In addition to the dopaminergic neurons in the nigrostriatal system, the properties of dopaminergic neurons in the mesolimbic system, such as the amygdala, are also of interest and importance because of their specific neuromodulatory effects in the pathophysiology of Parkinson’s disease (PD). Using the fast cyclic voltammetry (FCV) technique, we present evidence to indicate that electrically-evoked dopamine (DA) release from the amygdala, especially the central amygdaloid nucleus (CAN), of ovariectomized (OVX) female rats was significantly enhanced with increasing doses of estradiol benzoate (EB; 30, 50 and 100 μg/kg). Impaired DA release from the amygdala of an OVX rat PD model can also be increased by EB treatment (50μg/kg) to a level similar to that of controls. The well established neuroprotective effects of estrogen may be beneficial for reducing the dysfunction of dopaminergic neurons in mesolimbic structures of rat PD models and PD patients.

C31, consisting of 31 amino acid residues, is generated from the carboxyl terminal fragments (CTFs) of amyloid precursor protein (APP).It has been shown that C31 causes apoptosis in neurons and is present in brains of Alzheimer disease (AD) patients. Using whole-cell patch clamp techniques, we investigated effects of C31 on voltage-gated calcium channel (VGCC) currents and the protective effects of β-estradiol on PC12 cells. The results demonstrated that C31 induced a significant increase of the VGCC currents in PC12 cells, which was blocked by β-estradiol. These results suggest that modulation of intracellular calcium levels by VGCC may in part be involved in C31 induced neuronal death associated with AD.

The effects of intranigral iron injection on dopamine (DA) release and content in the caudate putamen(CPu)and their relationship to DA-related behavioral response were investigated in rats. Different concentrations of FeCl3 (10, 20, and 40μg) and saline were injected separately into the left substantia nigra. In some experiments, rats were pretreated with desferrioxamine or saline before iron injection. After 3 weeks, changes in behavioral response, DA release, and DA content in the CPu were determined. In all iron injection groups (10, 20, and 40μg), DA content in the lesioned side of the brain was significantly decreased, showing a significant linear correlation (R2 0.981, P＜0.01), and DA turnover ratio significantly increased (both P＜0.01, 0.01and 0.001 vs unlesioned sides, respectively). However, injection dosages of 10 or 20μg of iron did not lead to significant changes in DA release in the CPu or in behavioral response. At the 40-μg dosage, it was found that DA release in the lesioned side and rearing activity both were significantly reduced (all P＜0.01 vs unlesioned side or control) and apomorphine-induced rotation was observed. Pretreatment with desferrioxamine significantly inhibited the effect of iron on DA release and content. These results demonstrate that iron injection can damage dopaminergic neurons and suggest that DA release, rather than DA content, in the CPu is associated with DA-related behavioral changes in this PD model.

XIE JUN-XIA, MING TANG and CHUNYI ZHANG: Effect of cholecystokinin-8 mieroinjeetion into ventral tegmental area on dopamine release in nucleus accumbens of rats: An in vivo voltammclric study. Prog. Neuro-Psyehopharmaeol.& Biol.Psychiat.2001, 25 pp.427-434.

Isatin was a potent endogenous monoamine oxidase (MAO) inhibitor that is more active against MAO-B than MAO-A. The acute effects of isatin on apomorphine (APO)-induced rotations were evaluated in Parkinsonian rats induced by 6-hydroxydopamine (6-OHDA) lesion. Furthermore, the effects of isatin on DA release in caudate putamen (CPu) of model and normal rats were monitored using fast cyclic voltammetry (FCV). The contents of monoamine transmitters and their metabolites in CPu of model and normal rats were also analyzed by high performance liquid chromatography with electrochemical detection after administration of isatin. Here we show that isatin (100mg/kg,i.p.)apparently inhibited APO-induced rotations of Parkinsonian rats to 39.1±3.7% of the control (n＝12), while it had no apparent effects on electrical stimuli-induced DA release either in normal rats or in model rats. In addition, the content of 5-hydroxytryptamine but not DA was increased in both normal rats and model rats after isatin (100 mg/kg,i.p.) was administered (P＜0.01, n＝6). The content of 5-hydroxyindole acetic acid was not changed. These results suggest that isatin cannot increase DA levels in rat CPu. Therefore, the effects of isatin on APO-induced rotations of our Parkinsonian rats could not attribute to its inhibition of DA catabolism as a MAO inhibitor.