ELECTROPHYSIOLOGY OF CAT ASSOCIATION CORTICAL-CELLS IN-VIVO - INTRINSIC-PROPERTIES AND SYNAPTIC RESPONSES

1. The intrinsic properties and synaptic responses of association cortical neurons (n = 179) recorded from cat's areas 5 and 7 were studied in vivo. Intracellular recordings were performed under urethane anesthesia. Resting membrane potential (V(m)) was -71.7 +/- 1.2 (SE) mV, amplitude of action potential was 83.7 +/- 2.3 mV, and input resistance was 18.4 +/- 1.8 MOEMGA. Cells were identified ortho- and antidromically from lateroposterior and centrolateral thalamic nuclei and from homotopic foci in the contralateral cortex. Physiologically identified neurons were intracellularly stained with Lucifer yellow (LY) and found to be pyramidal-shaped elements (n = 21). 2. We classified the neurons as regular-spiking and intrinsically bursting cells. Regular-spiking cells were further classified as slow-and fast-adapting according to the adaptation of spike frequency during long-lasting depolarizing current pulses. 3. Regular-spiking, slow-adapting neurons had a monophasic afterhyperpolarization (AHP) or a biphasic AHP with fast and medium components (fAHP, mAHP). Slow-adapting behavior was observed in 84% (n = 119) of the regular-spiking cells. 4. Regular-spiking, fast-adapting cells only fired a train of spikes at the beginning of the pulse. Thereafter, the V(m) remained as a depolarizing plateau, occasionally triggering some spikes. These neurons had a monophasic AHP and represented 16% (n = 23) of the regular-spiking neurons. 5. Intrinsically bursting neurons (n = 37) were observed in 20% of neocortical cells at depolarized V(m). Their action potential was followed by a marked depolarizing afterpotential (DAP). Rhythmic (4-10 Hz) bursts occurred during long-lasting depolarizing current pulses. 6. Small (3-10 mV), fast (1.5-4 ms), all-or-none depolarizing potentials were triggered by depolarizing current pulses. They are tentatively regarded as dendritic spikes recorded from the soma because their rate of occurrence changed as a function of the V(m) and they were eventually blocked by hyperpolarization. 7. Synaptic stimulation of either thalamic or homotopic contralateral cortical areas elicited a sequence of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs). Two components of the EPSP were revealed. At a hyperpolarized V(m), the initial component of the EPSP increased in amplitude, whereas the secondary component was blocked. Repetitive (10 Hz) stimulation of the thalamus or contralateral cortex elicited incremental responses. The augmentation phenomenon was due to an increase in the secondary component of the EPSP. The cortically elicited augmenting responses survived extensive thalamic lesions. A short IPSP and a long-lasting IPSP were evoked by thalamic or cortical stimulation. The short IPSP had a reversal potential at about -70 mV and was reversed by increasing intracellular chloride concentration.