Figure 4. The thalamic mechanisms and regions involved in generating alpha oscillations.

(A) Electrophysiology and pharmacology results from Lorincz et al. (2009). In the lateral geniculate nucleus (LGN), the activation of high-threshold bursting (HBT) neurons can lead to either spiking or bursting in interneurons (IN), which results in the suppression of relay-mode (R-M) neuronal activity at the LGN alpha peak or trough, respectively. The activation of muscarinic acetylcholine (ACh) receptors generates alpha oscillations and can induce HT burst firing in a subset of relay cells, producing phase shifts in their spiking. Reproduced from (92); used with permission. (B) The comprehensive computational model by Vijayan and Kopell (2012) reproduced both these physiological and pharmacological results. It further emphasised the effect of low-level activation of glutamate receptors, together with AcCh agonists, in initiating alpha activity that biases relay cells to fire at certain alpha phases. Reproduced from (151); used with permission.