Synaptic impairment induced by paroxysmal ionic conditions in neocortex.

Area of Science:

• Neuroscience
• Electrophysiology
• Neocortical dynamics

Background:

• Seizures are characterized by altered extracellular ion concentrations, specifically reduced calcium ([Ca²⁺](o)) and increased potassium ([K⁺](o)).
• The impact of these ionic shifts on neuronal excitability and network synchrony in the neocortex remains incompletely understood.

Purpose of the Study:

• To investigate whether extracellular ionic changes during seizures are sufficient to alter synaptic neuronal responses and synchrony in the neocortex.
• To elucidate the specific roles of extracellular calcium and potassium in modulating neuronal function during seizure-like conditions.

Main Methods:

• In vivo and in vitro electrophysiological recordings from cat and rat neocortical neurons.
• Microstimulation techniques were employed to evoke neuronal responses.
• Experimentation involved manipulating extracellular potassium ([K⁺](o)) and calcium ([Ca²⁺](o)) concentrations to mimic seizure-like ionic environments.

Main Results:

• In vivo seizures abolished evoked synaptic responses.
• In vitro, elevated [K⁺](o) depolarized neurons, while elevated [Ca²⁺](o) hyperpolarized them.
• High [K⁺](o) (12 mm) abolished postsynaptic responses by blocking axonal spike propagation, whereas reduced [Ca²⁺](o) increased response failures but did not abolish them.

Conclusions:

• Concomitant changes in extracellular potassium and calcium during seizures significantly alter synaptic neuronal responses.
• These ionic shifts are major contributors to the observed decrease in long-range synchrony during neocortical seizures.