INTRODUCTION: Rebound depolarization (RD) is a neuronal mechanism in which membrane depolarization occurs following a period of hyperpolarization. This phenomenon often results in a burst of action potentials and effectively transforms inhibitory input into excitatory output, thereby influencing downstream synaptic activity. Despite its functional significance, the mechanisms underlying RD in cortical neurons remain incompletely understood.

AIM(S): The present study aimed to investigate the role of adrenergic receptor activation—specifically α1-, α2-, and β-adrenoceptors—in the generation of RD in pyramidal neurons of the medial prefrontal cortex (mPFC).

METHOD(S): Experiments were conducted on layer V pyramidal neurons in acute brain slices from adult male rats (58–65 days old). Whole-cell current-clamp recordings were performed in the presence of tetrodotoxin (TTX), DNQX, DL-AP5, and picrotoxin to block voltage-gated sodium channels and synaptic glutamatergic and GABAergic transmission, ensuring complete synaptic isolation. The effects of noradrenaline, cirazoline (α1-agonist), clonidine (α2-agonist), and isoproterenol (β-agonist) were assessed.

RESULTS: Application of noradrenaline, cirazoline, and isoproterenol reliably induced RD in mPFC pyramidal neurons. In contrast, application of clonidine did not produce significant changes in membrane potential or elicit RD.

CONCLUSIONS: These findings suggest that activation of α1- and β-adrenoceptors promotes RD in layer V pyramidal neurons of the mPFC, whereas α2-adrenoceptor activation does not. This receptor-specific modulation highlights a potential mechanism through which adrenergic signaling can influence cortical excitability and information processing.

FINANCIAL SUPPORT: The study was supported by the Medical University of Warsaw (grant number: FW3/1/F/MG/N/22, FW3/2/F/MG/N/22).