open access

https://hdl.handle.net/2115/43772

The dusp1 immediate early gene is regulated by natural stimuli predominantly in sensory input neurons

英語

ZENK

2010-07-15

Wiley-Liss

The Journal of Comparative Neurology

518(14)

2873-2901

Many immediate early genes (IEG) have activity-dependent induction in a subset of brain subdivisions or neuron types. However, none have been reported yet with regulation specific to thalamic-recipient sensory input neurons of the telencephalon or in the thalamic sensory input neurons themselves. Here, we report the first such gene, dual specificity phosphatase 1 (dusp1). Dusp1 is an inactivator of mitogen-activated protein kinase (MAPK), and MAPK in turn activates expression of egr1, one of the most commonly studied IEGs, as determined in cultured cells. We found that in the brain of naturally behaving songbirds and other avian species, hearing song, seeing visual stimuli, or performing motor behavior caused high dusp1 up-regulation respectively in auditory, visual, and somatosensory input cell populations of the thalamus and thalamic-recipient sensory input neurons of the telencephalic pallium, whereas high egr1 up-regulation occurred only in subsequently connected secondary and tertiary sensory neuronal populations of these same pathways. Motor behavior did not induce high levels of dusp1 expression in the motor-associated areas adjacent to song nuclei, where egr1 is up-regulated in response to movement. Our analysis of dusp1 expression in mouse brain suggests similar regulation in the sensory input neurons of the thalamus and thalamic-recipient layer IV and IV neurons of the cortex. These findings suggest that dusp1 has specialized regulation to sensory input neurons of the thalamus and telencephalon; they further suggest that this regulation may serve to attenuate stimulus-induced expression of egr1 and other IEGs, leading to unique molecular properties of forebrain sensory input neurons.

学術雑誌論文

Accepted Manuscript

This is the pre-peer-reviewed version of the following article: J. Comp. Neurol. 518:2873–2901, 2010., which has been published in final form at http://onlinelibrary.wiley.com/doi/10.1002/cne.22370/abstract

0021-9967

1096-9861

AA00695917