Dopaminergic stimulation up‐regulates the in vivo expression of brain‐derived neurotrophic factor (BDNF) in the striatum
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We investigated the effect of dopamine on the in vivo expression of brain‐derived neurotrophic factor (BDNF) in the striatum of mouse. BDNF mRNA expression in the striation, which was Quantified with the reverse transcriptase polymerase chain reaction, was up‐repulated from 2 h after oral administration of levodopa, a precursor of dopamine. The increase was sustained for 16 h. Co‐administrstion of haloperidol partially inhibited dopamine‐induced BDNF enhancement. These data suggest that dopaminergic stimulation directly promotes the expression of BDNF in the striatum in vivo.Ventral striatum
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Aim:To study the impairing compare of PQ and ES to the dopaminergic system and the acetylnergic system in the brain of C57BL mice. Methods:C57BL mice well administered orally with PA, MPTP, ES. Sponteneous behavior was monitored. The levels of AChR in the cortex, striatum, hippocampus and thalamus, the DAT and DAD 2R in the striatum were detected by autoradiography.Results:Comparing to the control group, there was no significant change in mAChR in the brain of PQ, ES and MPTP treated mice. However, DAT and DAD 2R were significantly decreased in the striatum.Conclusion:PQ and ES mainly damage the dopaminergic system, but has little effect on the acetylnergic system in the brain of mice.
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Evidence that L-dopa-induced rotational behavior is dependent on both striatal and nigral mechanisms
Parkinson's disease results from the death of the dopamine-containing neurons in the substantia nigra pars compacta (SNC). This is accompanied by a loss of dopamine in brain regions, such as the corpus striatum, which receives input from dopaminergic neurons in the substantia nigra (SN). Since the corpus striatum is the primary target for these dopaminergic neurons, it has long been thought that the corpus striatum is the principal region affected. It was, therefore, natural to assume that replenishing dopamine in the striatum might be an effective treatment for Parkinson's disease. In fact, the dopamine precursor L-dihydroxyphenylalanine (L-dopa), the current drug of choice for treatment of Parkinson's disease, is believed to exert its therapeutic effect by replenishing dopamine levels in the corpus striatum via enzymatic decarboxylation within the synaptic terminals of surviving nigrostriatal neurons (Hornykiewicz, 1974). However, dopamine is also synthesized, stored, and released from the dendrites of SNC neurons that arborize in the substantia nigra pars reticulata (SNR) (Cheramy et al., 1981). Using a classic animal model for Parkinson's disease (rats with a unilateral 6-hydroxydopamine lesion of the SN), we show that L-dopa is also converted to dopamine in significant amounts within the 6-OHDA-lesioned SN. Furthermore, in contrast to the situation in the striatum where dopamine levels are only elevated for a short time, dopamine levels in the SN remain elevated until the behavioral effects of L-dopa have subsided. This elevation of nigral dopamine levels produces rotation that can be blocked by injecting a selective D1 dopamine receptor antagonist (SCH 23390, 2 micrograms in 1 microliter) directly into the SN pars reticulata. Infusion of SCH 23390 into the ipsilateral striatum produced only a modest reduction in L-dopa-induced circling behavior. These results suggest that D1 dopamine receptors in the SN may be at least as important as D1 dopamine receptors in the striatum as a site for the effects of L-dopa. This may have important implications for the therapy of Parkinson's disease.
Pars compacta
Nigrostriatal pathway
Pars reticulata
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Microdialysis
3,4-Dihydroxyphenylacetic acid
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Ventral striatum
Reward system
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Many individuals with mental retardation exhibit chronic aberrant behaviors (CABs) that includes hyperactive, stereotyped, aggressive, and self-injurious behaviors. Brain imaging studies have found that several of these individuals have abnormalities in their dopaminergic neurotransmitter systems that are thought to be responsible in part, for the development of these behaviors. The present study evaluated the effects of a selective dopamine re-uptake blocker, GBR-12909 in three animal models of varying striatal dopamine concentrations. The three animal models included the neonatal 6-hydroxydopamine (6-OHDA)-lesioned rat, a model of dopamine neuronal depletion, the prenatal methylazoxymethanol (MAM)-exposed rat, a model of hyper-dopaminergic innervation and control rats, a model of normal dopaminergic function. The animals were given five daily injections of GBR-12909 and videotaped observations were conducted immediately following the injections and 6h later. The results of the study indicate that the MAM-treated rats exhibited more hyperactive behaviors than either the 6-OHDA or the control animals in response to the GBR-12909 injections. However, the 6-OHDA and control rats exhibited more self-injurious behaviors than the MAM rats. Interestingly, the topography of the self-injurious behavior exhibited differed from that we have previously observed in 6-OHDA lesioned rats following dopamine agonists and resembles the mouthing behaviors seen in some individuals with mental retardation, in particular those with Rett syndrome. These findings indicate the models of varying dopaminergic function interact differently with a dopamine re-uptake blocker than dopamine agonists and that the partially dopamine depleted model may model the behaviors seen in individuals with Rett syndrome.
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Experiments involving the use of behavioural, neurochemical and electrophysiological methods to explore the mechanisms mediating the effects of oestrogen on dopaminergic activity in the striatum on the female rat are described. Results have shown that oestrogen influences the activity of striatal dopamine terminals and dopamine-mediated behaviours in the female rat. These are rapid effects of oestrogen in the striatum, and are thought to be mediated by a novel membrane-associated receptor. How these novel effects of oestrogen may affect naturally occurring behaviours in the rat will be discussed.
Neurochemical
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