendrite-to-nucleus signaling is dependent on MEK1/2. Intriguingly, the activity of TrkB, the BDNF receptor, is required in the cell body for the induction of Arc and c-Fos mediated by dendritically applied BDNF. These results are consistent with the involvement of a signaling endosome-like pathway that conveys BDNF signals from the dendrite to the nucleus.gene expression | mRNA translation

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Presynaptic BDNF Promotes Postsynaptic Long-Term Potentiation in the Dorsal Striatum

Cited by 103 publications

References 43 publications

Maternal marginal iodine deficiency affects the expression of relative proteins during brain development in rat offspring

Maternal marginal iodine deficiency affects the expression of relative proteins during brain development in rat offspring

Brain networks in Huntington disease

Neurotrophin-mediated dendrite-to-nucleus signaling revealed by microfluidic compartmentalization of dendrites

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