Objective: To determine protein binding characteri stic and signal transmission pathway of melatonin（Mel） receptor(MR) in human e mbryonic peripheral organ tissues. Methods: MR was measured by radio ligand-binding assay and the effect of GTPγS on melatonin specific bindi ng was studied. Results: Mel specific binding sites were det ermined in 16 kinds of human embryonic tissue and this binding could be inhibit ed by GTPγS, supporting the theory that MR is coupled to inhibitory G-proteins system. Conclusion: MR is measured in human embryo tissue, the se results provide experimental data for elucidating the mechanism of the effect of Mel.

0.05).Conclusion CSNK1G1 gene may not be a susceptibility gene for sFS in the northern Chinese Han population.

The purpose of the present work was to study the effect of acute tetanization of the right caudate putamen nucleus (ATRC) on single neuronal interspike intervals (ISIs) in both laterodorsal thalamic nuclei (LDi), and electroencephalogram (EEG) wave interpeak intervals (IPIs) in both hippocampi (HPCi). Experiments were performed on 21 male Sprague-Dawley rats weighing 150~250 g. The seizures were induced by the ATRC (60 Hz, 2 s, 0.4~0.6 mA). Quadruple recordings were simultaneously carried out: two for single unit recordings from both LDi, and two for EEG recordings from both HPCi. The ATRC induced: (1) An interactive epileptic electrical network reconstructed in bilateral HPCi, which was driven by primary afterdischarges of single LD neuron. (2) A symmetric mirror-like ISI spot distribution of the LD neuronal firing before and after tetanus. (3) Gradually prolonged LD neuronal discharge intermittence was coherent with synchronous hippocampal EEG activities on the contralateral side. (4) Single LD neuronal spikes were phase- and time-locked to 20~25 Hz gamma oscillations in contralateral HPC. It suggests a particular temporal code patterning of single LD neuronal firing and its relationships to hippocampal EEG wave code in time series, the latter implies the LD neuronal encoding mechanisms of ATRC-induced epileptic electrical network in bilateral HPCi.
Action Potentials ; physiology ; Animals ; Caudate Nucleus ; physiology ; Electric Stimulation ; methods ; Electroencephalography ; Epilepsy ; etiology ; physiopathology ; Hippocampus ; physiology ; Lateral Thalamic Nuclei ; physiology ; Male ; Nerve Net ; physiology ; Neurons ; physiology ; Rats ; Rats, Sprague-Dawley ; Reaction Time ; physiology

The purpose of the present work was to study the role of unilateral hippocampal neural network in hippocampal epileptogenesis and its cellular mechanisms. Experiments were performed on 45 Sprague-Dawley adult rats. Acute tetanization (60 Hz, 2 s, 0.4 - 0.6 mA) of the right posterior dorsal hippocampus (ATPDH) was used to induce hippocampal epilepsy. The single unit discharges and the depth electrographs were synchronously recorded with a glass microelectrode and a pair of stainless concentric electrodes in the ipsilateral anterior dorsal hippocampus (HPC). The results demonstrated that: (1) some primary unit after-discharges were synchronized with electrographic after-discharges in the anterior dorsal HPC network after eight or nine tetanic trains were administered. Others desynchronized with 5 - 90 Hz primary depth electrographic after-discharges; (2) primary electrographic after-discharges were driven by primary unit after-discharges in the anterior dorsal HPC; (3) primary unit after-discharges were induced by brief primary electrographic after-discharges; and (4) plasticity of primary electrographic after-discharges and inhibition of single neuron firing were induced by repetitive ATPDH. The results suggest that hippocampal pathophysiologic network along the temporal-septal axis of the HPC is re-established by the repetitive ATPDH. There are plastic interactions between single neurons and its network during this re-establishment, which may be involved in the generation of "seizure oscillation". Over-activation of an intrinsic inhibition of the HPC along its temporal-septal axis might be involved in hippocampal network epileptogenesis.
Animals ; Electric Stimulation ; Epilepsy, Temporal Lobe ; physiopathology ; Evoked Potentials ; Hippocampus ; physiopathology ; Male ; Nerve Net ; physiopathology ; Neurons ; physiology ; Rats ; Rats, Sprague-Dawley

AIMTo investigate the neural network and cellular mechanisms of hippocampal epileptogenesis contralateral or ipsilateral to the side of acute tetanization (60 Hz, 2 s, 0.4 - 0.6 mA) of the posterior dorsal hippocampus (ATPDH).

METHODS10 trains of the ATPDH were administered into the CA1 basal dendritic region of the right hemisphere at an interval of 10 minutes.

RESULTS(1) The firing rate of CA1 single neuron in the right or the left hippocampus was inhibited respectively after the ATPDH, and the effects weakened gradually while the trains of the ATPDH increased. The inhibited firing rate and the transformed firing pattern from tonic one to clonic one were more obvious at the side contralateral to the stimulation (62.94% +/- 3.68%, 36.61% +/- 3.14%, P < 0.01). (2) Synchronous primary afterdischarges of depth EEG and single unit discharges were more commonly observed at the side ipsilateral to the ATPDH (P < 0.01). (3) Primary or secondary hippocampal network afterdischarges at high frequency were only found in CA1 region ipsilateral to the ATPDH. (4) Secondary afterdischarges of CA3 basal dendritic neural network were completely synchronized with those of subicular single neuron, which reoccurred and persisted several hours.

CONCLUSIONIt is possible that post-inhibition bursting of single neuron and recurrent network seizures in the hippocampus contralateral to the artificial focus be the important manifestation of the formation of "epileptic networks" across from one hemisphere to another.

Animals ; Electric Stimulation ; Hippocampus ; physiology ; Male ; Neural Pathways ; physiology ; Rats ; Rats, Sprague-Dawley ; Seizures ; etiology

AIMThe 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.

METHODSExperiments 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.

RESULTSChronic 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.

CONCLUSIONKindling 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.

Animals ; Behavior, Animal ; Caudate Nucleus ; Electric Stimulation ; Epilepsy ; physiopathology ; Kindling, Neurologic ; Male ; Rats ; Rats, Sprague-Dawley ; Seizures ; physiopathology

AIMTo 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).

METHODSExperiments 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).

RESULTS(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.

CONCLUSIONPathophysiological 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.

Animals ; Caudate Nucleus ; pathology ; physiopathology ; Corpus Callosum ; pathology ; physiopathology ; Disease Models, Animal ; Electric Stimulation ; Epilepsy ; pathology ; physiopathology ; Hippocampus ; pathology ; physiopathology ; Male ; Nerve Net ; Putamen ; pathology ; physiopathology ; Rats ; Rats, Sprague-Dawley

AIMTo 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.

METHODSExperiments 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.

RESULTS(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.

CONCLUSIONThe 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.

Animals ; Caudate Nucleus ; metabolism ; Epilepsy ; physiopathology ; Hippocampus ; metabolism ; Male ; Neurons ; metabolism ; Putamen ; metabolism ; Rats ; Rats, Sprague-Dawley

The purpose of the present study was to investigate the features of pathophysiological neural networks in rat temporal lobe epileptogenesis. To establish electrogenic epilepsy model, repetitive tetanization (60 Hz, 2 s, 0.4-0.6 mA) was delivered into the right dorsal hippocampus (HPC) of rat brain. Rats were divided into different groups. Experimental animals received tetanic stimulation once a day for 2, 4, 6, 8 or 10 days, respectively. Primary wet dog shakes (WEDS) of the animals were recorded daily during the stimulation to understand the development of behavioral seizures at early stage of epilepsy. The T(2)-weighted (T(2)-WI) spin-echo images were obtained from each experimental rat. The results demonstrated that T(2)-WI hyperintensity of experimental rats was observed in bilateral symmetric dorsal lateral ventricle (LV) areas at stimulating day 2 (n=4), in contralateral medial and ventral LV areas to the side of the electrode at stimulating day 6 (n=5), in contralateral ventral LV areas at stimulating day 8 (n=3), and in ipsilateral ventral LV areas at stimulating day 10 (n=4). Therefore the peak rate of primary WEDS appeared on stimulating day 4 in the experimental rats. Morphological identification demonstrated that the T(2)-WI signal abnormalities were related to the enlarged LV and pathological ventricular choroidea plexus hyperplasia. The results suggest that the development of rat brain abnormalities from dorsal LV to ventral LV at early stage of epilepsy can be measured by magnetic resonance image, which implies reorganization of pathophysiologically functional networks before kindling effect appear.
Animals ; Brain ; physiopathology ; Disease Progression ; Epilepsy, Temporal Lobe ; diagnosis ; pathology ; In Vitro Techniques ; Magnetic Resonance Imaging ; Male ; Rats ; Rats, Sprague-Dawley

The purpose of this work was to study the characteristics of rat brain abnormalities at two hemispheres at the early stage of electrogenic epilepsy. Experiments were performed on 37 male Sprague-Dawley rats. Chronically repetitive tetanization (60 Hz, 2 s, 0.4 - 0.6 mA) was used to stimulate the right dorsal hippocampus (DHPC) of the rat brain once a day for 2, 4, 6, 8 or 10 d, respectively. The T(2) weighted magnetic resonance image (T(2)-WI) were obtained from each experimental rat at the end of the experiments. Histological sections were obtained after experimentation. The results showed that the main pathologic changes at the early stage of epilepsy included: (1) T(2)-WI hyperintensification, the histological enlargement of lateral ventricle (LV) and pathological hyperplasia of ventricular choroidea plexus occurred. The pathological hyperplasia was symmetric in two hemispheres, but the LV enlargement was not. (2) Histologically enlarged LV area showed a resemblance to T(2)-WI hyperintensive area. Compared with the control rats, large T(2)-WI hyperintensive area (P=0.0259; P=0.0184; P=0.0184; P=0.0404; P=0.0259) and histologically enlarged LV area (P=0.0210; P=0.01; P=0.0100; P=0.0152) were present in chronically tetanized rats. (3) Dynamic characteristics of histologically enlarged LV area resembled to those of T(2)-WI hyperintensity area in chronically tetanized rats at different stimulating day. Lateralization of T(2)-WI hyperintensity was in accordance with that of T(2)-WI abnormal area and of histologically enlarged LV. These abnormalities were severe on the contralateral side on the stimulating day 6, or on the ipsilateral side on the stimulating day 10. These results imply characteristic propagation of brain abnormalities crossing to the opposite hemisphere at the early stage of an electrogenic rat epilepsy.
Animals ; Cerebral Cortex ; pathology ; physiopathology ; Electric Stimulation ; Epilepsy ; etiology ; pathology ; physiopathology ; Hippocampus ; physiopathology ; Magnetic Resonance Imaging ; Male ; Rats ; Rats, Sprague-Dawley ; Time Factors