Differential contribution of kainate receptors to excitatory postsynaptic currents in superficial layer neurons of the rat medial entorhinal cortex

West, Peter J.; Dalpé-Charron, Alexandre; Wilcox, Karen S.

doi:10.1016/j.neuroscience.2007.02.035

Cited by 22 publications

(22 citation statements)

References 69 publications

(120 reference statements)

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“…However, we varied the stimulation sites in our experiments but this made little difference, and we were generally unable to increase the incidence of observation of KAr-eEPSCs, or to elicit significant responses to single shock stimulation. These results are in agreement with those of West et al (2007). However, Beed et al (2009) suggested that KAr were largely sub-synaptic in Layer III, and that their activation was pathway specific, with an absence of response after stimulating in Layer I, but consistent responses observed when the stimulation electrode was moved to Layer II/III.…”

Section: Postsynaptic Gluk2 Receptors At Glutamate Synapsessupporting

confidence: 88%

“…We confirmed that KAr contribute a kinetically slow component to eEPSCs in Layer III of the EC (West et al, 2007;Beed et al, 2009). The lack of effect of ATPA on holding current and of UBP302 on sEPSCs or KAr-mediated eEPSCs in our studies suggest that GluK1-(or GluK3) containing receptors are not present postsynaptically, or are not accessed by synaptically released glutamate.…”

Section: Postsynaptic Gluk2 Receptors At Glutamate Synapsessupporting

confidence: 82%

“…Postsynaptic responses mediated by KAr in Layer III have been described (West et al, 2007;Beed et al, 2009). We confirmed the postsynaptic role of KAr and attempted to determine the subtype of receptor involved.…”

Section: Postsynaptic Kar At Glutamate Synapsesmentioning

confidence: 52%

“…Presynaptic KAr exist at excitatory (Agrawal and Evans, 1986;Frerking et al, 2001;Schmitz et al, 2001a) and inhibitory (Rodriguez-Moreno et al, 1997;Cossart et al, 2001) synapses where they act to increase or decrease transmitter release, or both, depending on factors including concentration of agonist, (Jiang et al, 2001;Schmitz et al, 2001a,b;Braga et al, 2003), synapse type (Cossart et al, 2001), the source of released glutamate (Contractor et al, 2003), and whether modulatory GPCRs are concurrently activated (Lourenco et al, 2010). Postsynaptic KAr, initially found at hippocampal mossy fibre synapses (Castillo et al, 1997;Vignes and Collingridge, 1997), have now been shown to participate in excitatory transmission at numerous sites (Kidd and Isaac, 1999;Ali, 2003;Pinheiro and Mulle, 2006) including the EC (West et al, 2007;Beed et al, 2009). …”

Section: Introductionmentioning

confidence: 99%

“…West et al (2007) demonstrated slow, KAr-mediated excitatory postsynaptic currents (EPSCs) at excitatory synapses on principal neurones of Layers II and III in the rat EC, although they were more prominent in Layer III. Beed et al (2009) confirmed this and provided evidence that postsynaptic KAr EPSCs were largely mediated by GluK2-containing receptors.…”

Section: Introductionmentioning

confidence: 99%

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Pre‐ and post‐synaptic functions of kainate receptors at glutamate and GABA synapses in the rat entorhinal cortex

Jane

Jones

2011

Hippocampus

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Oscillatory network activity in cortical areas is seen as vital to physiological processes of cognition, learning, and memory, and fundamental to disorders such as epilepsy. Increasing attention is being paid to the role of kainate receptors (KAr) in the generation of network oscillations and synchrony. The entorhinal cortex (EC) plays a key role in learning and memory, and is a major site of dysfunction in temporal lobe epilepsy. KAr have been implicated in oscillogenesis in the EC, but limited information is available concerning the physiological roles of KAr in synaptic transmission in this area. Here, we make a detailed analysis of KAr function in Layer III of the EC, a site known to be highly susceptible to oscillogenesis, using whole-cell patch clamp recording of evoked and spontaneous synaptic currents in rat brain slices. We demonstrate that KAr containing the GluK1-subunit act as facilitatory autoreceptors at glutamatergic synapses on pyramidal neurones in Layer III. In addition, GluK1-containing KAr mediate an excitatory drive at glutamatergic synapses on GABAergic interneurones. In contrast, a different KAr, which is likely to contain the GluK2-subunit mediates a slow postsynaptic excitation at glutamatergic synapses on principal neurones, and may also act as a heteroreceptor, facilitating GABA release at inhibitory terminals on principal neurones. Reducing [Mg(2+) ](o) , which we have previously shown can generate KAr-dependent slow network oscillations in Layer III, enhances both glutamate and GABA release. Both effects are partly sustained by increased activation of GluK1-containing KAr. Increased activation of the GluK1-containing autoreceptor also results in an enhancement of the postsynaptic response mediated by GluK2-containing receptors. Finally, spontaneous release of both transmitters shows a rhythmic periodicity in low-Mg, and, again, this is dependent on GluK1-containing KAr. The results show that KAr contribute a facilitatory function at multiple levels in the networks of the EC, and provide a basis for dissecting the role of these receptors in oscillogenesis in this area.

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Section: Postsynaptic Gluk2 Receptors At Glutamate Synapsessupporting

confidence: 88%

Section: Postsynaptic Gluk2 Receptors At Glutamate Synapsessupporting

confidence: 82%

Section: Postsynaptic Kar At Glutamate Synapsesmentioning

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Pre‐ and post‐synaptic functions of kainate receptors at glutamate and GABA synapses in the rat entorhinal cortex

Jane

Jones

2011

Hippocampus

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Phase precession and variable spatial scaling in a periodic attractor map model of medial entorhinal grid cells with realistic after‐spike dynamics

et al. 2011

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We present a model that describes the generation of the spatial (grid fields) and temporal (phase precession) properties of medial entorhinal cortical (MEC) neurons by combining network and intrinsic cellular properties. The model incorporates network architecture derived from earlier attractor map models, and is implemented in 1D for simplicity. Periodic driving of conjunctive (position × head-direction) layer-III MEC cells at theta frequency with intensity proportional to the rat's speed, moves an 'activity bump' forward in network space at a corresponding speed. The addition of prolonged excitatory currents and simple after-spike dynamics resembling those observed in MEC stellate cells (for which new data are presented) accounts for both phase precession and the change in scale of grid fields along the dorso-ventral axis of MEC. Phase precession in the model depends on both synaptic connectivity and intrinsic currents, each of which drive neural spiking either during entry into, or during exit out of a grid field. Thus, the model predicts that the slope of phase precession changes between entry into and exit out of the field. The model also exhibits independent variation in grid spatial period and grid field size, which suggests possible experimental tests of the model.

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Chronic ethanol and withdrawal effects on kainate receptor–mediated excitatory neurotransmission in the rat basolateral amygdala

Läck

Christian

Diaz

et al. 2009

Alcohol

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Withdrawal anxiety is a significant factor contributing to continued alcohol abuse in alcoholics. This anxiety is extensive, long-lasting, and develops well after the obvious physical symptoms of acute withdrawal. The neurobiological mechanisms underlying this prolonged withdrawal-induced anxiety are not well understood. The basolateral amygdala is a major emotional center in the brain and regulates the expression of anxiety. New evidence suggests that increased glutamatergic function in the basolateral amygdala may contribute to withdrawal-related anxiety following chronic ethanol exposure. Recent evidence also suggests that kainate-type ionotropic glutamate receptors are inhibited by intoxicating concentrations of acute ethanol. This acute sensitivity suggests potential contributions by these receptors to the increased glutamatergic function seen during chronic exposure. Therefore we examined the effect of chronic intermittent ethanol (CIE) and withdrawal (WD) on kainate receptor (KAR) mediated synaptic transmission in the basolateral amygdala (BLA) of Sprague Dawley rats. Our study showed that CIE, but not withdrawal, increased synaptic responses mediated by KARs. Interestingly, both CIE and WD occluded KAR-mediated synaptic plasticity. Finally, we found that BLA fEPSP responses were increased during CIE and WD via a mechanism that is independent from glutamate release from presynaptic terminals. Taken together, these data suggest that KARs might also contribute to postsynaptic increases in glutamatergic synaptic transmission during CIE and that the mechanisms responsible for the expression of KAR-dependent synaptic plasticity might be engaged by chronic ethanol exposure and withdrawal.

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Differential contribution of kainate receptors to excitatory postsynaptic currents in superficial layer neurons of the rat medial entorhinal cortex

Cited by 22 publications

References 69 publications

Pre‐ and post‐synaptic functions of kainate receptors at glutamate and GABA synapses in the rat entorhinal cortex

Pre‐ and post‐synaptic functions of kainate receptors at glutamate and GABA synapses in the rat entorhinal cortex

Phase precession and variable spatial scaling in a periodic attractor map model of medial entorhinal grid cells with realistic after‐spike dynamics

Chronic ethanol and withdrawal effects on kainate receptor–mediated excitatory neurotransmission in the rat basolateral amygdala

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