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

A unilateral microinjection of tumor necrosis factor alpha (TNFalpha) (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 TNFalpha injections were performed to determine Fos- and interleukin-1beta (IL1beta) immunoreactivity (IR). A unilateral microinjection of TNFalpha increased the number of Fos- and IL1beta-IR cells in the primary somatosensory cortex relative to the contralateral side that received heat-inactivated TNFalpha. These asymmetric TNFalpha-induced increases in the number of Fos- and IL1beta-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 IL1beta-IR cells double-labeled with glial fibrillary acidic protein (GFAP), suggesting that many of the IL1beta-IR cells were astrocytes. The number of the IL1beta-IR cells in the reticular thalamus increased significantly ipsilateral to the TNFalpha injection. Current results indicated that Fos- and IL1beta-IR may be utilized to study the functional neuroanatomy involved in the TNFalpha-mediated state-dependent enhancement of EEG slow wave activity.