Kainate Acts at Presynaptic Receptors to Increase GABA Release From Hypothalamic Neurons

Liu, Qingsong; Patrylo, Peter R.; Gao, Xiao‐Bing; Pol, Anthony N. van den

doi:10.1152/jn.1999.82.2.1059

Cited by 44 publications

(26 citation statements)

References 26 publications

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“…However, the use of novel benzodiazepine compounds (GYKI compounds), which act as selective antagonists of AMPA receptors (Paternain et al, 1995), has provided a means of demonstrating a distinct role of KARs in modulating synaptic transmission. Interestingly, several in vitro electrophysiological and pharmacological studies have shown that KARS mediate presynaptic effects on GABAergic and glutamatergic neurotransmission in various brain regions (Clarke et al, 1997;Lerma et al, 1997;Rodriguez-Moreno et al, 1997;Mulle et al, 1998;Rodriguez-Moreno and Lerma, 1998;Chittajallu et al, 1999;Liu et al, 1999;Min et al, 1999;Perkinton and Sihra, 1999;Chergui et al, 2000;Contractor et al, 2000;Frerking and Nicoll, 2000;Kamiya and Ozawa, 2000). Furthermore, the excitotoxic effects of KAR agonists were found to be greatly reduced in the CA3 region of the rat hippocampus after mossy fiber denervation (Debonnel et al, 1989).…”

Section: Abstract: Huntington's Disease; Excitotoxicity; Presynapticmentioning

confidence: 99%

“…Interestingly, recent evidence indicates that activation of GluR6-containing presynaptic kainate receptors facilitates glutamate exocytosis from cerebral cortex nerve terminals in a synaptosome preparation (Perkinton and Sihra, 1999). Similarly, kainate acts at presynaptic receptors to increase GABA release from hypothalamic neurons (Liu et al, 1999). However, kainate was found to downregulate GABAergic transmission in the rat hippocampus (Rodriguez-Moreno et al, 1997).…”

Section: Potential Functions Of Presynaptic Striatal Kainate Receptorsmentioning

confidence: 99%

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Subcellular and Subsynaptic Localization of Presynaptic and Postsynaptic Kainate Receptor Subunits in the Monkey Striatum

et al. 2001

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The localization and functions of kainate receptors (KARs) in the CNS are still poorly known. In the striatum, GluR6/7 and KA2 immunoreactivity is expressed presynaptically in a subpopulation of glutamatergic terminals and postsynaptically in dendrites and spines. The goal of this study was to further characterize the subcellular and subsynaptic localization of kainate receptor subunits in the monkey striatum. Immunoperoxidase data reveal that the relative abundance of GluR6/7-and KA2-immunoreactive terminals is homogeneous throughout the striatum irrespective of the differential degree of striatal degeneration in Huntington's disease. Pre-embedding and post-embedding immunogold data indicate that Ͼ70% of the presynaptic or postsynaptic GluR6/7 and KA2 labeling is expressed intracellularly. In material stained with the post-embedding immunogold method, approximately one-third of plasma membrane-bound gold particles labeling in axon terminals and spines is associated with asymmetric synapses, thereby representing synaptic kainate receptor subunits. On the other hand, Ͼ60% of the plasmamembrane bound labeling is extrasynaptic. Both GluR6/7 and KA2 labeling in glutamatergic terminals often occurs in clusters of gold particles along the membrane of large vesicular organelles located at various distances from the presynaptic grid. Anterograde labeling from the primary motor cortex or the centromedian thalamic nucleus indicate that both corticostriatal and thalamostriatal terminals express presynaptic GluR6/7 and KA2 immunoreactivity in the postcommissural putamen. In conclusion, these data demonstrate that kainate receptors in the striatum display a pattern of subcellular distribution different from other ionotropic glutamate receptor subtypes, but consistent with their metabotropic-like functions recently shown in the hippocampus.

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Section: Abstract: Huntington's Disease; Excitotoxicity; Presynapticmentioning

confidence: 99%

Section: Potential Functions Of Presynaptic Striatal Kainate Receptorsmentioning

confidence: 99%

Subcellular and Subsynaptic Localization of Presynaptic and Postsynaptic Kainate Receptor Subunits in the Monkey Striatum

et al. 2001

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“…In the present study, 20-100 jiM DOI induced only an enhancement of evoked NMDA receptor-mediated field 62 A. Chen et al / Neuroscience 119 (2003) [53][54][55][56][57][58][59][60][61][62][63] and intracellular recorded potentials in tlie amygdala. This effect was blocked both by the 5-HT2 antagonist ketanserin and by the S-HTzc receptor selective antagonist RSI02221.…”

Section: Enhancement Of Nmda-receptor Functions By Doimentioning

confidence: 50%

“…The biphasic effect of DOB was interpreted as an activation of protein kinase C (PKC) at low DOB concentration and calmodulin kinase 11 at high DOB concentration (Arvanov et al, 1999). Rahman and Neuman interpreted the same phenomenon as desensitization, but had to invoke more than one mechanism to explain its biphasic nature (Rahman and Neuman, 1993).In the present study, 20-100 jiM DOI induced only an enhancement of evoked NMDA receptor-mediated field 62 A. Chen et al / Neuroscience 119 (2003) [53][54][55][56][57][58][59][60][61][62][63] and intracellular recorded potentials in tlie amygdala. This effect was blocked both by the 5-HT2 antagonist ketanserin and by the S-HTzc receptor selective antagonist RSI02221.…”

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confidence: 65%

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Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala

Li¹,

Braga²,

Hough³

et al. 2005

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Public reporting burden for Ihis collection of information is estinnaled lo average 1 hour per response, including the time for reviewing inslojclions, searching existing data sources, gathering and malnlaining the data needed, and completing and reviewing this collection of Information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302 and to the Office of Management and Budget,. Washington, DC 20503 AGENCY USE ONLY (Leave blank) REPORT DATEMarch 2 004 REPORT TYPE AND DATES COVEREDAnnual (1 Feb 2003 -1 Feb 2004 TITLE AND SUBTITLE Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala AUTHOR(S)He Li, M.D., Ph.D. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Henry SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited ABSTRACT (Maximum 200 Words) 12b. DISTRIBUTION CODEPosttraumatic stress disorder (PTSD) is a syndrome of symptoms indicative of emotional dysfunction, which develop after exposure to life-threatening events. Prevalent symptoms are fear and anxiety, which become particularly intense during exposure to situations reminiscent of the traumatic events that precipitated the disease. The amygdala is a key component of the brain's neuronal network that determines the emotional significance of external events. Despite the central role of the amygdala in emotional behavior, little is known about the impact of stress on the amygdala's function. Clinical evidence indicates that norepinephrine and serotonin may participate in the synaptic plasticity phenomena that result in the memory of frightening events in PTSD. Our data indicate that the modulatory effects of norepinephrine and serotonin receptors on synaptic transmission, neuroplasticity and calcium homeostasis are altered in traumatically stressed rat amygdala. The results of this study may aid in the development of new strategies aimed at modifying and preventing the formation of traumatic memory, and thus could be useful for the treatment of combat PTSD in veterans. SUBJECT TERMS ~~~~Amygdala, post-traumatic stress disorder, serotonin, norepinephrine, calium signaling, adrenergic receptor, LTP, stress Conclusions 34References 35 Appendices 38 IntroductionIntense or chronic stress can have long-lasting consequences in an individual's health, and can be the cause of debiHtating mental ilhiesses. A very common mental ilhiess induced by traumatic stress is posttraumatic stress disorder (PTSD). PTSD is a syndrome of symptoms indicative of emotional dysfunction, which develop after exposure to life-threatening events, or very stressfiil situations of different nature. Prevalent symptoms are fear and anxiety, which become particularly intense during exposure to...

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Metabotropic signaling by kainate receptors

Rodrigues

Lerma

2012

WIREs Membr Transp Signal

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Kainate receptors (KARs) are members of the ionotropic glutamate receptor family. Despite their ubiquitous presence in the central nervous system, and in contrast to the better characterized N-methyl-D-aspartates (NMDARs) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs), the contribution of KARs to synaptic transmission has only been demonstrated in a few central synapses. However, there is now accumulating evidence that KARs are present on both sides of the synapse, where they play distinct and diverse roles. In addition to their contribution to synaptic transmission, KARs can regulate synaptic activity and plasticity either by presynaptically modulating neurotransmitter release at GABAergic and glutamatergic synapses, or by postsynaptically regulating neuronal excitability. This prominent neuromodulatory role of KARs has been further highlighted by the finding that these glutamate-gated ion-channels can also signal through G-proteins and other second messengers. This noncanonical metabotropic signaling of KARs was firmly established by demonstrating it to be independent of ion flux. The discovery of this dual signaling capacity of KARs constituted a breakthrough in understanding how they function and since then, an increasing number of metabotropic actions of KARs have been reported. It is now clear that this dual signaling underlies the diverse functions of KARs and defining this metabotropic component of the signaling system operated by KARs will be necessary to understand the physiological contributions of glutamate receptors.

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Kainate Acts at Presynaptic Receptors to Increase GABA Release From Hypothalamic Neurons

Cited by 44 publications

References 26 publications

Subcellular and Subsynaptic Localization of Presynaptic and Postsynaptic Kainate Receptor Subunits in the Monkey Striatum

Subcellular and Subsynaptic Localization of Presynaptic and Postsynaptic Kainate Receptor Subunits in the Monkey Striatum

Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala

Metabotropic signaling by kainate receptors

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