Objective To investigate the effect of ethanol on level of the main hippocampal subtype of muscarinic receptor(M1)in mice,and evalu?ate whether the content change on this receptor could be linked with alterations in cognition,so as to further reveal the mechanism of brain damage in?duced by ethanol. Methods Sixty female mice were randomly divided into four groups. The model mice were induced by intragastric administration of ethanol at dose of 8%,16%,and 32%respectively of 0.2 mL/10 g for 8 weeks according to the protocol,and control group were treated with intra?gastric administration of distilled water. The capability of learning and memory were examined by Morris water maze,and ELISA method was used to measure the M1 receptor content in hippocampus in each group of mice. Results Compared with first day,the mean escape latency period on the fifth day was significantly shortened in each group. There was no significant difference between ethanol and control group for the mean escape latency period on the fifth day. Compared with the control group,the active time in the target quadrant was significantly shortened in 16%and 32%ethanol group. M1 receptor content in hippocampus formation was significantly decreased in all the ethanol group mice. The ethanol concentration was nega?tive correlated with the M1 receptor content. Conclusion Chronic alcoholism can induce the memory impairment in mice,which might be associat?ed with the low level of M1 receptor subtype in hippocampus of mice.

Objective To investigate the effects of GR82334 caudal veins injection(iv)or intrathecal injection(ith)on the increase of dopamine (DA)content in rats anterior cingulate gyrus(ACG)induced by heavy current stimulation of saphenous nerve(SN). Methods Totally 42 male Wi-star rats were randomly divided into six groups,including control group,sham stimulation group,SN stimulation group,GR82334(ith)group,NS (ith)group,GR82334(iv)group,and NS(iv)group. At the end of the study,rats of different groups were sacrificed,then the right side ACG were collected and weighted. ACG samples were then homogenized with 0.1 mol/L perchloric acid solution. After spinning at 10 000 r/min(4℃)for 20 min,20μL of the supernatant were harvest from each sample. High performance liquid chromatography electrochemical detection was used to mea-sure DA content. Results Heavy current stimulation of SN caused obvious increase of the DA content in ACG. GR82334(iv or ith)antagonized the significant increase of DA content in ACG induced by the stimulating SN. However,GR82334(ith)did not completely antagonized the increase of DA content in ACG induced by electric stimulating SN. Conclusion The results indicated that there is connection between SN and the dopami-nergic nervous system in ACG,and SN afferent nociceptive signals can activate ACG dopaminergic neurons to release DA. Peripheral and central NK-1 receptors are involved in the process of significant increase of DA content in ACG induced by SN afferent signals. However,there are other central paths of SN information input to ACG to induce obvious increases of DA content,in which other neurotransmitters and receptors may be involved.

Objective To explore the effect of rhynchophylline and isorhynchophylline on headshakes behavior and levels of monoamine neurotransmitter in model rats with Tourette syndrome.Methods 40 Wistar rats were randomly divided into DOI-induced head-shakes rats (HSR group),haloperidol group,rhynchophylline group and isorhynchophylline group with 10 in each group.The inhibitory effects of rhynchophylline and isorhynchophylline were estimated by observing the HSR behavior.Dopamine (DA) and 5-hydroxytryptamine(5-HT) in the rat striatum were detected by the enzyme-linked immunosorbent assay (ELISA) method.The 5-HT2A receptor mRNA expression in prefrontal lobe cortex of the rats was measured by real-time PCR.Results Compared with HSR group,the head shakes of the rats in haloperidol group and isorhynchophylline group were significantly decreased(P＜0.01),and no change of head-shakes number was observed in rhynchophylline group (P＞0.05).There was no significant difference of head-shakes number between the haloperidol group and isorhynchophylline group(P＞0.05).Compared with HSR group,DA levels in the rat striatum were significantly decreased in isorhynchophylline group and haloperidol group((152.35± 5.80) μ~L vs (111.19±4.30) μg/L,(152.35±5.80) μg/L vs (126.42±3.17) μg/L,P＜0.01),while DA levels in the rat striatum in rhynchophylline group were not changed ((152.35±5.80) μg/L vs (142.71±5.51) μg/L,P＞0.05).There was no significant change of 5-HT2A receptor mRNA expression in rat prefrontal lobe cortex in every group(P＞0.05).Conclusion Isorhynchophylline may have an inhibitory effect on rats with DOI-induced HSR.Isorhynchophylline may decrease the DA levels in the rat stratum with DOI-induced HSR.Rhynchophylline has no significant inhibitory effect on head-shakes behavior and DA levels in the rat stratum with DOI-induced HSR.

Objective To study whether amputation of the tail extremity could induce change of Fos protein expression in mice ACC neurons , and explore the role of NK?1 receptor in the change. Methods Immunohistochemistry technique was adopted to study Fos protein expression change in mice ACC neurons at 0.25 h,0.5 h,1 h,2 h after amputation of the tail extremity 2.5 cm,and also the effect of NK?1 receptor antagonist GR82334(iv)or GR82334(ith)in the change. Results Fos protein expression in mice ACC neurons was significantly increased at 0.25 h,0.5 h after the amputation,and reached its peak at 1 h after the amputation,then started to decrease at 2 h after the amputation. GR82334(iv)com?pletely antagonized the significant augment in Fos protein expression in mice ACC neurons after the amputation ,but the antagonism of GR82334 (ith)was incomplete. Conclusion Amputation of the tail extremity could significantly increase the Fos protein expression of mice ACC neurons in a time?dependent manner. Both peripheral and central NK?1 receptors were involved in the process. However ,there are also central conduction pathways of other receptors and neurotransmitters involved in the significant augment in Fos protein expression in mice ACC neurons after amputa?tion.

Objective To perform a comparative study on membrane electrical properties of visceral and somatic nociceptive neurons of anterior cin?gulate gyrus(ACG)in cats,so as to provide the experimental basis for elucidating the mechanism of differences in perceptual qualities between vis?ceral pain and somatic pain from the membrane electrical aspects. Methods A total of 77 adult cats,female or male,weighting 2.0 to 3.5 kg were selected for the study. According to the properties of the greater splanchnic nerve(GSN)or saphenous nerve(SN)evoked responses of neurons in ACG and effect of morphine on the evoked responses,visceral nociceptive neurons(VNNs)having the long latency(≥50 ms)GSN evoked re?sponses or somatic nociceptive neurons(SNNs)having the long latency(≥50 ms)SN evoked responses were detected. With a glass microelectrode in vivo,a series of polarizing current of different intensity from-5 nA to+5 nA with a 50 ms duration were injected to these neurons in ACG,and the membrane electrical responses of these neurons were recorded. Finally,the membrane electrical parameters of these neurons were calculated. Re?sults Totally 254 VNNs and 172 SNNs were recorded in ACG. GSN evoked response threshold of VNNs were higher than SN evoked response threshold of SNNs. Compared with SNNs,the membrane resistance,the membrane capacity and the time constant of VNNs were larger. Conclusion Our data proved that there are some differences in the membrane electrical properties between VNNs and SNNs in ACG,which might be the mem?brane electrical basis for differences in perceptual qualities between visceral pain and somatic pain.