Thalamic control of neocortical activation: a critical re-evaluation

Bilateral intrathalamic injection of kainic acid in rats produces widespread destruction of thalamic neurons but does not abolish neocortical activation (generation of low voltage fast activity, LVFA). On the other hand, a combination of reserpine and scopolamine abolishes all LVFA but does not abolish thalamocortical transmission as assessed by recruiting responses, augmenting responses, and sensory evoked neocortical potentials. These facts show that thalamocortical transmission is neither necessary nor sufficient to produce neocortical activation. The classical view of neocortical activation as dependent on a reticulothalamocortical pathway seems to be incorrect. It appears, instead, that neocortical activation is dependent jointly on a cholinergic input from the basal forebrain and a serotonergic input from the brainstem.