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• W2000650034 abstract "Abstract The development of long‐lasting excitability changes after a single intracerebral injection1 of bicuculline (1 mM) in a restricted region of the anterior piriform cortex was studied by means of simultaneous, intra‐ and extracellular recordings in the isolated guinea‐pig brain preparation maintained in vitro by arterial perfusion. The transitory disinhibition induced by bicuculline revealed transient afterdischarges that were followed˜ by the activation of a synaptic potential mediated by the recurrent propagation of the focal epileptiform activity along cortico‐cortical associative fibres. The epileptiform associative potential persisted for the duration of the1 experiment. Both the induction and the long‐term expression of the epileptiform associative potential were dependent on the activation of glutamatergic receptors of the NMDA type, as demonstrated by perfusion with the NMDA receptor antagonist 2–aminopentanoic acid (AP5) (100 μM). After bicuculline washout, piriform cortex neurons responded to afferent stimulation with a burst discharge superimposed on a paroxysmal depolarizing potential. The early component of the burst was mediated by a Ca 2+ ‐dependent, non‐synaptic potential located at the proiimal apical dendrites and soma of layer 11–111 cells, since (i) it was abolished by membrane hyperpolarization, (ii) it was not affected by AP5, (iii) it was correlated with a current sink in layer II, as demonstrated by current source density analysis of field potential laminar profiles, and (iv) it was abolished by cadmium (2–5 mM) applied lbcally in layer II. The late component of the burst response (i) coincided in time with the extracellular epileptiform hssociative potential, (ii) increased linearly in amplitude during membrane hyperpolarization, (iii) was blocked by AP5, and (iv) was correlated with an extracellular sink in layer I b , where the associative fibres contact the distal apical dendrites of piriform cortex neurons. The results presented here indicate that a transient focal disinhibition promotes persistent intrinsic and synaptic excitability changes in piriform cortex neurons. These changes may be responsible for the propagation of epileptiform activity and for the induction of secondary epileptogenesis." @default.
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• W2000650034 date "1997-03-01" @default.
• W2000650034 modified "2023-10-04" @default.
• W2000650034 title "Persistent Excitability Changes in the Piriform Cortex of the Isolated Guinea-pig Brain after Transient Exposure to Bicuculline" @default.
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• W2000650034 doi "https://doi.org/10.1111/j.1460-9568.1997.tb01621.x" @default.
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