The Journal of Neurophysiology Vol. 86 No. 3 September 2001, pp. 1164-1178
Copyright ©2001 by the American Physiological Society

Network and Intrinsic Contributions to Carbachol-Induced Oscillations in the Rat Subiculum

 ¹Montreal Neurological Institute and Department of Neurology and Neurosurgery, McGill University, Montreal, Quebec H3A 2B4, Canada;  ²Neurological Institute, Tokyo Women's Medical College, Tokyo 162, Japan;  ³Istituto di Ricovero e Cura a Carattere Scientifico Neuromed, 86077 Pozzilli (Isernia); and  ⁴Ospedale San Paolo, Università degli Studi di Milano, 20142 Milan, Italy

D'Antuono, Margherita, Hiroto Kawasaki, Carmela Palmieri, and Massimo Avoli. Network and Intrinsic Contributions to Carbachol-Induced Oscillations in the Rat Subiculum. J. Neurophysiol. 86: 1164-1178, 2001. Low-frequency network oscillations occur in several areas of the limbic system where they contribute to synaptic plasticity and mnemonic functions that are in turn modulated by cholinergic mechanisms. Here we used slices of the rat subiculum (a limbic area involved in cognitive functions) to establish how network and single neuron (intrinsic) membrane mechanisms participate to the rhythmic oscillations elicited by the cholinergic agent carbachol (CCh, 50-100 µM). We have found that CCh-induced network oscillations (intraoscillatory frequency = 5-16 Hz) are abolished by an antagonist of non-N-methyl-D-aspartate (NMDA) glutamatergic receptors (n = 6 slices) but persist during blockade of GABA receptors (n = 16). In addition, during application of glutamate and GABA receptor antagonists, single subicular cells generate burst oscillations at 2.1-6.8 Hz when depolarized with steady current injection. These intrinsic burst oscillations disappear during application of a Ca²⁺ channel blocker (n = 6 cells), intracellular Ca²⁺ chelation (n = 6), or replacement of extracellular Na⁺ (n = 4) but persist in recordings made with electrodes containing a blocker of voltage-gated Na⁺ channels (n = 7). These procedures cause similar effects on CCh-induced depolarizing plateau potentials that are contributed by a Ca²⁺-activated nonselective cationic conductance (I_CAN). Network and intrinsic oscillations along with depolarizing plateau potentials were abolished by the muscarinic receptor antagonist atropine. In conclusion, our findings demonstrate that low-frequency oscillations in the rat subiculum rely on the muscarinic receptor-dependent activation of an intrinsic oscillatory mechanism that is presumably contributed by I_CAN and are integrated within the network via non-NMDA receptor-mediated transmission.