532 nm Low-Power Laser Irradiation Facilitates the Migration of GABAergic Neural Stem/Progenitor Cells in Mouse Neocortex.

BACKGROUND AND OBJECTIVE: Accumulating evidence has shown that low-power laser irradiation (LLI) affects cell proliferation and survival, but little is known about LLI effects on neural stem/progenitor cells (NSPCs). Here we investigate whether transcranial 532 nm LLI affects NSPCs in adult murine neocortex and in neurospheres from embryonic mice. STUDY DESIGN/MATERIALS AND METHODS: We applied 532 nm LLI (Nd:YVO4, CW, 60 mW) on neocortical surface via cranium in adult mice and on cultured cells from embryonic mouse brains in vitro to investigate the proliferation and migration of NSPCs and Akt expression using immunohistochemical assays and Western blotting techniques. RESULTS: In vivo experiments demonstrated that 532 nm LLI significantly facilitated the migration of GABAergic NSPCs that were induced to proliferate in layer 1 by mild ischemia. In vitro experiments using GABAergic NSPCs derived from embryonic day 14 ganglionic eminence demonstrated that 532 nm LLI for 60 min promoted the migration of GAD67-immunopositive NSPCs with a significant increase of Akt expression. Meanwhile, the LLI induced proliferation, but not migration, of NSPCs that give rise to excitatory neurons. CONCLUSION: It is concluded that 532 nm LLI promoted the migration of GABAergic NSPCs into deeper layers of the neocortex in vivo by elevating Akt expression.

[Lipids of neocortex after X-ray irradiation of the rat head at a dose of 200 Gy].

X-ray irradiation at a dose of 200 Gy with local exposure of the rat head induced the change of the lipid content in the neocortex tissue. The amount of phosphatidylinositol was decreased, the amount of free fatty acids, diglycerols, sphingomyelin was increased, and the amount of cholesterol had a growth trend in 2 h after X-ray exposition. The results testify in favor of participation of phosphatidylinositol- and sphingomyelin-relating signal systems and cholesterol in early stages of the cerebral radiation syndrome. We suggest that the change of the lipid content in early periods after the effect of a super-high dose of X-ray irradiation indicates the lipid dependence in the elimination of motion damages and the restoration of the functions of nerve cells. Effects on the lipid metabolism in the nerve tissue are promising for correcting the cerebral radiation syndrome.

Electric cortical stimulation suppresses epileptic and background activities in neocortical epilepsy and mesial temporal lobe epilepsy.

OBJECTIVE: To evaluate the suppressive effect of electric cortical stimulation upon the seizure onset zone and the non-epileptic cortex covered by subdural electrodes in patients with neocortical epilepsy and mesial temporal lobe epilepsy (MTLE). METHODS: Four patients with medically intractable focal epilepsy had implanted subdural electrodes for preoperative evaluation. Cortical functional mapping was performed by intermittently repeating bursts of electric stimulation, which consisted of 50 Hz alternating square pulse of 0.3 ms duration, 1-15 mA, within 5 s. The effect of this stimulation on the seizure onset zones and on the non-epileptic areas was evaluated by comparing spike frequency and electrocorticogram (ECoG) power spectra before and after stimulation. A similar comparison was performed in stimulation of 0.9 Hz of the seizure onset zones for 15 min. RESULTS: When the seizure onset zone was stimulated with high frequency, spike frequency decreased by 24.7%. Logarithmic ECoG power spectra recorded at stimulated electrode significantly decreased in 10-32 Hz band by high frequency stimulation of the seizure onset zone, and in 14-32 Hz band by high frequency stimulation of the non-epileptic area. Low frequency stimulation of the seizure onset zone produced 18.5% spike reduction and slight power decrease in 12-14 Hz. CONCLUSIONS: Both high and low frequency electric cortical stimulation of the seizure onset zone have a suppressive effect on epileptogenicity. Reduction of ECoG fast activities after electric cortical stimulation suggests the augmentation of inhibitory mechanisms in human cortex.

Time course of the effects of prenatal gamma irradiation on the dorsal lateral geniculate nucleus of Swiss mice.

A previous study reported that adult mice irradiated at the 16th embryonic day present a severe neuronal number reduction in the dorsal lateral geniculate thalamic nucleus. In the present study, we investigated the time course of the effects of prenatal irradiation on this thalamic nucleus. One day after irradiation, a great number of pyknotic figures were seen mainly in the cerebral proliferative zones. In the geniculate nucleus, only scattered pyknotic figures were identified. On the first week after birth, the geniculate nucleus presented frequent pyknotic figures. From five days after birth onwards, a severe shrinkage of the occipital cortex and a great reduction in the geniculate nucleus neuronal number were found. On the second week after birth this neuronal number reduction reached as high as 75%. At each postnatal analyzed age, severe volumetric geniculate nucleus shrinkage was combined to non-significant neuronal density variations. The presence of few pyknotic figures in the geniculate nucleus one day after irradiation and its delayed neuronal loss indicate an indirect effect of irradiation. We suggest that the effect upon the geniculate nucleus is secondary to the damage of the occipital cortex. A possible interpretation for thalamic neuronal loss is that geniculate neurons fail to establish cortical arbors after major target loss. In this case, the loss of trophic support should also be considered.