Dopaminergic stimulation up‐regulates the in vivo expression of brain‐derived neurotrophic factor (BDNF) in the striatum

Okazawa, Hitoshi; Murata, Miho; Watanabe, Masahiko; Kamei, Masaki; Kanazawa, Ichiro

doi:10.1016/0014-5793(92)81430-t

Cited by 134 publications

(48 citation statements)

References 31 publications

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“…Furthermore, endocannabinoids act as downstream effectors of D 2 R signaling in the inhibition of striatal synaptic transmission (Yin and Lovinger, 2006) and in the generation of corticostriatal long-term depression (Gerdeman et al, 2002(Gerdeman et al, , 2003. With respect to the interaction between DA and BDNF, it has been reported that acute administration of levodopa (Okazawa et al, 1992), dopamine, or direct D 1 R agonists (Kü ppers and Beyer, 2001;Williams and Undieh, 2009) upregulates BDNF signaling in the striatum. In contrast, other studies reported that both activation and inhibition of the DA system with, respectively, chronic cocaine (Fumagalli et al, 2007) and 6-OHDA treatment (Zhang et al, 2006) failed to affect striatal levels of BDNF.…”

Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum

Chiara¹,

Angelucci²,

Rossi³

et al. 2010

Journal of Neuroscience

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The role of brain-derived neurotrophic factor (BDNF) in emotional processes suggests an interaction with the endocannabinoid system. Here, we addressed the functional interplay between BDNF and cannabinoid CB 1 receptors (CB 1 Rs) in the striatum, a brain area in which both BDNF and CB 1 s play a role in the emotional consequences of stress and of rewarding experiences.BDNF potently inhibited CB 1 R function in the striatum, through a mechanism mediated by altered cholesterol metabolism and membrane lipid raft function. The effect of BDNF was restricted to CB 1 Rs controlling GABA-mediated IPSCs (CB 1 R (GABA) ), whereas CB 1 Rs modulating glutamate transmission and GABA B receptors were not affected. The action of BDNF on CB 1 R (GABA) function was tyrosine kinase dependent and was complete even after receptor sensitization with cocaine or environmental manipulations activating the dopamine (DA)-dependent reward system. In mice lacking one copy of the BDNF gene (BDNF The present study identifies a novel mechanism of CB 1 R regulation mediated by BDNF and cholesterol metabolism and provides some evidence that DA D 2 R-dependent modulation of striatal CB 1 R activity is mediated by this neurotrophin.

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Section: Discussionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum

Chiara¹,

Angelucci²,

Rossi³

et al. 2010

Journal of Neuroscience

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“…BDNF signals through the tyrosine kinase receptor B (TrkB) and through the p75 receptor (Huang and Reichardt, 2001). Both BDNF and TrkB are expressed by DA neurons (Okazawa et al, 1992;Nishio et al, 1998;Numan and Seroogy, 1999;Venero et al, 2000). Postmortem studies of PD patients using in situ hybridization, immunohistochemistry, and Western blot analysis demonstrate that reduced levels of BDNF within the SNC accompany the disease condition (Mogi et al, 1999;Parain et al, 1999;Howells et al, 2000;Chauhan et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Brain-Derived Neurotrophic Factor Is Required for the Establishment of the Proper Number of Dopaminergic Neurons in the Substantia Nigra Pars Compacta

Baquet¹,

Bickford²,

Jones³

2005

J. Neurosci.

270

190

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Brain-derived neurotrophic factor (BDNF) has been implicated in regulating neuronal survival, differentiation, and synaptic plasticity. Reduced expression of BDNF within the substantia nigra accompanies the deterioration of dopaminergic neurons in Parkinson's disease (PD) patients. Analysis of the effects of long-term BDNF absence from the CNS has been difficult because of the early postnatal lethality of BDNF Ϫ/Ϫ mice. Mice with a floxed BDNF allele were bred with Wnt1-Cre mice to generate Wnt-BDNF KO mice that lack BDNF from the midbrain-hindbrain (MHB). These mice are viable but exhibit hindlimb clutching and poor rotarod performance. Tyrosine hydroxylase (TH)-positive neuron numbers in the substantia nigra pars compacta (SNC) were estimated using stereological methods, revealing a persistent ϳ23% reduction of these cells at postnatal day 21 (P21) in Wnt-BDNF KO mice compared with controls. The diminishment of TH-expressing neurons was present at birth and continued through P120. This deficit appears selective for the dopaminergic population, because at P21, total neuron number within the SNC, defined as neuronal nuclei protein-positive cells, was not significantly reduced. Interestingly, and similar to observations in PD patients, SNC neuron subpopulations are not equally affected. Calbindin-and calretininexpressing SNC populations show no significant difference between Wnt-BDNF KO mice and controls. Thus, BDNF depletion from the MHB selectively leads to reduced TH expression in a subpopulation of neurons, but it remains unclear whether these cells are lost.

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“…Final washing was performed in 1 x SSC at 50°C. Full-length cDNA of rat t&B was amplified with two sets of RT-PCR reactions which amplified divided portions of rat trkB cDNA as described previously [30]. The PCR products were subcloned into pBluescript and used for the hybridization after confirming the sequence.…”

Section: Resultsmentioning

confidence: 99%

“…For the screening of the cDNA library, we amplified DNA fragment of the porcine trkC [23] using the reverse transcriptase PCR (RT-PCR) technique as described previously [30]. The amplified fragment was subcloned into the pBluescript (Stratagene, USA).…”

Section: Isolation and Characterization Of Chicken Trkc Cdna Clonesmentioning

confidence: 99%

Molecular cloning and expression of a novel truncated form of chicken trkC

1993

Self Cite

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The trk family of tyrosine protein kinase genes serves crucial roles for the development of the nervous system and the survival of neurons. The members of this gene family, trk, trkB and trkC, bind a distinct neurotrophin of the nerve growth factor (NGF) gene family, and trigger the intracellular signals which elicit trophic and differentiating effects on neurons. Adding to these neurotrophic receptor kinases, the truncated forms without the tyrosine kinase domain have been cloned and characterized. It has been thought that the existence of truncated forms is limited to trkB; however, very recently the truncated trkC has been cloned in rat [(1993) Neuron 10,963-974; Neuron 10,975-9901. We independently approached and molecularly cloned a truncated form which belongs to the chicken trkC. The truncated trkC possesses the binding and the transmembrane domains but not the tyrosine kinase domain. Northern blot analysis shows that the truncated form is preferentially expressed in the adult central nervous system. The truncated form is scarcely expressed during the embryonic stages. The conservation of the truncated trkC beyond species suggests they have specific functions.

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Dopaminergic stimulation up‐regulates the in vivo expression of brain‐derived neurotrophic factor (BDNF) in the striatum

Cited by 134 publications

References 31 publications

Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum

Brain-Derived Neurotrophic Factor Controls Cannabinoid CB1 Receptor Function in the Striatum

Brain-Derived Neurotrophic Factor Is Required for the Establishment of the Proper Number of Dopaminergic Neurons in the Substantia Nigra Pars Compacta

Molecular cloning and expression of a novel truncated form of chicken trkC

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