Glial cells have important physiological roles of regulating neuronal excitability and preventing epilepsy.

Later, Yu Zhou and colleagues in the Silva lab discovered that CREB modulates memory allocation by regulating neuronal excitability.

It plays a role in regulating neuronal excitability throughout the nervous system.

In mammalian CNS neurons, K2.1 is a predominant delayed rectifier K current that regulates neuronal excitability, action potential duration, and tonic spiking.

The K2.2 protein is activated before membrane hyperpolarization and is thought to regulate neuronal excitability by contributing to the slow component of synaptic AHP.

They may regulate A-type currents, and hence neuronal excitability, in response to changes in intracellular calcium.

These modulations of K conductances serve as common mechanisms for regulating excitability and synaptic strength.

When NK receptors are stimulated, they can generate various second messengers, which can trigger a wide range of effector mechanisms that regulate cellular excitability and function.

This indicates that RNA editing here may be a mechanism for regulating neuronal excitability by stabilising receptor signalling.

Their diverse functions include regulating neurotransmitter release, heart rate, insulin secretion, neuronal excitability, epithelial electrolyte transport, smooth muscle contraction, and cell volume.