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1.
Epilepsy Res ; 204: 107384, 2024 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-38879905

RESUMEN

At least 3 months after systemic treatment with pilocarpine to induce status epilepticus, Long-Evans and Sprague-Dawley rats were video-EEG monitored for seizures continuously for 1 month. Rats were then perfused, hippocampi were processed for Nissl staining, and hilar neurons were quantified. Seizure frequency in Long-Evans rats was 1/10th of that in Sprague-Dawley rats, and more variable. Hilar neuron loss was also less severe in Long-Evans rats. However, there was no correlation between hilar neuron loss and seizure frequency in either strain. The low and variable seizure frequency suggests limited usefulness of pilocarpine-treated Long-Evans rats for some epilepsy experiments.


Asunto(s)
Electroencefalografía , Neuronas , Pilocarpina , Ratas Long-Evans , Ratas Sprague-Dawley , Convulsiones , Animales , Pilocarpina/toxicidad , Ratas , Convulsiones/inducido químicamente , Convulsiones/tratamiento farmacológico , Convulsiones/fisiopatología , Neuronas/efectos de los fármacos , Neuronas/patología , Masculino , Especificidad de la Especie , Hipocampo/efectos de los fármacos , Hipocampo/patología , Modelos Animales de Enfermedad , Estado Epiléptico/inducido químicamente , Estado Epiléptico/patología , Estado Epiléptico/tratamiento farmacológico
2.
J Neurosci ; 2022 Aug 19.
Artículo en Inglés | MEDLINE | ID: mdl-35995562

RESUMEN

Temporal lobe epilepsy is common, but mechanisms of seizure initiation are unclear. We evaluated seizure initiation in female and male rats that had been systemically treated with pilocarpine, a widely used model of temporal lobe epilepsy. Local field potential recordings from many brain regions revealed variable sites of earliest recorded seizure activity, but mostly the ventral hippocampal formation. To test whether inactivation of the ventral hippocampal formation would reduce seizures, mini-osmotic pumps were used to continually and focally deliver tetrodotoxin. High doses of tetrodotoxin infused unilaterally into the ventral hippocampal formation blocked seizures reversibly but also reduced local field potential amplitudes in remote brain regions, indicating distant effects. A lower dose did not reduce local field potential amplitudes in remote brain regions but did not reduce seizures when infused unilaterally. Instead, seizures tended to initiate in the contralateral ventral hippocampal formation. Bilateral infusion of the lower dose into the ventral hippocampal formation reduced seizure frequency 85%. Similar bilateral treatment in the amygdala was not effective. Bilateral infusion of the dorsal hippocampus reduced seizure frequency, but only 17%. Together, these findings reveal that the ventral hippocampal formation is a primary bilaterally independent epileptogenic zone, and the dorsal hippocampus is a secondary epileptogenic zone in pilocarpine-treated rats. This is consistent with many human patients, and the results further validate the local field potential method for identifying seizure onset zones. Finally, the findings are more consistent with a focal mechanism of ictogenesis rather than one involving a network of interdependent nodes.SIGNIFICANCE STATEMENT:To better understand how seizures start, investigators need to know where seizures start in the animal models they study. In the widely used pilocarpine-treated rat model of temporal lobe epilepsy, earliest seizure activity was most frequently recorded in the ventral hippocampal formation. Confirming the primary role of the ventral hippocampal formation, seizure frequency was reduced most effectively when it was inactivated focally, bilaterally, and continually with infused tetrodotoxin. These findings suggest the ventral hippocampal formation is the primary site of seizure initiation in this animal model of temporal lobe epilepsy, consistent with findings in many human patients.

3.
Epilepsy Res ; 184: 106965, 2022 08.
Artículo en Inglés | MEDLINE | ID: mdl-35724601

RESUMEN

Pathology in the dentate gyrus, including sclerosis, is a hallmark of temporal lobe epilepsy, and reduced inhibition to dentate granule cells may contribute to epileptogenesis. The perisomatic-targeting axonal boutons of parvalbumin-expressing interneurons decrease in proportion with granule cells in temporal lobe epilepsy. In contrast, dendrite-targeting axonal boutons of somatostatin-expressing interneurons sprout exuberantly in temporal lobe epilepsy. A third major class of GABAergic interneurons expresses cannabinoid receptor type 1 (CB1) on their terminal boutons, but there is conflicting evidence as to whether these boutons are increased or decreased in temporal lobe epilepsy. Naturally occurring temporal lobe epilepsy in California sea lions, with unilateral or bilateral sclerosis, offers the benefit of neuroanatomy and neuropathology akin to humans, but with the advantage that the entirety of both hippocampi from control and epileptic brains can be studied. Stereological quantification in the dentate gyrus revealed that sclerotic hippocampi from epileptic sea lions had fewer CB1-labeled boutons than controls. However, the reduction in the number of granule cells was greater, resulting in increased CB1-labeled boutons per granule cell in sclerotic hippocampi at temporal levels. This suggests that although CB1-expressing boutons are decreased in sclerotic dentate gyri, surviving cells have enhanced innervation from these boutons in epileptic sea lions.


Asunto(s)
Epilepsia del Lóbulo Temporal , Epilepsia , Leones Marinos , Animales , Giro Dentado/patología , Epilepsia/patología , Epilepsia del Lóbulo Temporal/patología , Humanos , Interneuronas/fisiología , Receptores de Cannabinoides , Esclerosis/patología
4.
eNeuro ; 8(6)2021.
Artículo en Inglés | MEDLINE | ID: mdl-34819310

RESUMEN

Temporal lobe epilepsy remains a common disorder with no cure and inadequate treatments, potentially because of an incomplete understanding of how seizures start. CA1 pyramidal cells and many inhibitory interneurons increase their firing rate in the seconds-minutes before a spontaneous seizure in epileptic rats. However, some interneurons fail to do so, including those identified as putative interneurons with somata in oriens and axons targeting lacunosum-moleculare (OLM cells). Somatostatin-containing cells, including OLM cells, are the primary target of inhibitory vasoactive intestinal polypeptide and calretinin-expressing (VIP/CR) bipolar interneuron-selective interneurons, type 3 (ISI-3). The objective of this study was to test the hypothesis that in epilepsy inhibition of OLM cells by ISI-3 is abnormally increased, potentially explaining the failure of OLM recruitment when needed most during the ramp up of activity preceding a seizure. Stereological quantification of VIP/CR cells in a model of temporal lobe epilepsy demonstrated that they survive in epileptic mice, despite a reduction in their somatostatin-expressing (Som) cell targets. Paired recordings of unitary IPSCs (uIPSCs) from ISI-3 to OLM cells did not show increased connection probability or increased connection strength, and failure rate was unchanged. When miniature postsynaptic currents in ISI-3 were compared, only mIPSC frequency was increased in epileptic hippocampi. Nevertheless, spontaneous and miniature postsynaptic potentials were unchanged in OLM cells of epileptic mice. These results are not consistent with the hypothesis of hyperinhibition from VIP/CR bipolar cells impeding recruitment of OLM cells in advance of a seizure.


Asunto(s)
Epilepsia del Lóbulo Temporal , Péptido Intestinal Vasoactivo , Animales , Hipocampo , Interneuronas , Ratones , Células Piramidales , Ratas
5.
Epilepsia ; 61(5): 856-867, 2020 05.
Artículo en Inglés | MEDLINE | ID: mdl-32242932

RESUMEN

OBJECTIVE: The present study tested whether ictal onset sites are regions of more severe interneuron loss in epileptic pilocarpine-treated rats, a model of human temporal lobe epilepsy. METHODS: Local field potential recordings were evaluated to identify ictal onset sites. Electrode sites were visualized in Nissl-stained sections. Adjacent sections were processed with proximity ligation in situ hybridization for glutamic acid decarboxylase 2 (Gad2). Gad2 neuron profile numbers at ictal onset sites were compared to contralateral regions. Other sections were processed with immunocytochemistry for reelin or nitric oxide synthase (NOS), which labeled major subtypes of granule cell layer-associated interneurons. Stereology was used to estimate numbers of reelin and NOS granule cell layer-associated interneurons per hippocampus. RESULTS: Ictal onset sites varied between and within rats but were mostly in the ventral hippocampus and were frequently bilateral. There was no conclusive evidence of more severe Gad2 neuron profile loss at sites of earliest seizure activity compared to contralateral regions. Numbers of granule cell layer-associated NOS neurons were reduced in the ventral hippocampus. SIGNIFICANCE: In epileptic pilocarpine-treated rats, ictal onset sites were mostly in the ventral hippocampus, where there was loss of granule cell layer-associated NOS interneurons. These findings suggest the hypothesis that loss of granule cell layer-associated NOS interneurons in the ventral hippocampus is a mechanism of temporal lobe epilepsy.


Asunto(s)
Epilepsia/inducido químicamente , Neuronas GABAérgicas/patología , Pilocarpina/farmacología , Animales , Encéfalo/patología , Encéfalo/fisiopatología , Modelos Animales de Enfermedad , Epilepsia/patología , Epilepsia/fisiopatología , Femenino , Glutamato Descarboxilasa/metabolismo , Hipocampo/patología , Hipocampo/fisiopatología , Hibridación in Situ , Masculino , Óxido Nítrico Sintasa/metabolismo , Ratas , Ratas Sprague-Dawley , Proteína Reelina , Convulsiones/inducido químicamente , Convulsiones/patología , Convulsiones/fisiopatología
6.
Neurotoxicology ; 66: 128-137, 2018 05.
Artículo en Inglés | MEDLINE | ID: mdl-29625197

RESUMEN

Harmful blooms of domoic acid (DA)-producing algae are a problem in oceans worldwide. DA is a potent glutamate receptor agonist that can cause status epilepticus and in survivors, temporal lobe epilepsy. In mice, one-time low-dose in utero exposure to DA was reported to cause hippocampal damage and epileptiform activity, leading to the hypothesis that unrecognized exposure to DA from contaminated seafood in pregnant women can damage the fetal hippocampus and initiate temporal lobe epileptogenesis. However, development of epilepsy (i.e., spontaneous recurrent seizures) has not been tested. In the present study, long-term seizure monitoring and histology was used to test for temporal lobe epilepsy following prenatal exposure to DA. In Experiment One, the previous study's in utero DA treatment protocol was replicated, including use of the CD-1 mouse strain. Afterward, mice were video-monitored for convulsive seizures from 2 to 6 months old. None of the CD-1 mice treated in utero with vehicle or DA was observed to experience spontaneous convulsive seizures. After seizure monitoring, mice were evaluated for pathological evidence of temporal lobe epilepsy. None of the mice treated in utero with DA displayed the hilar neuron loss that occurs in patients with temporal lobe epilepsy and in the mouse pilocarpine model of temporal lobe epilepsy. In Experiment Two, a higher dose of DA was administered to pregnant FVB mice. FVB mice were tested as a potentially more sensitive strain, because they have a lower seizure threshold, and some females spontaneously develop epilepsy. Female offspring were monitored with continuous video and telemetric bilateral hippocampal local field potential recording at 1-11 months old. A similar proportion of vehicle- and DA-treated female FVB mice spontaneously developed epilepsy, beginning in the fourth month of life. Average seizure frequency and duration were similar in both groups. Seizure frequency was lower than that of positive-control pilocarpine-treated mice, but seizure duration was similar. None of the mice treated in utero with vehicle or DA displayed hilar neuron loss or intense mossy fiber sprouting, a form of aberrant synaptic reorganization that develops in patients with temporal lobe epilepsy and in pilocarpine-treated mice. FVB mice that developed epilepsy (vehicle- and DA-treated) displayed mild mossy fiber sprouting. Results of this study suggest that a single subconvulsive dose of DA at mid-gestation does not cause temporal lobe epilepsy in mice.


Asunto(s)
Epilepsia del Lóbulo Temporal/inducido químicamente , Hipocampo/efectos de los fármacos , Ácido Kaínico/análogos & derivados , Toxinas Marinas/toxicidad , Efectos Tardíos de la Exposición Prenatal/inducido químicamente , Animales , Femenino , Edad Gestacional , Hipocampo/metabolismo , Hipocampo/fisiopatología , Ácido Kaínico/administración & dosificación , Ácido Kaínico/toxicidad , Toxinas Marinas/administración & dosificación , Ratones , Embarazo
7.
Cell Rep ; 20(9): 2156-2168, 2017 Aug 29.
Artículo en Inglés | MEDLINE | ID: mdl-28854365

RESUMEN

Although Netos are considered auxiliary subunits critical for kainate receptor (KAR) function, direct evidence for their regulation of native KARs is limited. Because Neto KAR regulation is GluK subunit/Neto isoform specific, such regulation must be determined in cell-type-specific contexts. We demonstrate Neto1/2 expression in somatostatin (SOM)-, cholecystokinin/cannabinoid receptor 1 (CCK/CB1)-, and parvalbumin (PV)-containing interneurons. KAR-mediated excitation of these interneurons is contingent upon Neto1 because kainate yields comparable effects in Neto2 knockouts and wild-types but fails to excite interneurons or recruit inhibition in Neto1 knockouts. In contrast, presynaptic KARs in CCK/CB1 interneurons are dually regulated by both Neto1 and Neto2. Neto association promotes tonic presynaptic KAR activation, dampening CCK/CB1 interneuron output, and loss of this brake in Neto mutants profoundly increases CCK/CB1 interneuron-mediated inhibition. Our results confirm that Neto1 regulates endogenous somatodendritic KARs in diverse interneurons and demonstrate Neto regulation of presynaptic KARs in mature inhibitory presynaptic terminals.


Asunto(s)
Dendritas/metabolismo , Interneuronas/metabolismo , Proteínas Relacionadas con Receptor de LDL/metabolismo , Proteínas de la Membrana/metabolismo , Red Nerviosa/metabolismo , Inhibición Neural , Receptores de Ácido Kaínico/metabolismo , Receptores Presinapticos/metabolismo , Animales , Ritmo Gamma , Activación del Canal Iónico , Ácido Kaínico , Ratones Noqueados , Ratones Mutantes , Mutación/genética , Regiones Promotoras Genéticas/genética , Subunidades de Proteína/metabolismo , ARN Mensajero/genética , ARN Mensajero/metabolismo , Receptores de N-Metil-D-Aspartato
9.
Neuron ; 85(6): 1257-72, 2015 03 18.
Artículo en Inglés | MEDLINE | ID: mdl-25754824

RESUMEN

Circuit computation requires precision in the timing, extent, and synchrony of principal cell (PC) firing that is largely enforced by parvalbumin-expressing, fast-spiking interneurons (PVFSIs). To reliably coordinate network activity, PVFSIs exhibit specialized synaptic and membrane properties that promote efficient afferent recruitment such as expression of high-conductance, rapidly gating, GluA4-containing AMPA receptors (AMPARs). We found that PVFSIs upregulate GluA4 during the second postnatal week coincident with increases in the AMPAR clustering proteins NPTX2 and NPTXR. Moreover, GluA4 is dramatically reduced in NPTX2(-/-)/NPTXR(-/-) mice with consequent reductions in PVFSI AMPAR function. Early postnatal NPTX2(-/-)/NPTXR(-/-) mice exhibit delayed circuit maturation with a prolonged critical period permissive for giant depolarizing potentials. Juvenile NPTX2(-/-)/NPTXR(-/-) mice display reduced feedforward inhibition yielding a circuit deficient in rhythmogenesis and prone to epileptiform discharges. Our findings demonstrate an essential role for NPTXs in controlling network dynamics highlighting potential therapeutic targets for disorders with inhibition/excitation imbalances such as schizophrenia.


Asunto(s)
Potenciales de Acción/fisiología , Proteína C-Reactiva/metabolismo , Interneuronas/metabolismo , Red Nerviosa/crecimiento & desarrollo , Proteínas del Tejido Nervioso/metabolismo , Parvalbúminas/metabolismo , Sinapsis/metabolismo , Animales , Animales Recién Nacidos , Proteína C-Reactiva/deficiencia , Modelos Animales de Enfermedad , Ratones , Ratones Noqueados , Proteínas del Tejido Nervioso/deficiencia
10.
J Neurosci ; 34(2): 622-8, 2014 Jan 08.
Artículo en Inglés | MEDLINE | ID: mdl-24403160

RESUMEN

Neto1 and Neto2 auxiliary subunits coassemble with NMDA receptors (NMDARs) and kainate receptors (KARs) to modulate their function. In the hippocampus, Neto1 enhances the amplitude and prolongs the kinetics of KAR-mediated currents at mossy fiber (MF)-CA3 pyramidal cell synapses. However, whether Neto1 trafficks KARs to synapses or simply alters channel properties is unresolved. Therefore, postembedding electron microscopy was performed to investigate the localization of GluK2/3 subunits at MF-CA3 synapses in Neto-null mice. Postsynaptic GluK2/3 Immunogold labeling was substantially reduced in Neto-null mice compared with wild types. Moreover, spontaneous KAR-mediated synaptic currents and metabotropic KAR signaling were absent in CA3 pyramidal cells of Neto-null mice. A similar loss of ionotropic and metabotropic KAR function was observed in Neto1, but not Neto2, single knock-out mice, specifically implicating Neto1 in regulating CA3 pyramidal cell KAR localization and function. Additional controversy pertains to the role of Neto proteins in modulating synaptic NMDARs. While Immunogold labeling for GluN2A at MF-CA3 synapses was comparable between wild-type and Neto-null mice, labeling for postsynaptic GluN2B was robustly increased in Neto-null mice. Accordingly, NMDAR-mediated currents at MF-CA3 synapses exhibited increased sensitivity to a GluN2B-selective antagonist in Neto1 knockouts relative to wild types. Thus, despite preservation of the overall MF-CA3 synaptic NMDAR-mediated current, loss of Neto1 alters NMDAR subunit composition. These results confirm that Neto protein interactions regulate synaptic localization of KAR and NMDAR subunits at MF-CA3 synapses, with implications for both ionotropic and metabotropic glutamatergic recruitment of the CA3 network.


Asunto(s)
Región CA3 Hipocampal/metabolismo , Lipoproteínas LDL/metabolismo , Proteínas de la Membrana/metabolismo , Fibras Musgosas del Hipocampo/metabolismo , Receptores de Ácido Kaínico/metabolismo , Receptores de N-Metil-D-Aspartato/metabolismo , Animales , Proteínas Relacionadas con Receptor de LDL , Masculino , Ratones , Ratones Noqueados , Técnicas de Placa-Clamp , Sinapsis/metabolismo
11.
J Neurosci ; 30(26): 8993-9006, 2010 Jun 30.
Artículo en Inglés | MEDLINE | ID: mdl-20592220

RESUMEN

Perisomatic inhibition from basket cells plays an important role in regulating pyramidal cell output. Two major subclasses of CA1 basket cells can be identified based on their expression of either cholecystokinin (CCK) or parvalbumin. This study examined their fates in the mouse pilocarpine model of temporal lobe epilepsy. Overall, immunohistochemical labeling of GABAergic boutons in the pyramidal cell layer of CA1 was preserved in the mouse model. However, CCK-labeled boutons in this layer were chronically reduced, whereas parvalbumin-containing boutons were conserved. Immunohistochemistry for cannabinoid receptor 1 (CB(1)), another marker for CCK-containing basket cells, also labeled fewer boutons in pilocarpine-treated mice. Hours after status epilepticus, electron microscopy revealed dark degenerating terminals in the pyramidal cell layer with lingering CCK and CB(1) immunoreactivity. In mice with recurrent seizures, carbachol-induced enhancement of spontaneous IPSCs (sIPSCs) originating from CCK-containing basket cells was accordingly reduced in CA1 pyramidal cells. By suppressing sIPSCs from CCK-expressing basket cells, a CB(1) agonist reverted the stimulatory effects of carbachol in naive mice to levels comparable with those observed in cells from epileptic mice. The agatoxin-sensitive component of CA1 pyramidal cell sIPSCs from parvalbumin-containing interneurons was increased in pilocarpine-treated mice, and miniature IPSCs were reduced, paralleling the decrease in CCK-labeled terminals. Altogether, the findings are consistent with selective reduction in perisomatic CA1 pyramidal cell innervation from CCK-expressing basket cells in mice with spontaneous seizures and a greater reliance on persisting parvalbumin innervation. This differential alteration in inhibition may contribute to the vulnerability of the network to seizure activity.


Asunto(s)
Región CA1 Hipocampal/fisiopatología , Colecistoquinina/metabolismo , Epilepsia del Lóbulo Temporal/fisiopatología , Neuronas/fisiología , Animales , Región CA1 Hipocampal/efectos de los fármacos , Región CA1 Hipocampal/ultraestructura , Modelos Animales de Enfermedad , Epilepsia del Lóbulo Temporal/inducido químicamente , Epilepsia del Lóbulo Temporal/patología , Potenciales Postsinápticos Inhibidores/efectos de los fármacos , Masculino , Ratones , Vías Nerviosas/efectos de los fármacos , Vías Nerviosas/fisiopatología , Vías Nerviosas/ultraestructura , Neuronas/efectos de los fármacos , Neuronas/ultraestructura , Parvalbúminas/metabolismo , Pilocarpina , Terminales Presinápticos/efectos de los fármacos , Terminales Presinápticos/fisiología , Terminales Presinápticos/ultraestructura , Células Piramidales/efectos de los fármacos , Células Piramidales/fisiopatología , Células Piramidales/ultraestructura , Receptor Cannabinoide CB1/agonistas , Receptor Cannabinoide CB1/metabolismo , Estado Epiléptico/inducido químicamente , Estado Epiléptico/patología , Estado Epiléptico/fisiopatología , Ácido gamma-Aminobutírico/metabolismo
12.
Water Environ Res ; 80(6): 490-6, 2008 Jun.
Artículo en Inglés | MEDLINE | ID: mdl-18686924

RESUMEN

Dimensionally stable anodes (DSAs) demonstrate potential for the electrochemical treatment of industrial waste streams and disinfection of effluent. Oxidation by laboratory-prepared tin oxide DSAs was compared with that of commercially available ruthenium oxide, iridium oxide, and mixed metal oxide DSAs, using hexanol as a probe molecule. The performance of the four anodes was similar in two-chamber reactors, in which the anode cell was separated from the cathode cell by a Nafion membrane, which allows transmission of current between the chambers, but not passage of chemical constituents. The anodes were then evaluated in single-cell reactors, which are more representative of potential treatment and disinfection applications. However, in the single-cell reactors, the tin oxide anodes were significantly more effective at oxidation and generated higher quality cyclic voltammograms than the other DSAs. These results suggest that tin oxide anodes have greater potential than the three commercially available DSAs tested for industrial waste stream treatment and effluent disinfection.


Asunto(s)
Electrodos , Compuestos de Estaño/química , Comercio , Concentración de Iones de Hidrógeno , Oxidación-Reducción , Oxígeno/química
13.
J Neurosci ; 23(9): 3588-96, 2003 May 01.
Artículo en Inglés | MEDLINE | ID: mdl-12736329

RESUMEN

Little is known about the expression and possible functions of unopposed gap junction hemichannels in the brain. Emerging evidence suggests that gap junction hemichannels can act as stand-alone functional channels in astrocytes. With immunocytochemistry, dye uptake, and HPLC measurements, we show that astrocytes in vitro express functional hemichannels that can mediate robust efflux of glutamate and aspartate. Functional hemichannels were confirmed by passage of extracellular lucifer yellow (LY) into astrocytes in nominal divalent cation-free solution (DCFS) and the ability to block this passage with gap junction blocking agents. Glutamate/aspartate release (or LY loading) in DCFS was blocked by multivalent cations (Ca2+, Ba2+, Sr2+, Mg2+, and La3+) and by gap junction blocking agents (carbenoxolone, octanol, heptanol, flufenamic acid, and 18alpha-glycyrrhetinic acid) with affinities close to those reported for blockade of gap junction intercellular communication. Glutamate efflux via hemichannels was also accompanied by greatly reduced glutamate uptake. Glutamate release in DCFS, however, was not significantly mediated by reversal of the glutamate transporter: release did not saturate and was not blocked by glutamate transporter blockers. Control experiments in DCFS precluded glutamate release by volume-sensitive anion channels, P2X7 purinergic receptor pores, or general purinergic receptor activation. Blocking intracellular Ca2+ mobilization by BAPTA-AM or thapsigargin did not inhibit glutamate release in DCFS. Divalent cation removal also induced glutamate release from intact CNS white matter (acutely isolated optic nerve) that was blocked by carbenoxolone, suggesting the existence of functional hemichannels in situ. Our results indicated that astrocyte hemichannels could influence CNS levels of extracellular glutamate with implications for normal and pathological brain function.


Asunto(s)
Astrocitos/metabolismo , Uniones Comunicantes/metabolismo , Ácido Glutámico/metabolismo , Ácido Glicirretínico/análogos & derivados , Adenosina Trifosfato/metabolismo , Sistema de Transporte de Aminoácidos X-AG/antagonistas & inhibidores , Sistema de Transporte de Aminoácidos X-AG/metabolismo , Animales , Ácido Aspártico/metabolismo , Astrocitos/citología , Astrocitos/efectos de los fármacos , Transporte Biológico/efectos de los fármacos , Transporte Biológico/fisiología , Calcio/metabolismo , Carbenoxolona/farmacología , Cationes Bivalentes/farmacología , Células Cultivadas , Quelantes/farmacología , Conexina 43/metabolismo , Ácido Flufenámico/farmacología , Colorantes Fluorescentes/farmacocinética , Uniones Comunicantes/efectos de los fármacos , Ácido Glutámico/farmacocinética , Ácido Glicirretínico/farmacología , Heptanol/farmacología , Inmunohistoquímica , Lantano/farmacología , Octanoles/farmacología , Ratas
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