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Ishii, T. et al.

Toshiaki Ishii, Ryuta Suenaga, Wataru Iwata, Ryouhei Miyata, Ryu Fujikawa, Yoshikage Muroi,

Bilateral lesions of the mesencephalic trigeminal sensory nucleus stimulate hippocampal neurogenesis but lead to severe deficits in spatial memory resetting.

The mesencephalic trigeminal sensory nucleus (Me5), which receives signals originating from oral proprioceptors, becomes active at weaning and contributes to the acquisition of active exploratory behavior [Ishii, T., Furuoka, H., Kitamura, N., Muroi, Y., and Nishimura, M. (2006) Brain Res. 1111, 153-161]. Because cognitive functions play a key role in animal exploration, in the present study we assessed the role of Me5 in spatial learning and memory in the water maze. Mice with bilateral Me5 lesions exhibited severe deficits in both a reversal learning and a reversal probe test compared with sham-operated mice. In spite of these reversal tests, Me5 lesions had no effect on a hidden platform test. These results suggest that Me5-lesioned mice show a perseveration of the previously learned spatial strategy rather than an inability to learn a new strategy, resulting in reduced spatial memory resetting. Moreover, adult neurogenesis in the dentate gyrus of the hippocampus, which has been proposed to have a causal relationship to spatial memory, was stimulated in Me5-lesioned mice. Thus, a stimulation of hippocampal neurogenesis observed after Me5 lesions may lead to a rigidity and perseverance of the previously learned strategy because of inferential overuse of past memories in a novel situation. These results suggest that Me5 contributes to spatial memory resetting by controlling the rate of hippocampal neurogenesis through an ascending neuronal pathway to the hippocampus.[1]

References

Bilateral lesions of the mesencephalic trigeminal sensory nucleus stimulate hippocampal neurogenesis but lead to severe deficits in spatial memory resetting. Ishii, T., Suenaga, R., Iwata, W., Miyata, R., Fujikawa, R., Muroi, Y. Brain Res. (2010) [Pubmed]

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