Calcium currents in respiratory neurons of the cat in vivo.

Under in vivo conditions, periodic burst discharges of medullary respiratory neurons of mature cat typically start with a rebound depolarization when inhibition through antagonistic neurons stops. This rebound can be blocked by ionophoretically applied extracellular Cd2+. A similar Cd(2+)-sensitive rebound depolarization is triggered by hyperpolarizing current pulses even in the presence of extracellular tetrodotoxin (TTX) and tetraethylammonium (TEA). In current-clamp mode, the current/voltage (I/V) curves rectify outwardly at positive voltages, and this rectification is blocked by Cd2+. Intracellular injection of the L-type Ca(2+)-channel blocker methoxy-verapamil changes the spontaneous activity patterns of neurons. In those neurons that typically show augmenting patterns, the membrane depolarization is slowed down, while in those neurons that have a declining pattern, voltage changes become augmenting. Voltage-clamp measurements reveal a transient, low-voltage-activated T-type Ca2+ current. The current is deinactivated at -100 mV and almost completely inactivated at -60 mV. Depolarizing voltage commands starting from more positive holding potentials evoke sustained Ca2+ currents that reach a maximum at 0 mV. The sustained L-type Ca2+ currents are completely blocked by extracellular Cd2+. We conclude that low- and high-voltage-activated Ca2+ currents are expressed in all types of respiratory neurons and play an essential role in rhythm generation and pattern formation in adult cats in vivo.