ABSTRACT
Objective To investigate the influences of anterior thalamic nucleus (ANT) stimulation on neurogenesis in hippocampus of epileptic rats. Methods Thirty-two male SD rats were randomly alloca-ted to normal-control group ( n＝8),control-stimulation group ( n＝8),sham-stimulation group ( n＝8) and model-stimulation group(n＝8).Eqileptic SD rat model was established by using microinjection of kainic acid in hippocampal CA3 area,and administered 48 h continuous ANT stimulation in the chronic stage.Epileptic seizures were monitored and counted.The levels of Ki-67,a neurogenesis protein in hippocampus was deter-mined by Western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Results The epi-lepsy seizure rate was (5.9±2.2) per week in the sham-stimulation group and (2.9±1.1) per week in model-stimulation group.Compared with sham-stimulated rats, ANT stimulation reduced seizures by 50.8%(P＜0.05).Western blot analysis revealed that the relative levels of Ki-67 in the hippocampus of model-stimula-tion group significantly higher than that of the sham-stimulation group((0.44±0.15) vs (0.19±0.73),P＜0.05).qRT-PCR analysis showed that relative levels of Ki-67 mRNA in the hippocampus of model-stimula-tion group were significantly higher than that of the sham-stimulation group((0.45±0.10) vs (0.15±0.06), P＜0.05). Conclusion Chronic ANT stimulation can promote neurogenesis in epileptic rats,which may be a principle mechanism of the beneficial effect of ANT stimulation on epilepsy.
ABSTRACT
It has been suggested that epileptic seizures can be interrupted by deep brain stimulation (DBS) of various deep brain structures which may exert a therapeutic control on seizure generators or correspond to ictal onset zone themselves. Several groups have used DBS in drug-resistant epilepsy cases for which resective surgery cannot be applied. The promising subcortical brain structures are anterior and centromedian nucleus of the thalamus, subthalamic nucleus, and other nuclei to treat epilepsy in light of previous clinical and experimental data. Recently two randomized trials of neurostimulation for controlling refractory epilepsy employed the strategies to stimulate electrodes placed on both anterior thalamic nuclei or near seizure foci in response to electroencephalographically detected epileptiform activity. However, the more large-scale, long-term clinical trials which elucidates optimal stimulation parameters, ideal selection criteria for epilepsy DBS should be performed before long.
Subject(s)
Anterior Thalamic Nuclei , Brain , Deep Brain Stimulation , Electrodes , Epilepsy , Intralaminar Thalamic Nuclei , Light , Patient Selection , Seizures , Subthalamic Nucleus , ThalamusABSTRACT
It has been suggested that epileptic seizures can be interrupted by deep brain stimulation (DBS) of various deep brain structures which may exert a therapeutic control on seizure generators or correspond to ictal onset zone themselves. Several groups have used DBS in drug-resistant epilepsy cases for which resective surgery cannot be applied. The promising subcortical brain structures are anterior and centromedian nucleus of the thalamus, subthalamic nucleus, and other nuclei to treat epilepsy in light of previous clinical and experimental data. Recently two randomized trials of neurostimulation for controlling refractory epilepsy employed the strategies to stimulate electrodes placed on both anterior thalamic nuclei or near seizure foci in response to electroencephalographically detected epileptiform activity. However, the more large-scale, long-term clinical trials which elucidates optimal stimulation parameters, ideal selection criteria for epilepsy DBS should be performed before long.
Subject(s)
Anterior Thalamic Nuclei , Brain , Deep Brain Stimulation , Electrodes , Epilepsy , Intralaminar Thalamic Nuclei , Light , Patient Selection , Seizures , Subthalamic Nucleus , ThalamusABSTRACT
Objective To examine the synaptic structure and glutamatergic transmitter of the pathway linking the anterior thalamic nucleus(ATN) and the subicular complex. Methods The HRP tracing and post embedding immunogold technique were used. Results In the anterior thalamic nucleus,anterograde HRP labelled terminals contained clear round synaptic vesicles and several mitochondria,and formed asymmetric synaptic contacts with HRP-labelled or non-HRP labelled dendrites.The highest densities of immunogold particles following glutamate immunostaining were found in HRP-labelled terminals and similar axon terminals devoid of HRP reaction product,They formed asymmetric synaptic contacts(Gray type Ⅰ) with dendrites.The average density of those immunogold particles was more than 3 times higher than that of the gold particles in the dendrites of their contacts and over 6 times higher than that of the particles in the terminals that formed symmetric synapses(Gray type Ⅱ).In two serial GABA immunogold reactive sections,Gray tpye Ⅱ terminals were heavily labeled whereas Gray type Ⅰterminals displayed a very slight labelling.In glutamate immunogold reactive sections,Gray type Ⅱ terminals were slightly labeled.A GABA positive terminal which formed symmetric synapses with HRP-labeled dendrites and the terminal which formed asymmetric synapses converged on the same dendrite.Conclusion The terminals of projection neurons in the pathway linking the anterior thalamic nucleus and the subicular complex are glutamatergic.In anterior thalamic nucleus corticothalamic projection neuron terminals form asymmetric synaptic contacts with HRP-labelled thalamocortical projection neurons by axo-dendritic synapses.