Acclimatization to middle altitude hypoxia protects against developmental and cognitive deficits caused by acute fetal hypoxia in mice / 生理学报

Acute fetal hypoxia (AFH) can elicit postnatal motor deficits and cognitive impairments. To test whether lifelong acclimatization to middle altitude (MA) hypoxia has protective effects on the impairments caused by AFH, ICR mice bred at 1 900 m altitude for 6-7 generations were evaluated under AFH. On gestation day 9 (GD 9), 13 (GD 13) or 17 (GD 17), pregnant mice received a single exposure to acute hypoxia (7% O, 6 h). Physiological and neurodevelopmental behaviors, motor function (open field), spatial learning and memory (Morris water maze), and anxiety level (elevated plus maze) were examined in the offspring from neonate to adulthood. In the neonatal age, among all the physiological and behavioral landmarks, almost no differences were found in the hypoxia groups. In the juvenile period, no obvious impairments of motor function and anxiety level were found in the hypoxia groups. In the adult period, no obvious impairment of motor function was found in hypoxia groups; Interestingly, AFH groups' offspring showed normal or enhanced long-term spatial memory ability after AFH. These data suggest that AFH cause little abnormalities in the offspring of MA-adapted mice. To further investigate the underlying mechanisms, the neuronal numbers in behavior-related brain areas (accumbens nucleus, basal amygdala and hippocampus) were counted, and the physiological parameters of the blood were measured. The morphological data showed that no obvious neuronal necrosis was found in all hypoxia groups. In addition, blood tests showed that red blood corpuscle count, hemoglobin concentration and hematocrit levels in mice raised at MA were markedly higher in both males and females, compared with controls raised at the sea level. These data suggest that lifelong acclimatization to MA hypoxia has protective effects against development delay, motor deficits and spatial learning and memory impairments induced by AFH, and the protective effects may be due to higher hemoglobin concentration and hematocrit levels in the blood. The findings may provide a better understanding of fetal hypoxia and potential intervention treatments.

Characteristics of neural information encoding in epileptic networks involved in rat caudate putamen-hippocampi / 中国应用生理学杂志

<p><b>AIM</b>To study the characteristics of neural information encoding of the epileptic networks involved caudate-putamen(CPu) and the hippocampi induced by tetanization of the right CPu in rats.</p><p><b>METHODS</b>Experiments were performed on 59 SD rats. Acute or chronic tetanization of the right CPu (ATRC or CTRC) (60Hz,0.4-0.6 mA, 2 s) was used to induce rat epilepsy.</p><p><b>RESULTS</b>(1) The bursting or primary unit afterdischarges of single neurons were asymmetric in dual hippocampi induced by the ATRC. (2) Continuous sharp waves were observed in ipsilateral or contralateral CPu induced by the CTRC. The oscillatory network seizures with phase shift appeared between two sharp waves in ipsilateral CPu. The frequency of oscillatory waves was negatively correlated with the time and fluctuated from 70 Hz to 110 Hz, then to 35 Hz, and finally to 30 Hz. (3) In the contralateral side primary network after discharges in the CPu were induced by the CTRC. Therefore, the characteristic primary network afterdischarges could be shifted from the CPu or to the HPC, but amplified. On the other hand, HPC sharp waves could be depressed when the CPu network seizures occurred.</p><p><b>CONCLUSION</b>The reestablishment of CPu-hippocampal epileptic networks could be transhemispherically promoted by over-activation of the right CPu network, in which bilateral hippocampal neuronal network and CPu neural network were involved in some particular pathophysiological information encoding.</p>

Characteristics of electrographic and behavioral seizures induced by chronic tetanization of the right caudate-putamen in rats / 中国应用生理学杂志

<p><b>AIM</b>The electrographic and behavioral kindling effects were induced by chronic tetanization of the right caudate-putamen (CPu) to study the target-behavior expression involved in the CPu or hippocampus (HPC) network abnormalities.</p><p><b>METHODS</b>Experiments were performed on 58 SD rats. Tetanization (60Hz,0.4 - 0.6mA, 2s) was delivered into the CPu or the HPC, once a day, for 7-12 days. Animal behaviors were observed every day and depth electrographs were recorded at the beginning or at the end of the experiments.</p><p><b>RESULTS</b>Chronic tetanization of the CPu or of the HPC induced: (1) Rhythmic sharp waves in the CPu and paroxysmal epileptiform events in the HPC electrographs. (2) Primary behavioral seizures, secondary behavioral seizures, and kindling effects, including wet dog shakes (WEDS), rearing, face washing, immobility, chewing and head nodding. (3) Lower rate of primary WEDS (P < 0.01), and higher rate of secondary WEDS (P < 0.01) in the CPu-tetanized rats. (4) Longer silent period of behavioral seizures before kindling appeared in the CPu-tetanized rats.</p><p><b>CONCLUSION</b>Kindling effects in the CPu-tetanized rats resembles those in the HPC-tetanized rats. The CPu might participate in the origin of epileptic focus and be involved in reestablishment of limbic epileptic networks, which may be responsible for the target-behavioral seizures.</p>

Network interactions between caudate putamen and hippocampus contralateral to the right tetanized corpus callosum in rats / 中国应用生理学杂志

<p><b>AIM</b>To study the role of epileptic neural networks reestablished in contralateral caudate putamen (CPu)-hippocampus(HPC) by using chronic tetanization of the right corpus callosum (CTRCC).</p><p><b>METHODS</b>Experiments were performed on 50 SD rats under anaesthesia. The left CPu (LCPu) and the left HPC(LHPC) electrographs were synchronously recorded after acute tetanization following CTRCC (60 Hz, 0.4-0.6 mA, 2 s).</p><p><b>RESULTS</b>(1) In contralateralization to the side implanted interconvertible network inhibition between the CPu and the HPC were induced by combinedly using chronic and acute tetanization of the RCC. (2) Electrographic kindling in the LCPu or in the LHPC was recorded after CTRCC. (3) In case the LCPu or the LHPC electrographs were not kindled after CTRCC, hypsarrhythmia in the LCPu and reduced sharp waves in the HPC were induced b y repetitive tetanization of the RCC once again. Primary afterdischarges in the LCPu or in the LHPC electrographs were evoked by combinedly using chronic and acute tetanization of the RCC.</p><p><b>CONCLUSION</b>Pathophysiological neural networks in the CPu and in the HPC might be reestablished in another side of hemispheres by chronic over-activation of the right CC, which is related to epileptogenesis. Abnormal interactions between the two functional neural networks might be involved in formation of secondary epileptic focus.</p>