Alkalosis leads to the over-activity of cortical principal neurons

Alkalosis patients manifest anxiety, manic and convulsion. The elevation of mood and behavior is hypothetically a scenario that alkalosis resets the functional status of neuronal networks to overexcitation. In addition to the downregulation of inhibitory neurons, we examined whether alkalosis upregulates the functions of cortical principal neurons by electrophysiological approach. High extracellular pH condition downgrades inhibitory postsynaptic current frequency, as well as upregulates excitatory synaptic events and spike production in cortical principal neurons. Their functional upregulation is associated with the decreases of spike refractory period and threshold potential. Alkalosis downregulates GABA release from inhibitory neurons and upregulates the functions of principal neurons, which lead to imbalance between inhibitory and excitatory networks for the elevated mood and behaviors.

► Alkalosis downgrades GABA release from cortical inhibitory neuron. ► Alkalosis upgrades excitatory synaptic transmission on cortical pyramidal neurons. ► Alkalosis upgrades the abilities of encoding spikes at cortical pyramidal neurons. ► Balance among neurons shifts to overexcitation for brain deficits in alkalosis.