[Effects of co-exposure to paraquat and maneb on system of substantial nigra and striatum in rats].

OBJECTIVE: To investigate the effects of exposure of paraquat and maneb on the behavior, the morphology and electrical activity of the Substantia nigra and striatum, and to discuss the relationship between this two pesticides and Parkinson's disease. METHODS: 37 rats were divided randomly into 3 groups: control group (n = 11), paraquat (10 mg/kg) group (n = 13) and combinative group of paraquat (10 mg/kg) and maneb (30 mg/kg) (n = 13), and were exposed twice a week for 6 weeks by intraperitoneal injection. The behavior of animals in the declined-plane, the vertical-grid and the open-field test were observed. The morphology of substantia nigral neurons were investigated by HE pathology. The spontaneous discharge of striatum neurons were recorded after exposure. RESULTS: Compared to the control group and the pre-exposure group, both the numbers of animals sliding down from the declined-plane and the latency of rats' moving on the vertical-grid significantly increased, and the animals' autonomic movement decreased significantly (P < 0.05, P < 0.001). After the combinative exposure, the neurons of the Substantial nigra pars compacta (SNPc) were progressively impaired, the cell density of the paraquat group [(82.17 ± 12.91) n/mm(2)] and the combined group [(41.15 ± 6.44) n/mm(2)] were lower than that in control group (143.10 ± 20.85 n/mm(2)] (P < 0.01). In the paraquat group (5.97 ± 7.30 Hz) and the combined group [(6.95 ± 9.87) Hz], the average discharge rates of the striatum neurons were increased significantly compared to the control group [(1.78 ± 5.05) Hz] (P < 0.01). The bursting discharge was increased significantly in the combined group (22.3%) compared to the control group (9.8%) and the paraquat group (5.6%) (P < 0.05, P < 0.01). CONCLUSION: The co-exposure of paraquat and maneb could induce similar symptoms to Parkinsonism syndrome of rats such as rigidity, moving reduction and etc, and the combined exposure had a certain enhanced effect compared to alone paraquat exposure. The combinative exposure of paraquat and maneb could cause neural loss in SNPc and it is involved with the enhanced electrophysiological activity in striatum. The synergy toxicity of paraquat and maneb in nigrostriatal system is related to Parkinson's disease.

Morpho-physiologic characteristics of dorsal subicular network in mice after pilocarpine-induced status epilepticus.

The goal of this study was to examine the morpho-physiologic changes in the dorsal subiculum network in the mouse model of temporal lobe epilepsy using extracellular recording, juxtacellular and immunofluorescence double labeling, and anterograde tracing methods. A significant loss of total dorsal subicular neurons, particularly calbindin, parvalbumin (PV) and immunopositive interneurons, was found at 2 months after pilocarpine-induced status epilepticus (SE). However, the sprouting of axons from lateral entorhinal cortex (LEnt) was observed to contact with surviving subicular neurons. These neurons had two predominant discharge patterns: bursting and fast irregular discharges. The bursting neurons were mainly pyramidal cells, and their dendritic spine density and bursting discharge rates were increased significantly in SE mice compared with the control group. Fast irregular discharge neurons were PV-immunopositive interneurons and had less dendritic spines in SE mice when compared with the control mice. When LEnt was stimulated, bursting and fast irregular discharge neurons had much shorter latency and stronger excitatory response in SE mice compared with the control group. Our results illustrate that morpho-physiologic changes in the dorsal subiculum could be part of a multilevel pathologic network that occurs simultaneously in many brain areas to contribute to the generation of epileptiform activity.

GABA mediaties the inhibitory effect of lateral amygdaloid nucleus stimulation on the acoustic response of neurons in A I cortex: An in vivo microiontophoretic study.

Experiments were performed on Sprague Dawley rats with multibarrel microelectrode technique. The effects of acoustic response of A I cortex neurons produced by electrical stimulation of lateral amygdaloid nucleus (LA) and the influence of GABA were observed. Experimental results showed that iontophoretic administration of GABA caused a pronounced inhibition of the electrical activity of A-I neurons. Blockade of GABA(A) with bicuculline (BIC) facilitated the acoustic response. The acoustic response of A-I neurons was inhibited when the LA was stimulated. Iontophoretic application of GABA resulted in a similar inhibitory effect as that of LA stimulation. Blockade of GABA(A) with bicuculline reversed the inhibitory effect of LA stimulation on the acoustic response of A-I neurons. In contrast, application of strychnine, a glycine receptor antagonist, could not reverse the inhibitory effect of LA. Baclofen, a GABA(B) agonist, did not affect the acoustic response of the auditory neurons. These results indicate that GABA is the ultimate transmitter which mediates the LA stimulation-induced inhibition of the acoustic response of A-I neurons in rats, possibly via the GABA(A) receptor.