Unilateral cortical application of tumor necrosis factor α induces asymmetry in Fos- and interleukin-1β-immunoreactive cells within the corticothalamic projection

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A unilateral microinjection of tumor necrosis factor alpha (TNFα) (150 ng) onto the primary somatosensory cortex induces state-dependent asymmetries in electroencephalographic (EEG) slow wave activity during non-rapid eye movement sleep in rats [H. Yoshida, Z. Peterfi, F. Garcia-Garcia, R. Kirkpatrick, T. Yasuda, J.M. Krueger, State-specific asymmetries in EEG slow wave activity induced by local application of TNF alpha, Brain Res. 1009 (2004) 129–136]. In the current study, analogous TNFα injections were performed to determine Fos- and interleukin-1β (IL1β) immunoreactivity (IR). A unilateral microinjection of TNFα increased the number of Fos- and IL1β-IR cells in the primary somatosensory cortex relative to the contralateral side that received heat-inactivated TNFα. These asymmetric TNFα-induced increases in the number of Fos- and IL1β-IR cells were evident along the outside surface of the cortex (mainly layers II and III) in a restricted rostral to caudal zone. Asymmetrical increases in the number of Fos-IR cells were also observed in the subcortical region that receives the main cortical projection from the somatosensory cortex, the somatic region of the reticular nucleus of the thalamus (reticular thalamus). The IL1β-IR cells double-labeled with glial fibrillary acidic protein (GFAP), suggesting that many of the IL1β-IR cells were astrocytes. The number of the IL1β-IR cells in the reticular thalamus increased significantly ipsilateral to the TNFα injection. Current results indicated that Fos- and IL1β-IR may be utilized to study the functional neuroanatomy involved in the TNFα-mediated state-dependent enhancement of EEG slow wave activity.