Kainate receptor-mediated heterosynaptic facilitation in the amygdala

Li, He; Chen, Aiqin; Xing, Guoqiang; Wei, Mei Ling; Rogawski, Michael A.

doi:10.1038/88432

Cited by 103 publications

(117 citation statements)

References 45 publications

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“…fEPSPs baseline was recorded for 10 minutes and ATPA was applied for 15 minutes. During the 15 minute ATPA application, the amplitude and slope of fEPSPs decreased below baseline, similar to that seen in other laboratories (Li et al, 2001). fEPSP amplitude and slope rapidly (in <5 min) returned to baseline levels after removing ATPA from the slice.…”

Section: Acute Ethanol and Ubp 296 Block Atpa Induced Synaptic Plastisupporting

confidence: 87%

“…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%

“…The GluR5 agonist ATPA has been used to stimulate increases in synaptic facilitation and this has been suggested to take place through recruitment of additional excitatory synapses (Li et al, 2001). To examine the neurophysiological ramifications of acute ethanol inhibition of KA-Rmediated synaptic transmission, we used fEPSPs to examine increases in synaptic strength induced by the kainate receptor agonist ATPA.…”

Section: Acute Ethanol and Ubp 296 Block Atpa Induced Synaptic Plastimentioning

confidence: 99%

“…Using fEPSPs, we wanted to examine neurophysiological endpoints related to KA-R activation in the BLA. Recently, the KA-R agonist ATPA was shown to increase synaptic strength in BLA principal neurons, potentially through recruitment of excitatory synapses (Li et al, 2001). Further, in the CA1 region of the hippocampus, long term ATPA application led to an enduring increase in the number of glutamatergic synapses in that region (Vesikansa et al, 2007).…”

Section: Atpa-induced Synaptic Plasticity Is Inhibited By Acute Ethanolmentioning

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 and Ubp 296 Block Atpa Induced Synaptic Plastisupporting

confidence: 87%

Section: Acute Ethanol Dose Dependently Decreased Ka Mediated Epscsmentioning

confidence: 78%

Section: Acute Ethanol and Ubp 296 Block Atpa Induced Synaptic Plastimentioning

confidence: 99%

Section: Atpa-induced Synaptic Plasticity Is Inhibited By Acute Ethanolmentioning

confidence: 99%

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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Ionotropic Glutamate Receptors

Bleakman

Alt

Lodge

et al. 2007

Handbook of Contemporary Neuropharmacology

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Since their discovery in the 1950s, ionotropic glutamate receptors represent a class of receptor proteins that mediate fast excitatory transmission in the central nervous system. In this chapter, we describe the extensive studies of agents that act at the various subtypes of ionotropic glutamate receptor and how these agents have been used to delineate the physiological and pathophysiological roles of these receptors.

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Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure‐Like Activities

Li,

Shi,

Zhao

et al. 2024

Advanced Science

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The corticostriatal connection plays a crucial role in cognitive, emotional, and motor control. However, the specific roles and synaptic transmissions of corticostriatal connection are less studied, especially the corticostriatal transmission from the anterior cingulate cortex (ACC). Here, a direct glutamatergic excitatory synaptic transmission in the corticostriatal projection from the ACC is found. Kainate receptors (KAR)‐mediated synaptic transmission is increased in this corticostriatal connection both in vitro and in vivo seizure‐like activities. GluK1 containing KARs and downstream calcium‐stimulated adenylyl cyclase subtype 1 (AC1) are involved in the upregulation of KARs following seizure‐like activities. Inhibiting the activities of ACC or its corticostriatal connection significantly attenuated pentylenetetrazole (PTZ)‐induced seizure. Additionally, injection of GluK1 receptor antagonist UBP310 or the AC1 inhibitor NB001 both show antiepileptic effects. The studies provide direct evidence that KARs are involved in seizure activity in the corticostriatal connection and the KAR‐AC1 signaling pathway is a potential novel antiepileptic strategy.

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Kainate receptor-mediated heterosynaptic facilitation in the amygdala

Cited by 103 publications

References 45 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

Ionotropic Glutamate Receptors

Increased GluK1 Subunit Receptors in Corticostriatal Projection from the Anterior Cingulate Cortex Contributed to Seizure‐Like Activities

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