We tried to avoid the spreading of drugs to other regions of the hippocampus by restricting the volume of microinjections to 0.2 μL. Considering this, our findings suggest that the severity of convulsive reactions promotion info induced by peripheral treatment with PTZ, rather than cholinergic mechanisms of the dH, may also be mediated by other areas of the CNS, for example, the entorhinal cortex (Stringer 1996), amygdaloid complex (Galvis-Alonso et al. 2004; Foresti et al. 2008), other structures Inhibitors,research,lifescience,medical of the hippocampal formation (Rodrigues et al. 2004; Lan et al. 2007),
and the corpora quadrigemina (Garcia-Cairasco 2002; Doretto et al. 2009). Additionally, the severity of convulsive reactions may possibly be modulated by the substantia nigra, pars reticulata, and inhibitory pathways that modulate Inhibitors,research,lifescience,medical aversive stimulus-induced defensive responses
(Coimbra and Brandão 1993; Eichenberger et al. 2002; Ribeiro et al. 2005; Castellan-Baldan et al. 2006), as well as epileptogenic activity (Rodrigues et al. 2004; Rossetti et al. 2011, 2012). In conclusion, the neuroanatomical substrates identified Inhibitors,research,lifescience,medical in the present work reinforce the involvement of the pain inhibitory system in pain control and suggest that the nuclei connected to the dH are critically involved in the elaboration of postictal antinociception. A reduction in dH activity, caused by blocking local synapses with cobalt chloride, decreased postictal analgesia, confirming dH involvement in the elaboration of antinociception induced by tonic-clonic seizures. Furthermore, our findings suggest that the muscarinic and Sorafenib Tosylate nicotinic cholinergic pathways from the dH exert Inhibitors,research,lifescience,medical an important role in the organization of postictal antinociception, possibly modulated by input to the dH from both prosencephalic areas and from the endogenous pain inhibitory Inhibitors,research,lifescience,medical system. Elucidation of the neurochemistry
of the antinociceptive process evoked by convulsive seizures may represent an important step toward understanding the neural basis of the control of pain. Acknowledgments This work was supported by FAPESP (proc. 96/08574-9, 02/01496-5, and 07/01174-1), CAPES (AUX-PE-PNPD Anacetrapib 2400/2009, proc. 23038.027801/2009-37), and FAEPA (proc. 537/1995 and 70/2002). L. I. Bolognesi was the recipient of a Scientific Initiation scholarship sponsored by FAPESP (08/03402-4). A. Twardowschy was a Doctorate (Sc.D.; process 2008/00531-8) student and a Post-Doctoral (process 2011/20381-3) researcher supported by FAPESP. R. L. de Freitas was the recipient of a Scientific Initiation scholarship (process 01/03752-6), a Magister Scientiae (M.Sc.) fellowship (process 03/05256-1) sponsored by FAPESP, a Scientiae Doctor (Sc.D.). Fellowship sponsored by CAPES and is a Post-Doctorate researcher supported by FAPESP (process 2009/17258-5). N. C.