AIM: To study the effects of dopamine depletion on the phosphorylation level, intracellular distribution, and mRNA expression of DARPP-32 in the ischemic striatum and to elucidate the mechanisms underlying the ischemic injury. METHODS: A complex model of SN lesioning with 6-OHDA to deplete dopamine and four vessels occlusion for inducing forebrain ischemia was constructed in rats. DARPP-32 was investigated with autoradiogram, immunohistochemistry and in situ hybridization. RESULTS: The [32P]phosphate incorporation of DARPP-32 was reduced in vitro following ischemia. However, the [32P]phosphate incorporation, the numbers of positive neurons, and mRNA expression of DARPP-32 were increased in SN lesioning plus ischemic rats with denervated striatum. CONCLUSION: Dopamine depletion reduced the DARPP-32 phosphorylation in vivo following ischemia, and protected DARPP-32 immunoreactivity and mRNA expression level against the reduction induced by ischemia.
AIM: To study the effects of dopamine depletion on the phosphorylation level, intracellular distribution, and mRNA expression of DARPP-32 in the ischemic striatum and to elucidate the mechanisms underlying the ischemic injury. METHODS: A complex model of SN lesioning with 6-OHDA to deplete dopamine and four vessels occlusion for inducing forebrain ischemia was constructed in rats. DARPP-32 was investigated with autoradiogram, immunohistochemistry and in situ hybridization. RESULTS: The [32P]phosphate incorporation of DARPP-32 was reduced in vitro following ischemia. However, the [32P]phosphate incorporation, the numbers of positive neurons, and mRNA expression of DARPP-32 were increased in SN lesioning plus ischemicrats with denervated striatum. CONCLUSION:Dopamine depletion reduced the DARPP-32 phosphorylation in vivo following ischemia, and protected DARPP-32 immunoreactivity and mRNA expression level against the reduction induced by ischemia.