Associative EPSP‐‐spike potentiation induced by pairing orthodromic and antidromic stimulation in rat hippocampal slices.

Jester, Jennifer M.; Campbell, Lee W.; Sejnowski, T. J.

doi:10.1113/jphysiol.1995.sp020696

Cited by 66 publications

(57 citation statements)

References 34 publications

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“…Paired orthodromic and antidromic stimulation has also been used previously to produce an extracellular associative E-S potentiation that was expressed without LTP (Jester et al, 1995). E-S potentiation had not yet been examined intracellularly using an associative LTP induction protocol.…”

Section: Discussionmentioning

confidence: 99%

“…There has been considerable debate as to the mechanisms underlying E-S potentiation, with studies focusing on increased neuronal excitability (Abraham et al, 1985;Taube and Schwartzkroin, 1988;Wathey et al, 1992;Jester et al, 1995;Daoudal et al, 2002) and decreased efficacy of inhibition (Wilson et al, 1981;Abraham et al, 1987;Chavez-Noriega et al, 1989;Tomasulo et al, 1991;McMahon and Kauer, 1997;Lu et al, 2000;Chevaleyre and Castillo, 2003;Staff and Spruston, 2003). There is substantial evidence that a major component of E-S potentiation relies on GABAergic inhibition, because E-S potentiation is mimicked and occluded Chavez-Noriega et al, 1989;Tomasulo et al, 1991;Lu et al, 2000) or reduced (Daoudal et al, 2002;Staff and Spruston, 2003) by GABA A receptor (GABA A R) antagonists (but see Jester et al, 1995;Evans and Viola-McCabe, 1996).…”

Section: Introductionmentioning

confidence: 99%

“…There is substantial evidence that a major component of E-S potentiation relies on GABAergic inhibition, because E-S potentiation is mimicked and occluded Chavez-Noriega et al, 1989;Tomasulo et al, 1991;Lu et al, 2000) or reduced (Daoudal et al, 2002;Staff and Spruston, 2003) by GABA A receptor (GABA A R) antagonists (but see Jester et al, 1995;Evans and Viola-McCabe, 1996). Several possible explanations exist for the dependence of E-S potentiation on intact inhibition.…”

Section: Introductionmentioning

confidence: 99%

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Timing and Balance of Inhibition Enhance the Effect of Long-Term Potentiation on Cell Firing

Marder

Buonomano²

2004

J. Neurosci.

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The role of a neuron in neural processing is ultimately determined by whether or not it fires an action potential in a given context. Studies on synaptic plasticity have focused primarily on changes in EPSPs, and not on whether plasticity translates into changes in firing. However, this issue has been addressed by examining EPSP-spike (E-S) potentiation, which enhances the ability of an EPSP of a fixed slope to elicit spikes after long-term potentiation (LTP). Although LTP is thought to underlie learning and memory, E-S potentiation could play an equally important role by potentiating the neuronal input-output function. Here, we used a combined experimental and theoretical approach to examine both the mechanisms underlying E-S potentiation as well as the role of inhibition in shaping the input-output function of neurons. Whereas previous studies examined tetanus-LTP, in which inhibitory synapses may have undergone plasticity, here we examined pairing-induced associative LTP. We determined that although intact inhibition was necessary for pairinginduced E-S potentiation, inhibitory plasticity was not. We further established using computer simulations that a primary mechanism of E-S potentiation was a change in the relative recruitment and latency of inhibitory neurons. Although these studies do not exclude the presence of additional mechanisms of E-S potentiation that may be engaged depending on the induction protocol, they do establish that under intact pharmacology, LTP of the Schaffer collateral to CA1 pyramidal neuron synapses will produce E-S potentiation as a result of changes in the balance and timing of excitation and inhibition.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Timing and Balance of Inhibition Enhance the Effect of Long-Term Potentiation on Cell Firing

Marder

Buonomano²

2004

J. Neurosci.

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“…During an E-S potentiation, input specificity is strongly reduced, whether in vitro in CA1 (Jester et al 1995) or in vivo in the DG (Abraham et al 1985). Given the effect of AmmTX3 on E-S potentiation, we can therefore assume that in a behavioral context, AmmTX3 infusion could decrease the signal-to-noise ratio during information encoding.…”

Section: Ammtx3 Prolongs the E-s Component Of Ltpmentioning

confidence: 99%

Kv4 potassium channels modulate hippocampal EPSP-spike potentiation and spatial memory in rats

Truchet¹,

Manrique²,

Sréng³

et al. 2012

Learn. Mem.

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Kv4 channels regulate the backpropagation of action potentials (b-AP) and have been implicated in the modulation of longterm potentiation (LTP). Here we showed that blockade of Kv4 channels by the scorpion toxin AmmTX3 impaired reference memory in a radial maze task. In vivo, AmmTX3 intracerebroventricular (i.c.v.) infusion increased and stabilized the EPSP-spike (E-S) component of LTP in the dentate gyrus (DG), with no effect on basal transmission or short-term plasticity. This increase in E-S potentiation duration could result from the combination of an increase in excitability of DG granular cells with a reduction of GABAergic inhibition, leading to a strong reduction of input specificity. Radioactive in situ hybridization (ISH) was used to evaluate the amounts of Kv4.2 and Kv4.3 mRNA in brain structures at different stages of a spatial learning task in naive, pseudoconditioned, and conditioned rats. Significant differences in Kv4.2 and Kv4.3 mRNA levels were observed between conditioned and pseudoconditioned rats. Kv4.2 and Kv4.3 mRNA levels were transiently up-regulated in the striatum, nucleus accumbens, retrosplenial, and cingulate cortices during early stages of learning, suggesting an involvement in the switch from egocentric to allocentric strategies. Spatial learning performance was positively correlated with the levels of Kv4.2 and Kv4.3 mRNAs in several of these brain structures. Altogether our findings suggest that Kv4 channels could increase the signal-to-noise ratio during information acquisition, thereby allowing a better encoding of the memory trace.

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“…This rapid and short-lasting reduction of I A via an inactivation curve shift during the initial period of potentiation can induce an initial and signifi cant enhancement of excitability throughout the neuron. In fact, activity-dependent changes in somatic I A channels are not unique because various conditioning stimuli for synaptic plasticity actively influence the expression and kinetic properties of several ion channels [1,53,[57][58][59][60] . Furthermore, it is possible that the I A -mediated enhancement of somatic excitability directly affects the properties and/or expression of other voltage-dependent ion channels, and thus modifi es membrane conductance and cellular signaling cascades (for review see Reyes 2001 [61] ).…”

Section: Modifi Cationsmentioning

confidence: 99%

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

et al. 2014

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In the mammalian brain, information encoding and storage have been explained by revealing the cellular and molecular mechanisms of synaptic plasticity at various levels in the central nervous system, including the hippocampus and the cerebral cortices. The modulatory mechanisms of synaptic excitability that are correlated with neuronal tasks are fundamental factors for synaptic plasticity, and they are dependent on intracellular Ca 2+ -mediated signaling. In the present review, the A-type K + (I A ) channel, one of the voltage-dependent cation channels, is considered as a key player in the modulation of Ca 2+ infl ux through synaptic NMDA receptors and their correlated signaling pathways. The cellular functions of I A channels indicate that they possibly play as integral parts of synaptic and somatic complexes, completing the initiation and stabilization of memory.

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Associative EPSP‐‐spike potentiation induced by pairing orthodromic and antidromic stimulation in rat hippocampal slices.

Cited by 66 publications

References 34 publications

Timing and Balance of Inhibition Enhance the Effect of Long-Term Potentiation on Cell Firing

Timing and Balance of Inhibition Enhance the Effect of Long-Term Potentiation on Cell Firing

Kv4 potassium channels modulate hippocampal EPSP-spike potentiation and spatial memory in rats

Roles of somatic A-type K+ channels in the synaptic plasticity of hippocampal neurons

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