GluR5 kainate receptor mediated synaptic transmission in rat basolateral amygdala in vitro

He, Luping; Rogawski, Michael A.

doi:10.1016/s0028-3908(98)00109-9

Cited by 91 publications

(73 citation statements)

References 26 publications

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“…First, our results confirm previous findings (Li and Rogawski, 1998) that stimulation of the external capsule evokes synaptic responses mediated by KA-Rs in BLA neurons. These responses were specifically inhibited by the kainate receptor-selective antagonist UBP 296.…”

Section: Acute Ethanol Inhibits Ka Epscs Via a Postsynaptic Mechanismsupporting

confidence: 91%

“…Previous studies have reported that KA EPSCs can be recorded by stimulation of the external capsule and the amplitude of these responses can be markedly enhanced by using short stimulus trains (Li et al, 2001;Li and Rogawski, 1998). Therefore, in our first experiments, KA EPSCs were evoked in BLA neurons by stimulus trains delivered to the external capsule (Fig.…”

Section: Acute Ethanol Dose Dependently Decreased Ka Mediated Epscsmentioning

confidence: 78%

“…KA-Rs consist of five possible subunits, GLUR 5-7 , needed for functional channels, and KA 1-2 (Braga et al, 2004). Receptors containing GLUR 5,6 and KA 2 have been shown to be highly expressed in the BLA and contribute postsynaptically to glutamatergic excitatory postsynaptic potentials (EPSPs) (Li and Rogawski, 1998). KA-Rs expressed in neuronal cultures (Valenzuela et al, 1998;Valenzuela and Cardoso, 1999) and in the rat hippocampus (Weiner et al, 1999) are inhibited by acute ethanol exposure.…”

Section: Acute Ethanol Inhibits Ka Epscs Via a Postsynaptic Mechanismmentioning

confidence: 99%

“…While the physiological role of AMPA and NMDA receptors in the amygdala with respect to alcohol have been fairly well characterized, the role of KA-Rs in mediating the effects of ethanol has only begun to emerge with the development of pharmacological tools that have allowed the separation of AMPA-and KA-receptor mediated responses (reviewed in (Pinheiro and Mulle, 2006). For example, KA-Rs contribute to postsynaptic glutamatergic excitatory responses in the BLA (Li and Rogawski, 1998) and also mediate a form of long-lasting heterosynaptic facilitation in this brain region (Li et al, 2001). We have previously demonstrated that KA-Rs in the rat hippocampus are potently inhibited by acute ethanol (Carta et al, 2003;Weiner et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

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Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

et al. 2008

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The neurobiological mechanisms governing alcohol-induced alterations in anxiety-like behaviors are not fully understood. Given that the amygdala is a major emotional center in the brain and regulates the expression of both learned-fear and anxiety, neurotransmitter systems within the basolateral amygdala represent likely mechanisms governing the anxiety-related effects of acute ethanol exposure. It is well established that, within the glutamatergic system, N-methyl-D-aspartate (NMDA)-type receptors, are particularly sensitive to intoxicating concentrations of ethanol. However, recent evidence suggests that kainate-type glutamate receptors are sensitive to ethanol as well. Therefore, we examined the effect of acute ethanol on kainate receptor (KA-R)-mediated synaptic transmission in the basolateral amygdala (BLA) of Sprague Dawley rats. Acute ethanol decreased KA-R-mediated excitatory postsynaptic currents (EPSCs) in the BLA in a concentrationdependent manner. Ethanol also inhibited currents evoked by focal application of the kainate receptor agonist (R, S)-2-amino-3-(3-hydroxy-5-tert-butylisoxazol-4-yl) propanoic acid (ATPA), and ethanol inhibition of kainate EPSCs was not associated with a change in paired-pulse ratio, suggesting a postsynaptic mechanism of ethanol action. The neurophysiological consequences of this acute sensitivity were tested by measuring ethanol's effects on KA-R-dependent modulation of synaptic plasticity. Acute ethanol, like the GluR5-specific antagonist (RS)-3-(2-carboxybenzyl)willardiine (UBP 296), robustly diminished ATPA-induced increases in synaptic efficacy. Lastly, to better understand the relationship between KA-R activity and anxiety-like behavior, we bilaterally microinjected ATPA directly into the BLA. We observed an increase in measures of anxiety-like behavior, assessed in the light/dark box, with no change in locomotor activity. This evidence suggests that kainate receptors in the BLA are inhibited by pharmacologically relevant concentrations of ethanol and may contribute to some of the acute anxiolytic effects of this drug.

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Section: Acute Ethanol Inhibits Ka Epscs Via a Postsynaptic Mechanismsupporting

confidence: 91%

Section: Acute Ethanol Dose Dependently Decreased Ka Mediated Epscsmentioning

confidence: 78%

Section: Acute Ethanol Inhibits Ka Epscs Via a Postsynaptic Mechanismmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

et al. 2008

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“…Postsynaptic KARs are found in the hippocampus (Castillo et al, 1997;Vignes and Collingridge, 1997;Cossart et al, 1998;Frerking et al, 1998), cortex Isaac, 1999, 2001), cerebellum (Bureau et al, 2000), amygdala (Li and Rogawski, 1998), spinal cord (Li et al, 1999), and retina (DeVries and Schwartz, 1999;DeVries, 2000), and, like AMPARs, KARs are activated by glutamate release under normal conditions. At most of these synapses the EPSC mediated by KARs has a much smaller amplitude than that of AMPARs and much slower kinetics.…”

mentioning

confidence: 99%

AMPA Receptors and Kainate Receptors Encode Different Features of Afferent Activity

Frerking

Ohliger-Frerking

2002

J. Neurosci.

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Postsynaptic kainate receptors (KARs) have been found in the CNS along with AMPA receptors (AMPARs), but because KARmediated EPSCs are much smaller and slower than AMPARmediated EPSCs, it remains unclear whether these postsynaptic KARs are functionally significant. In this study we measured KAR-and AMPAR-mediated EPSPs in hippocampal interneurons, and then we used these EPSPs in a model to examine the effects of afferent firing on each receptor. In this model the KARs generated a large tonic depolarization when activated by a small population of afferent fibers firing asynchronously at physiologically relevant firing rates (1-5 Hz). At 3-5 Hz this tonic depolarization exceeded the peak depolarization mediated by AMPARs in response to the same afferent activity. We also found that, unlike AMPARs, KARs did not generate large oscillations in membrane potential during theta rhythms. When simulated EPSCs were injected into interneurons to mimic afferents firing at 5 Hz, we found that currents simulating KARs elicited more spiking than currents simulating AMPARs. We also found that simulated AMPARs, but not KARs, could transmit presynaptic theta rhythms into postsynaptic spiking at the theta rhythm. Our results suggest that synaptically activated KARs have a strong influence on membrane potential and that AMPARs and KARs differ in their ability to encode temporal information.

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Synaptic drive at developing synapses: Transient upregulation of kainate receptors

Zundert¹,

Zhao

Constantine‐Paton

2010

Developmental Neurobiology

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At the onset of a period of intense synaptic refinement initiated by synchronized eye-opening (EO), rapid changes in post-synaptic NMDA receptor and AMPA receptor currents (NMDARcs, AMPARcs) occur within the superficial visual layers of the rodent superior colliculus (sSC; Lu and Constantine-Paton, 2004). Subsequently, evoked non-NMDARc amplitudes increase, but by 2 weeks after EO (AEO) they decrease significantly. Here, using whole-cell patch-clamp recording, we demonstrate that small, slowly desensitizing excitatory kainate receptor currents (KARcs) are responsible for the rise and subsequent fall in non-NMDARcs. The increase in KAR transmission parallels inhibitory GABAA responses that plateau at 7 days AEO. By 2 weeks AEO, KARcs are gone. AMPARcs remain unchanged during the appearance and disappearance of the KARcs, despite increases in sSC neuropil activity and continued refinement of inputs to individual sSC neurons. We suggest that in the interval of heightened activity, before SC inhibition matures, many AMPARcs desensitize and are relatively ineffective at relieving the Mg2+ block on NMDARs. This transient appearance of slowly desensitizing, long-duration KARcs may provide increased membrane depolarization necessary for NMDAR function and continuation of synaptic refinement.

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GluR5 kainate receptor mediated synaptic transmission in rat basolateral amygdala in vitro

Cited by 91 publications

References 26 publications

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

Ethanol inhibition of kainate receptor-mediated excitatory neurotransmission in the rat basolateral nucleus of the amygdala

AMPA Receptors and Kainate Receptors Encode Different Features of Afferent Activity

Synaptic drive at developing synapses: Transient upregulation of kainate receptors

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