“…Changes in the regional and cellular expression of different trophic molecules, belonging either to the GDNF or to the neurotrophin family, and relevant receptors have been previously reported in the developing and adult rat nervous system (Maisonpierre et al, 1990; Treanor et al, 1996; Trupp et al, 1996; Buj‐Bello et al, 1997; Molliver et al, 1997; Nosrat et al, 1997; Sanicola et al, 1997; Suvanto et al, 1997; Widenfalk et al, 1997; Lenhard and Suter‐Crazzolara, 1998; Masure et al, 1998, 1999; Naveilhan et al, 1998; Worby et al, 1998; Yu et al, 1998; Åkerud et al, 1999; Burazin and Gundlach, 1999; Baudet et al, 2000; Airaksinen and Saarma, 2002). From a clinical perspective, it is interesting that the GDNF family ligands and receptors have been shown to undergo dynamic and differential changes in their expression following epileptic seizures induced in different experimental models (Trupp et al, 1997; Reeben et al, 1998; Kokaia et al, 1999; Chen et al, 2001) and forebrain ischemia (Kokaia et al, 1999; Ardvinsson et al, 2001; Miyazaki et al, 2001, 2002; Sarabi et al, 2001, 2003), indicating that the regulation of endogenous GDNF family signalling mechanisms may be critical for the determination of neuronal fate after brain insults, and that the structural changes and/or functional reorganization that occur in adult brain in the post‐insult period may depend upon the adaptive response of these molecules. Indeed, it has been shown that the intraventricular infusion of GDNF prevents kindling‐induced increases of the hilar area and sprouting of the mossy fibres in the rat (Li et al, 2000) and inhibits kainate‐mediated seizures (Martin et al, 1995) and that GDNF and ART prevent excitotoxic‐induced hippocampal neuronal loss (Bonde et al, 2000; Cheng et al, 2004).…”