Chemical characteristics of callosal neurons in the frontal and occipital cortex of Wistar rat were studied by means of combined method of HRP retrograde tracing andimmunocytochemistry of glutamate (Glu) and ?-aminobutyric acid (GABA). Glutamate containing callosal neurons were large or medium sized pyramidal cells and mainly localized in layers Ⅱ/Ⅲ, Ⅴ and Ⅵ. They tended to appear in clusters. GABA containing callosal neurons were also found. They were medium sized nonpyramidal cells with round, elliptic, or fusiform soma and were mostly localized in layers Ⅴ and Ⅵ. They also tended to appear in clusters. The percentage of GABA containing callosal neurons (about 8% and 10% in frontal and occipital cortex respectively)was much less than that of glutamate containing callosal neurons (about 17% and 29% in frontal and occipital cortex respectively). These results further confirmed that part of callosal cells used glutamate as an excitatory transmitter and firstly confirmed that some callosal neurons contained an inhibitory transmitter GABA morphologically. In view of the existence of GABA containing callosal neurons, it also suggested that at least in rat cerebral cortex,some GABA containing neurons had longer projections than local circuit neurons. According to the results of ours and other authors, we suggested that callosal system was the one that contained different kinds of neurotransmitters, and that diversification of the transmitters and their interaction in the callosal system was one of the neuroanatomical bases of the complicated and advanced functions of the callosal neurons.

To study the significance of the pathological changes of axon and myelin sheath in injured brainstem.The neurofilament and myelin basic protein was demonstrated immunohistochemically,and the pathological changes of axons and myelin sheathes in human brainstem following trauma were observed.In the injured brainstem,irregular swelling and disconnecting axons could be found as early as 0 5h after injury, while pathological changes in myelin sheaths such as tortuous change,partial peeling off from axon and intermittent disappearance could be observed at 19～22h after injury.However,in the normal brainstem,there were no evident changes in axons and myelin sheaths.Pathological changes of axon and myelin sheath in brainstem would occur after trauma,which could be used for postmortem diagnosis of brainstem injury.

0.05～0.2?l of HRP (Sigma Ⅵ) were introduced into the periaqueduetal gray (PAG) of 45 rats at the superior collicular level, each brain was sectioned and processed with DAB, BDHC, O-D and TMB reactions. 29 were chosen for analysis and according to the locations of the injection center and the extent of reaction, were divided into 3 groups:1. The injection center was found in the lateral part of PAG; the reaction only involved a small area within PAG (11 rats), labeled cells were seen in PAG, tectum, reticular formation (RF) and dorsal raphe nucleus.2. The injection center was in the dorsolateral part of PAG; the reaction area extended out of PAG to the nearby RF and tectum (9 rats); labeled cells were seen in the structures mentioned in group 1 as well as in habenular nucleus (hn), parafascicular nucleus (PFN), hypothalamic nuclei (anterior, posterior, ventromedial, dorsomedial, lateral), thalamic nuclei (lateral, reticular, medial part of ventral nucleus), paraventricular gray (PVG), nucleus of the optic tract, nucleus of posterior commissure (NPC), parabigeminal nucleus (PBN), locus ceruleus, ventral nucleus of lateral geniculate body, entopeduncular nucleus.3. The injection center was in the lateral or ventrolateral part of PAG, the reaction area extended to the nearby RF, tegmentum and part of tectum (9 rats), labeled cells were seen in the structures mentioned in group 1 as well as in substantia nigra, H_1, H_2, zona inserta, HN, PFN, PVG, NPC, PBN, locus ceruleus, pretectral area and nuclei of hypothalamus. In this group 3 rats were processed with TMB reaction. Labeled cells were seen not only in the above-mentioned structures but also in the deep layers of anterior cingulate cortex (areas 23 and 24), nucleus raphe magnus, nucleus reticularis gigantocellularis, periventricular gray of 4th ventricle, dentate nucleus of cerebellum, lamina Ⅴ～Ⅶ of cervical spinal cord (the other segments were left out), preoptic and supraoptic nuclei, suprachiasmatic nucleus, anterior nucleus of mammillary body, medial nucleus of amygdaloid nucleus, spinal nucleus of nerve Ⅴ. The labelled cells were seen chiefly in the ipsilateral side. Neuronal connections also were analysed according to the disparity in labelled structures.

AIM: To study the neuroprotective effect and possible mechanism of ganglioside GM 1 on neonatal hypoxic-ischemic-encephalopathy(HIE). METHODS: A rat model of neonatal HIE was established, then the pathological changes and expressions of nitric oxide synthase (NOS) in the brain tissues were investigated in different periods after hypoxia-ischemia (HI) and the subseqent changes of the above results after GM 1 administrated. RESULTS: The damage of the brain exposed to HI were alleviated significantly after GM 1 administrated. The levels of NOS expressions in the brain tissue increased after HI. GM 1 could inhibit NOS expressions induced by HI. CONCLUSION: GM 1 may have some protective effects on neonatal HIE, and the possible mechanism is related to the partial inhibition of NOS expression.