Peripheral nerve injury influences the disinhibition induced by focal ischaemia in the rat motor cortex Tama ´s Farkas a , Eniko ˝ Racekova b , Zsolt Kis a , Szatma ´r Horva ´th a , Jozef Burda b , Jan Galik b , Jo ´zsef Toldi a, * a Department of Comparative Physiology, University of Szeged, Ko ¨ze ´p fasor 52, H-6726 Szeged, Hungary b Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovakia Received 4 February 2003; accepted 12 February 2003 Abstract Photothrombotic lesions were produced in the rat primary motor cortex, and the brain excitability was assessed in a paired-pulse stimulation protocol by transcranial recording, in parallel at 16 points of the frontal cortex, including the insulted and the surrounding areas. The cortical lesion reduced the inhibition in the extended frontal cortex, with a delay of a few minutes. Unilateral facial nerve transection, however, accelerated the widespread disinhibition. Although the mechanism is not clear in detail, both peripheral and central injury-induced disinhibition may have a significant impact on the recovery of the function. q Elsevier Science Ireland Ltd. All rights reserved. Keywords: Nerve injury; Cortical disinhibition; Focal ischaemia; Rose Bengal; Motor cortex; Facial nerve It is well known that both deafferentation of a sensory cortex [2] and deefferentation of the primary motor cortex (MI) [13] induce a reduction in cortical inhibition, during which different types of cortico-cortical connections are modu- lated in efficacy. The functional meaning of such a change is still obscure, but its importance is unquestionable from both theoretical and clinical aspects (mention may be made of phantom pain and synkinesia). No less interesting and important a topic is the ischaemia-induced plastic changes in the cortex (we may consider stroke). Schiene et al. [14] recently described an enlargement of the cortical vibrissa representation in the surroundings of an ischaemic cortical lesion. Extended brain disinhibition has been demonstrated following an ischae- mia-induced focal cortical lesion [1]. Both denervation and ischaemia-induced cortical changes indicate that widespread remote decreases in inhibition are a common feature of these peripheral and central injuries. Among the questions that may arise, the most important one is how these remote effects favour or impair the recovery of function. As the first step in the investigation of this complex problem, in the present work we have examined whether the two manipulations interact or not in causing disinhibition. The experimental procedures used in this study followed the protocol for animal care approved by the European Communities Council Directives (86/609/EEC). A total of 30 Sprague–Dawley adult rats of either sex were anaes- thetized with i.p. injections of a mixture of Ketavet (10.0 mg/100 g) and Rompun (xylasine, 0.8 mg/100 g). The rats were placed into a stereotaxic frame and the skull was exposed. On the left side, above the MI, the skull was thinned with a dental drill from about 2 mm posterior to 5 mm anterior of the bregma, and from 0.5 to 5 mm lateral of the midline. In the course of the operation, we also exposed the right side facial nerve (n7), including its postauricular branch. The cortical photothrombotic (pt) lesion was carried out by i.v. injection of Rose Bengal (1.3 mg/100 g) and cold light exposure, as described by Buchkremer-Ratzmann and Witte [1]. There were two main groups of animals: the controls (n ¼ 10) and the lesioned animals (n ¼ 20). In the ten controls, either illumination was applied (n ¼ 4) or Rose Bengal was given without cold light application (n ¼ 3). In three animals, neither Rose Bengal nor light exposure was applied. In three of the 20 lesioned rats, only a pt lesion was 0304-3940/03/$ - see front matter q Elsevier Science Ireland Ltd. All rights reserved. doi:10.1016/S0304-3940(03)00230-1 Neuroscience Letters 342 (2003) 49–52 www.elsevier.com/locate/neulet * Corresponding author. Tel.: þ 36-62-544153; fax: þ 36-62-544291. E-mail address: toldi@bio.u-szeged.hu (J. Toldi).