| 11530219 |
Louvel J, Papatheodoropoulos C, Siniscalchi A, Kurcewicz I, Pumain R, Devaux B, Turak B, Esposito V, Villemeure JG, Avoli M: GABA-mediated synchronization in the human neocortex: elevations in extracellular potassium and presynaptic mechanisms. Neuroscience. 2001;105(4):803-13.
Field potential and extracellular [K (+)] ([K (+)](o)) recordings were made in the human neocortex in an in vitro slice preparation to study the synchronous activity that occurs in the presence of 4-aminopyridine (50 microM) and ionotropic excitatory amino acid receptor antagonists. Under these experimental conditions, negative or negative-positive field potentials accompanied by rises in [K (+)](o) (up to 4.1 mM from a baseline of 3.25 mM) occurred spontaneously at intervals of 3-27 s. Both field potentials and [K (+)](o) elevations were largest at approximately 1000 microm from the pia. Similar events were induced by neocortical electrical stimuli. Application of medium containing low [Ca (2+)]/high [Mg (2+)] (n=3 slices), antagonism of the GABA (A) receptor (n=7) or mu-opioid receptor activation (n=4) abolished these events. Hence, they represented network, GABA-mediated potentials mainly reflecting the activation of type A receptors following GABA release from interneurons. The GABA (B) receptor agonist baclofen (10-100 microM, n=11) reduced and abolished the GABA-mediated potentials (ID (50)=18 microM). Baclofen effects were antagonized by the GABA (B) receptor antagonist CGP 35348 (0.1-1 mM, n=6; ID (50)=0.19 mM). CGP 38345 application to control medium increased the amplitude of the GABA-mediated potentials and the concomitant [K (+)](o) rises without modifying their rate of occurrence. The GABA-mediated potentials were not influenced by the broad-spectrum metabotropic glutamate agonist (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (100 microM, n=10), but decreased in rate with the group I receptor agonist (S)-3,5-dihydroxyphenylglycine (10-100 microM, n=9). Our data indicate that human neocortical networks challenged with 4-aminopyridine generate glutamatergic-independent, GABA-mediated potentials that are modulated by mu-opioid and GABA (B) receptors presumably located on interneuron terminals. These events are associated with [K (+)](o) elevations that may contribute to interneuron synchronization in the absence of ionotropic excitatory synaptic transmission. |
1(0,0,0,1) |