Lesion was made individually to the verious cortical areas in 14 adult cats.Thecorticofugal fibers terminating into vestibular nuclei were traced in sections by meansof modified Nauta silver staining method.The majority of cortical efferents which terminated to the vestibular nuclei deri-ved from somato-sensory area Ⅰ.A few fibers originated from the cortical motorareas,and some fibers derived from vestibular area and somatosensory area Ⅱ.Thefibers originated from the visual and auditory areas were not observed.The corticovestibular fibers descended within the pyramidal tract.These fibersleft pyramidal tract at the level of pons.Then,most of them reached to the vesti-bular nuclei ipsilaterally,and others reached bilaterally.Terminal degeneration was present throughout the whole extent of the vestibularnuclei.The total number of preterminal degenerating fibers in the nuclei was small.The anatomical and functional significance of our findings are discussed.

Lesion was made individually to the various cortical areas in 14 rats.The cortico- fugal fibers terminating into cochlear nuclei were traced in sections by means of the modified Nauta and Fink-Heimer silver staining method.The results were as follows: 1.After damaging the auditory area or somato-sensory area 1(SI)of the cerebral cortex unilaterally,degenerating fibers were found bilaterally in the ventral and dorsal cochlear nuclei.This result showed that the above cortical areas have direct descending connection with the cochlear nuclei. 2.No degenerating fibers were found in the cochlear nuclei after the ablation of the motor or visual area of the cerebral cortex,which demonstrated that the cochlear nuclei do not receive descending fibers from the above cortical areas. 3.The pathway from the cerebral cortex to the cochlear nuclei was:The descending fibers which originated from the auditory area or SI area ipsilaterally passed through the capsula interna and basis pedunculi,and part of these fibers passed dorsally and downward to the lateral portion of the reticular formation of the midbrain;and from there the fibers passed through the lemniscus lateralis and dorsal acustic stria to the cochlear nuclei of the ipsilateral side.The cochlear nuclei in contralateral side also received the corticofugal fibers by way of the dorsal acustic stria.These fibers might cross to the contralateral side at the region in the posterior commissure,superior colliculus commissure and inferior colliculus commissure.

Objective: To investigate the characteristic of nasal mucosa absorption in vivo of tetramethylpyrazine hydrochloride (TMP HCl) in rats. Methods: The nasal circulatory perfusion test of TMP HCl was performed in rats.Results: The absorption rate constants was increased with the increasing of the concentration of TMP HCl; The absorption rate constants was increased with the elevating of pH values at the pH value range of 4.70～7.00. Conclusion:When the pH value of nasal circulatory perfusion liquid of TMP HCl is 7.00, the nasal mucosa absorption is optimal.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.

AIM:To investigate the effect of gastro-din on the expression of brain-derived neurotroph-ic factor(BDNF)and interleukin-6(IL-6)in the stria-tum of cerebral ischemia rats,and to explore the potential mechanism of gastrodin in treating cere-bral ischemia.METHODS:The rats were randomly divided into four groups:normal,sham,model,and gastrodin groups,each consisting of 10 rats.After successful modeling using middle cerebral artery occlusion(MCAO),the gastrodin group received in-traperitoneal injection of gastrodin injection at a dose of 10 mg/kg once a day for 14 consecutive days.Pathological changes in striatal neurons were observed using Nissl staining.Immunohistochemis-try was utilized to detect positive expression of BDNF and IL-6 proteins in the striatum.Additional-ly,immunoblot analysis was performed to deter-mine the expression levels of BDNF and IL-6 pro-teins in the striatum.RESULTS:Nissl staining re-vealed clear and intact structures of striatal neu-rons in the normal and sham groups,with tightly arranged cells.In the model group,the number of cells was significantly reduced compared to the sham group(P＜0.01),and there was a noticeable cytosolic atrophy and loose cell arrangement.The gastrodin group showed a significant increase in the number of Nissl-positive neurons compared to the model group(P＜0.01),and there was also a sig-nificant improvement in cell morphology.The re-sults of immunohistochemistry and immunoblot were consistent,and there was no statistically sig-nificant difference in BDNF and IL-6 protein expres-sion between the normal group and the sham group(P＞0.05).Compared to the sham group,the model group showed a decrease in the protein ex-pression level of BDNF in the striatum on the isch-emic side(P＜0.01)and an increase in the protein expression level of IL-6(P＜0.05,P＜0.01).In con-trast,the gastrodin group showed an increase in the protein expression level of BDNF in the stria-tum on the ischemic side(P＜0.05,P＜0.01)and a decrease in the protein expression level of IL-6(P＜0.05,P＜0.01)compared to the model group.CON-CLUSION:Gastrodin has a significant protective ef-fect on striatal injury caused by cerebral ischemia,and its mechanism may be related to the up-regula-tion of the anti-inflammatory factor BDNF and the down-regulation of the pro-inflammatory factor IL-6.