| The present study examined the neurobiological mechanisms underlying neocortical activation induced by electrical stimulation of the rat inferior colliculus (IC) in two separate experiments. Both experiments used 100-Hz electrical stimulation of the IC to elicit neocortical activation, which was indicated by a reduction in neocortical activity in the delta frequency range (0.5--4 Hz) and the concurrent appearance of low-voltage, fast activity in the electrocorticogram (ECoG). In the first experiment, treatment with the muscarinic anatagonist scopolamine (1 mg/kg; i.p.), or the serotonergic antagonist methiothepin (1 mg/kg; i.p.), reduced the suppression of ECoG activity in the delta frequency range, suggesting that acetylcholine and serotonin are both involved in IC-induced neocortical activation. Conversely, treatment with saline (1 mg/kg; i.p.), the peripherally acting muscarinic antagonist, methyl-scopolamine (1 mg/kg; i.p.), or both (1 mg/kg each; i.p.), failed to alter ECoG activation elicited by IC stimulation. It was also found that combined treatment with scopolamine and methiothepin (1 mg/kg each; i.p.) completely abolished the suppression of ECoG delta activity, suggesting that non-cholinergic and non-serotonergic input to the neocortex is insufficient to maintain IC-induced neocortical activation. In the second experiment, infusions of the anesthetic lidocaine (2%, 1 mul) in the basal forebrain (BF), raphe nuclei, or both, were found to reduce the suppression of ECoG delta activity following IC stimulation. These results suggested that the BF and raphe both play a role in IC-induced neocortical activation. Taken together the data suggest that the IC exerts its activating influence on the neocortex via cholinergic and serotonergic projections to the cortex that originate in the BF and raphe, respectively. |
