Glutamatergic excitation suppresses latent cortical pacemaking

Local glutamate-receptor antagonism in awake rabbit cortex reveals a recovery-dependent cortical population pacemaker, producing stereotyped LFP and multi-unit bursts separated by quiescence.

• Why it matters: Glutamatergic excitation is the cortex’s main excitatory drive, but it can mask latent timing mechanisms; separating recovery-dependent pacemaking from disinhibited epileptiform bursting is a key gap.
• What they did: The authors combined near-threshold susceptibility and spike-history-dependent loss of excitability to propose an availability reservoir, then tested it in awake rabbit cortex using local glutamate-receptor antagonism and graded GABAergic inhibition.
• The result: Increasing GABAergic inhibition progressively reduced burst size and recurrence before abolishing the pacemaker regime, while reducing GABAergic inhibition under baseline conditions produced epileptiform activity with different timing and intra-burst structure.