Fig 1.
Spontaneous hippocampal epileptiform discharges in CA3 and CA1 under nonsynaptic conditions.
(A) Simultaneous recording of synchronous epileptiform activity induced in synaptic blockers aCSF: (1) bursts of discharges, (2) single epileptiform discharges, (3) epileptiform discharges appear simultaneously in CA3 and CA1, while population spikes only in CA1. (B) Nonsynaptic population spikes appear in low-Ca2+ aCSF: (4) epileptiform activity is not synchronized between CA3-CA1 hippocampal zones.
Fig 2.
CA3-CA1 synchronization of epileptiform discharges induced in aCSF with AMPA, NMDA, GABA antagonists depends on synaptic connections.
(A) Blockade of the synchronous epileptiform discharges following 15 μM CdCl2 application: (1) burst of epileptiform discharges and (2) single epileptiform discharges become less synchronized (3) following 15 μM CdCl2 application and nonsynaptic population spikes (4) appear in CA1. (B) Simultaneous extracellular (upper trace) and intracellular (bottom trace) recording in CA1 during perfusion with synaptic blockers aCSF reveals synaptic currents appear during epileptiform discharges.
Fig 3.
Effect of mechanical separation of CA3 and CA1 hippocampal zones on epileptiform discharges in synaptic blockers aCSF.
(1) Burst of discharges synchronized between CA3-CA1. (2) Epileptiform discharges disappear in CA1, but not in CA3 after the separation was made between two recording sites.
Fig 4.
Effect of cholinergic antagonists on CA3-CA1 synchronous epileptiform discharges induced in synaptic blockers aCSF.
(A) Application of atropine does not block CA3-CA1 synchronous discharges: (1) burst of discharges in synaptic blockers aCSF, (2) synchronous epileptiform discharges appear during atropine application. (B) Application of d-tubocurarine blocks CA3-CA1 synchronous epileptiform discharges: (3) burst of discharges in synaptic blockers aCSF, (4) reduction of the discharges after tubocurarine application, (5) epileptiform discharges decrease under tubocurarine application.
Table 1.
Effect of cholinergic antagonists on CA3-CA1 synchronization of epileptiform discharges.
Fig 5.
Nicotinic receptors contribute to synchronous discharges in synaptic blockers aCSF.
(A) Effect of nonselective nicotinic antagonist mecamylamine on CA3-CA1 synchronous epileptiform discharges induced in synaptic blockers aCSF: (1) single epileptiform discharges; (2) decrease in epileptiform discharges following 50 μM MEC application; (3) epileptiform discharges after mecamylamine wash out. (B) Simultaneous extracellular (up) and patch clamp recording (bottom) in synaptic blockers aCSF: (4) neuron voltage clamped at -70 mV, (5) neuron voltage clamped at zero mV.
Fig 6.
Effect of selective nicotinic antagonists on spontaneous epileptiform discharges in synaptic blockers aCSF.
(A) Application of α7 nAChRs antagonist MLA (100 nM) does not stop synchronous discharges: (1) burst of discharges in synaptic blockers aCSF; (2) burst of discharges during MLA application; (3) single field discharges in presence of MLA and (4) after wash out. (B) Synchronous burst of discharges appears in (1) synaptic blockers aCSF, (2) after DhβE application, and after perfusion was returned to synaptic blockers aCSF (3). (C) Summary data of the effect of cholinergic antagonists on cross-correlation between CA3 and CA1 field potential in synaptic blockers aCSF.
Fig 7.
Effect of the cholinergic antagonists on hippocampal SLA activity.
(A) Reduction of the bicuculline-evoked SLA following MEC application. (B) Application of α7 nAChRs antagonist MLA and α4β2 antagonist DhβE has no effect on bicuculline-evoked SLA. (C) Application of MEC has no effect on 4-AP induced SLA.