Integration of synaptic excitation to generate an action potential (excitatory postsynaptic potential-spike coupling or E-S coupling) determines the neuronal output. Bidirectional synaptic plasticity is well established in the hippocampus, but whether active synaptic integration can display potentiation and depression remains unclear. We show here that synaptic depression is associated with an N-methyl-D-aspartate receptor-dependent and long-lasting depression of E-S coupling. E-S depression is input-specific and is expressed in the presence of ␥-aminobutyric acid type A and B receptor antagonists. In single neurons, E-S depression is observed without modification of postsynaptic passive properties. We conclude that a decrease in intrinsic excitability underlies E-S depression and is synergic with glutamatergic long-term depression.I ntegration of synaptic inputs to produce an action potential at the axon hillock is a complex operation that depends on two critical factors: the distribution of voltage-gated ion channels in the dendrites and the passive electrical properties upon which these active channels are superimposed (1). Synaptic potentials have been shown to be shaped by intrinsic voltage-gated conductances located in the dendrites and the soma (2), but the dynamics of active synaptic integration remains poorly understood. We addressed here the question as to whether synaptic integration is modified after induction of long-term synaptic potentiation and depotentiation.In the area CA1, homosynaptic long-term potentiation (LTP) of excitatory synaptic transmission is induced by high-frequency stimulation (HFS, 100 Hz) of the afferent fibers (3). In parallel, the probability of discharge of the postsynaptic neurons in response to a given excitatory postsynaptic potential (EPSP) is enhanced (4-7). This second component has been called EPSPto-Spike potentiation (E-S potentiation, E-S P) which is complementary to LTP and functionally important. The reversal of LTP preserves a potential for network plasticity and appears essential for any model of memory (8). Long-term synaptic depotentiation has been reported in the area CA1 (9), but the reversal of E-S P has never been clearly established (10, 11). We show here that E-S depression (E-S D) is expressed concomitantly with long-term depression (LTD). E-S D is largely independent of synaptic inhibition but requires N-methyl-D-aspartate (NMDA) receptor (NMDAR) activation for its induction. We provide evidence for an activity-dependent decrease of the intrinsic excitability of CA1 pyramidal neurons that acts in synergy with LTD. MethodsSlice Preparation. Hippocampal slices (400 m) were obtained from 3-to 6-week-old rats according to institutional guidelines. Slices were cut in a solution (280 mM sucrose͞26 mM NaHCO 3 ͞10 mM D-glucose͞1.3 mM KCl͞1 mM CaCl 2 ͞10 mM MgCl 2 ), and were maintained for 1 h at room temperature in oxygenated (95% O 2 ͞5% CO 2 ) artificial cerebrospinal fluid (ACSF; 125 mM NaCl͞2.5 mM KCl͞0.8 mM NaH 2 PO 4 ͞26 mM NaHCO 3 ͞3 mM CaCl 2 ͞2 mM Mg...

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Excitability changes of the dorsal lateral geniculate nucleus were recorded in male albino rats (Wistar strain) with chronically implanted electrodes. Both averaged postsynaptic and presynaptic evoked responses showed clear circadian rhythms under a constant dark condition. The circadian rhythmicity of the evoked responses was not as a result of motor activity or due to the sleep-wakefulness changes which might show circadian rhythms independently. Circadian rhythms of antidromic and orthodromic evoked responses were abolished after bilateral suprachiasmatic nucleus lesions. These results suggest that the circadian rhythm generated in the suprachiasmatic nucleus significantly affects visual information transmission in the lateral geniculate nucleus.

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