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1.
Eur J Neurosci ; 50(1): 1700-1711, 2019 07.
Artigo em Inglês | MEDLINE | ID: mdl-30687962

RESUMO

Ca2+ -induced Ca2+ release (CICR) via type-3 ryanodine receptor enhances neurotransmitter release in frog motor nerve terminals. To test a possible role of synaptic vesicle in CICR, we examined the effects of loading of EGTA, a Ca2+ chelator, into synaptic vesicles and depolymerization of actin fibers. Intravesicular EGTA loading via endocytosis inhibited the ryanodine sensitive enhancement of transmitter release induced by tetanic stimulation and the associated rises in intracellular-free Ca2+ ([Ca2+ ]i : Ca2+ transients). Latrunculin A, a depolymerizer of actin fibers, enhanced both spontaneous and stimulation-induced transmitter release, but inhibited the enhancement of transmitter release elicited by successive tetanic stimulation. The results suggest a possibility that the activation of CICR from mobilized synaptic vesicles caused the enhancement of neurotransmitter release.


Assuntos
Actinas/efeitos dos fármacos , Compostos Bicíclicos Heterocíclicos com Pontes/farmacologia , Quelantes de Cálcio/farmacologia , Cálcio/metabolismo , Fenômenos Eletrofisiológicos , Neurônios Motores/metabolismo , Terminações Pré-Sinápticas/metabolismo , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Transmissão Sináptica/efeitos dos fármacos , Vesículas Sinápticas/metabolismo , Tiazolidinas/farmacologia , Animais , Ácido Egtázico/farmacologia , Estimulação Elétrica , Ranidae
2.
Cell Calcium ; 49(6): 400-14, 2011 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-21514957

RESUMO

We studied how mitochondrial uncoupling by ß(3)-adrenergic stimulation elicits Ca(2+) signals in rodent brown adipocytes by fluorometry of Ca(2+) concentrations ([Ca(2+)](i), [Ca(2+)](m) and [Ca(2+)](ER)) in the cytoplasm, mitochondria and the endoplasmic reticulum (ER), respectively, and mitochondrial membrane potential, using fura-2, rhod-5N, cameleon and rhodamine 123. Immunoblotting demonstrated α(1A)- and ß(3)-adrenergic receptor and UCP1 in adipocytes, while RT-PCR revealed the mRNA of type 3, 7 and 9 adenylate cyclase, UCP1, UCP2, UCP3 and type 1 and 2 inositoltrisphosphate receptors. Isoproterenol and BRL37344, ß-agonist, caused triphasic rises in [Ca(2+)](i) (ß-responses) with mitochondrial depolarization in adipocytes. BRL37344 transiently decreased [Ca(2+)](m). ß-Responses were blocked by propranolol, ß-antagonist, H-89, protein kinase A blocker, and knockout of UCP1 gene. The late phase of ß-responses was depressed by a Ca(2+) free, EGTA solution, U73122, a phospholipase C blocker, and thapsigargin, ER-Ca(2+) pump blocker, and by transfecting siRNA for type 2 IP(3)R. Intracellular loading of BAPTA/AM depressed the late phase more strongly than the initial phase. ß-Agonists, phenylephrine, α-agonist, and cyclopiazonic acid, ER-Ca(2+) pump blocker, decreased [Ca(2+)](ER). Thus, the mitochondrial uncoupling by ß(3)-adrenergic activation causes Ca(2+) release from mitochondria and subsequently from the ER and further evokes plasmalemmal Ca(2+) entries, including the store-operated Ca(2+) entry.


Assuntos
Adipócitos Marrons/fisiologia , Cálcio/metabolismo , Retículo Endoplasmático/metabolismo , Mitocôndrias/metabolismo , Receptores Adrenérgicos beta 3/metabolismo , Adipócitos Marrons/citologia , Adipócitos Marrons/efeitos dos fármacos , Agonistas de Receptores Adrenérgicos beta 3/farmacologia , Antagonistas de Receptores Adrenérgicos beta 3/farmacologia , Animais , Células Cultivadas , Corantes Fluorescentes/química , Receptores de Inositol 1,4,5-Trifosfato/antagonistas & inibidores , Receptores de Inositol 1,4,5-Trifosfato/genética , Receptores de Inositol 1,4,5-Trifosfato/metabolismo , Canais Iônicos/genética , Canais Iônicos/metabolismo , Potencial da Membrana Mitocondrial , Camundongos , Camundongos Endogâmicos C57BL , Proteínas Mitocondriais/genética , Proteínas Mitocondriais/metabolismo , Propranolol/farmacologia , Interferência de RNA , RNA Interferente Pequeno , Ratos , Ratos Wistar , Receptores Adrenérgicos alfa 1/química , Receptores Adrenérgicos alfa 1/metabolismo , Receptores Adrenérgicos beta 3/química , Fosfolipases Tipo C/metabolismo , Proteína Desacopladora 1
3.
Eur J Neurosci ; 32(6): 948-62, 2010 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-20796022

RESUMO

We studied the effects of varying extracellular Ca(2+) ([Ca(2+) ](o) ) and Ca(2+) channel density and intracellular loading of Ca(2+) chelators on stimulation-induced rises in intracellular Ca(2+) ([Ca(2+) ](i) ) in frog motor nerve terminals with Ca(2+) imaging. The slowly waxing and waning components of rises in [Ca(2+) ](i) induced by repetitive tetani were suppressed by blockers of Ca(2+) pumps of the endoplasmic reticulum (thapsigargin and cyclopiazonic acid) and a blocker of ryanodine receptors [8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride] without affecting the initial quickly-rising component, thus reflecting the priming (and then subsequent rapid activation) and inactivation phases of Ca(2+) -induced Ca(2+) release (CICR) from the endoplasmic reticulum. A short tetanus-induced rise in [Ca(2+) ](i) was proportional to [Ca(2+) ](o) , whereas the component of CICR was non-linearly related to [Ca(2+) ](o) with saturation at 0.9 mm. The progressive blockade of Ca(2+) channels by ω-conotoxin GVIA caused proportional decreases in CICR and short tetanus-induced [Ca(2+) ](i) rises. Intracellular loading of BAPTA and EGTA reduced the magnitude of CICR as well as short tetanus-induced rises in [Ca(2+) ](i) with a greater effect of BAPTA than EGTA on CICR. The time to peak and the half decay time of CICR were prolonged by a low [Ca(2+) ](o) or Ca(2+) channel blocker or [Ca(2+) ](i) chelators. These results suggest that ryanodine receptors sense the high [Ca(2+) ](i) transient following single action potentials for triggering CICR, whereas the priming and inactivation processes of CICR sense a slower, persisting rise in [Ca(2+) ](i) during and after action potential trains. A model is presented that includes CICR activation in elementary units.


Assuntos
Cálcio/fisiologia , Neurônios Motores/metabolismo , Inibição Neural/fisiologia , Terminações Pré-Sinápticas/metabolismo , Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo , Animais , Neurônios Motores/fisiologia , Terminações Pré-Sinápticas/fisiologia , Ranidae , Canal de Liberação de Cálcio do Receptor de Rianodina/biossíntese
4.
J Physiol ; 586(14): 3365-84, 2008 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-18483065

RESUMO

We studied inactivation of Ca(2+)-induced Ca(2+) release (CICR) via ryanodine receptors (RyRs) in bullfrog sympathetic neurons. The rate of rise in [Ca(2+)](i) due to CICR evoked by a depolarizing pulse decreased markedly within 10-20 ms to a much slower rate despite persistent Ca(2+) entry and little depletion of Ca(2+) stores. The Ca(2+) entry elicited by the subsequent pulse within 50 ms, during which the [Ca(2+)](i) level remained unchanged, did not generate a distinct [Ca(2+)](i) rise. This mode of [Ca(2+)](i) rise was unaffected by a mitochondrial uncoupler, carbonyl cyanide p-trifluromethoxy-phenylhydrazone (FCCP, 1 microm). Paired pulses of varying interval and duration revealed that recovery from inactivation became distinct >or= 50 ms after depolarization and depended on [Ca(2+)](i). The inactivation was prevented by BAPTA (>or= 100 microm) but not by EGTA (

Assuntos
Sinalização do Cálcio/fisiologia , Cálcio/metabolismo , Neurônios/fisiologia , Rana catesbeiana/fisiologia , Sistema Nervoso Simpático/fisiologia , Potenciais de Ação , Animais , Cafeína/farmacologia , Fármacos do Sistema Nervoso Central/farmacologia , Relação Dose-Resposta a Droga , Ácido Egtázico/análogos & derivados , Ácido Egtázico/farmacologia , Mitocôndrias/metabolismo , Neurônios/efeitos dos fármacos , Rianodina/farmacologia , Tapsigargina/farmacologia
5.
Am J Physiol Cell Physiol ; 292(2): C896-908, 2007 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-16987997

RESUMO

How the endoplasmic reticulum (ER) and mitochondria communicate with each other and how they regulate plasmalemmal Ca(2+) entry were studied in cultured rat brown adipocytes. Cytoplasmic Ca(2+) or Mg(2+) and mitochondrial membrane potential were measured by fluorometry. The sustained component of rises in cytoplasmic Ca(2+) concentration ([Ca(2+)](i)) produced by thapsigargin was abolished by removing extracellular Ca(2+), depressed by depleting extracellular Na(+), and enhanced by raising extracellular pH. FCCP, dinitrophenol, and rotenone caused bi- or triphasic rises in [Ca(2+)](i), in which the first phase was accompanied by mitochondrial depolarization. The FCCP-induced first phase was partially inhibited by oligomycin but not by ruthenium red, cyclosporine A, U-73122, a Ca(2+)-free EGTA solution, and an Na(+)-free solution. The FCCP-induced second phase paralleling mitochondrial repolarization was partially blocked by removing extracellular Ca(2+) and fully blocked by oligomycin but not by thapsigargin or an Na(+)-deficient solution, was accompanied by a rise in cytoplasmic Mg(2+) concentration, and was summated with a high pH-induced rise in [Ca(2+)](i), whereas the extracellular Ca(2+)-independent component was blocked by U-73122 and cyclopiazonic acid. The FCCP-induced third phase was blocked by removing Ca(2+) but not by thapsigargin, depressed by decreasing Na(+), and enhanced by raising pH. Cyclopiazonic acid-evoked rises in [Ca(2+)](i) in a Ca(2+)-free solution were depressed after FCCP actions. Thus mitochondrial uncoupling causes Ca(2+) release, activating Ca(2+) release from the ER and store-operated Ca(2+) entry, and directly elicits a novel plasmalemmal Ca(2+) entry, whereas Ca(2+) release from the ER activates Ca(2+) accumulation in, or release from, mitochondria, indicating bidirectional mitochondria-ER couplings in rat brown adipocytes.


Assuntos
Adipócitos Marrons/fisiologia , Cálcio/metabolismo , Retículo Endoplasmático/fisiologia , Mitocôndrias/fisiologia , Adipócitos Marrons/efeitos dos fármacos , Animais , Sinalização do Cálcio , Carbonil Cianeto p-Trifluormetoxifenil Hidrazona/farmacologia , Células Cultivadas , Ciclosporina/farmacologia , Retículo Endoplasmático/efeitos dos fármacos , Retículo Endoplasmático/metabolismo , Inibidores Enzimáticos/farmacologia , Estrenos/farmacologia , Concentração de Íons de Hidrogênio , Indóis/farmacologia , Líquido Intracelular/metabolismo , Magnésio/metabolismo , Potencial da Membrana Mitocondrial , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Oligomicinas/farmacologia , Pirrolidinonas/farmacologia , Ratos , Rotenona/farmacologia , Sódio/metabolismo , Tapsigargina/farmacologia , Desacopladores/farmacologia
6.
Neurosci Res ; 57(3): 339-46, 2007 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-17173996

RESUMO

The role of cyclic ADP-ribose (cADPR) and its synthetic enzyme, CD38, as a downstream signal of muscarinic acetylcholine receptors (mAChRs) was examined in neuroblastoma cells expressing M1 mAChRs (NGM1). NGM1 cells were further transformed with both wild-type and mutant (C119K/C201E) human CD38. The dual transformed cells exhibited higher cADPR formation than ADPR production and elevated intracellular free Ca(2+) concentrations ([Ca(2+)](i)) in response to ACh. These phenotypes were analyzed in detail in a representative CD38 clone. The intracellular cADPR concentration by ACh application was significantly increased by CD38 overexpression. Digital image analysis by a confocal microscopy revealed that topographical distribution of the sites of Ca(2+) release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca(2+) signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.


Assuntos
ADP-Ribosil Ciclase 1/metabolismo , ADP-Ribosil Ciclase/metabolismo , Acetilcolina/metabolismo , Sinalização do Cálcio/fisiologia , ADP-Ribose Cíclica/metabolismo , Receptores Muscarínicos/metabolismo , ADP-Ribosil Ciclase 1/genética , Acetilcolina/farmacologia , Animais , Cálcio/metabolismo , Sinalização do Cálcio/efeitos dos fármacos , Linhagem Celular Tumoral , Células Clonais/efeitos dos fármacos , Células Clonais/metabolismo , Humanos , Camundongos , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Fenótipo , Ratos , Receptores Muscarínicos/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/fisiologia , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/fisiologia
7.
Cell Calcium ; 38(6): 557-67, 2005 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-16157373

RESUMO

Ca(2+)-induced Ca2+ release (CICR) occurs in frog motor nerve terminals after ryanodine receptors (RyRs) are primed for activation by conditioning large Ca2+ entry. We studied which type of RyR exists, whether CICR occurs without conditioning Ca2+ entry and how RyRs are primed. Immunohistochemistry revealed the existence of RyR3 in motor nerve terminals and axons and both RyR1 and RyR3 in muscle fibers. A blocker of RyR, 8-(N,N-diethylamino)octyl 3,4,5-trimethoxybenzoate hydrochloride (TMB-8) slightly decreased rises in intracellular Ca2+ ([Ca2+]i) induced by a short tetanus (50 Hz, 1-2s), but not after treatment with ryanodine. Repetitive tetani (50 Hz for 15s every 20s) produced repetitive rises in [Ca2+]i, whose amplitude overall waxed and waned. TMB-8 blocked the waxing and waning components. Ryanodine suppressed a slow increase in end-plate potentials (EPPs) induced by stimuli (33.3 Hz, 15s) in a low Ca2+, high Mg2+ solution. KN-62, a blocker of Ca(2+)/calmoduline-activated protein kinase II (CaMKII), slightly reduced short tetanus-induced rises in [Ca2+]i, but markedly the slow waxing and waning rises produced by repetitive tetani in both normal and low Ca2+, high Mg2+ solutions. Likewise, KN-62, but not KN-04, an inactive analog, suppressed slow increases in EPP amplitude and miniature EPP frequency during long tetanus. Thus, CICR normally occurs weakly via RyR3 activation by single impulse-induced Ca2+ entry in frog motor nerve terminals and greatly after the priming of RyR via CaMKII activation by conditioning Ca2+ entry, thus, facilitating transmitter exocytosis and its plasticity.


Assuntos
Cálcio/fisiologia , Exocitose/fisiologia , Neurônios Motores/fisiologia , Junção Neuromuscular/metabolismo , Neurotransmissores/metabolismo , Canal de Liberação de Cálcio do Receptor de Rianodina/classificação , Canal de Liberação de Cálcio do Receptor de Rianodina/fisiologia , Animais , Cálcio/metabolismo , Neurônios Motores/metabolismo , Músculo Esquelético/inervação , Junção Neuromuscular/fisiologia , Terminações Pré-Sinápticas/metabolismo , Terminações Pré-Sinápticas/fisiologia , Ranidae
8.
Eur J Neurosci ; 20(2): 419-26, 2004 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-15233751

RESUMO

We have studied whether Ca(2+)-induced Ca(2+) release (CICR) is involved in the mechanism of long-term potentiation (LTP) at nicotinic synapses of bullfrog sympathetic ganglia. Fast excitatory postsynaptic potentials (fast EPSPs) were recorded in a low-Ca(2+), high-Mg(2+) solution and quantal analysis was applied. The conditioning stimulation of the B-type preganglionic nerve at 20 Hz for 4 min consistently enhanced the amplitude and quantal content of fast EPSP for > 2 h, but only sometimes enhanced the quantal size. The LTP of quantal content produced by the conditioning tetanus was blocked by thapsigargin, a blocker of Ca(2+) pumps at Ca(2+) stores, applied before or after the conditioning tetanus, and by Xestospongin C, a blocker of inositoltrisphosphate (IP(3)) receptors, applied before the tetanus. It was not, however, blocked by ryanodine, a blocker and/or activator of ryanodine receptors, or by propranolol, a blocker of beta-adrenergic receptors. Thus the long-lasting activity of the preganglionic nerve at a high frequency causes the LTP of impulse-evoked transmitter release by the activation of CICR from thapsigargin-sensitive Ca(2+) stores in the nerve terminals. It is likely that a large Ca(2+) entry into the nerve terminals during tetanic activity primes ryanodine-insensitive Ca(2+) release channels for activation.


Assuntos
Cálcio/metabolismo , Inibidores Enzimáticos/farmacologia , Gânglios Simpáticos/citologia , Potenciação de Longa Duração/efeitos dos fármacos , Terminações Pré-Sinápticas/efeitos dos fármacos , Tapsigargina/farmacologia , Antagonistas Adrenérgicos beta/farmacologia , Animais , Relação Dose-Resposta à Radiação , Estimulação Elétrica/métodos , Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos , Potenciais Pós-Sinápticos Excitadores/fisiologia , Técnicas In Vitro , Potenciação de Longa Duração/efeitos da radiação , Compostos Macrocíclicos , Oxazóis/farmacologia , Terminações Pré-Sinápticas/fisiologia , Terminações Pré-Sinápticas/efeitos da radiação , Propranolol/farmacologia , Rana catesbeiana , Rianodina/farmacologia , Fatores de Tempo
9.
Eur J Neurosci ; 15(8): 1291-8, 2002 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-11994123

RESUMO

The depressant action of adenosine on acetylcholine release at frog motor nerve terminals was studied by intracellular recording and Ca(2+)-imaging techniques. Adenosine (200 microm) quickly and reversibly decreased the amplitude and quantal content of end-plate potentials (EPPs) with no change in quantal size in a low-Ca(2+), high-Mg(2+) solution, and EPP amplitude in normal Ringer containing d-tubocurarine. Likewise, adenosine (200 microm) reduced miniature EPP (MEPP) frequency, but not amplitude, in a high-K(+) (6 mm) solution. Adenosine (40-200 microm), however, did not affect single or repetitive impulse(s)-induced rises in Ca(2+) in the nerve terminals or its basal level. Adenosine (100-200 microm) reduced the Ca(2+)-independent enhancement of MEPP frequency caused by hypertonicity. EPPs induced by tetanic stimulation (33 Hz) in Ringer with d-tubocurarine initially increased in amplitude within 10 stimuli and then declined to the minimum. Adenosine (200 microm) decreased EPP amplitude in the initial phase of the tetanus, but enhanced it in the middle phase, thus prolonging the decay of EPP amplitude. The total sum of these EPPs, reflecting the readily releasable pool of vesicles and its refilling, however, was not changed. The results suggest that adenosine inhibits a Ca(2+)-independent step of transmitter exocytosis at frog motor nerve terminals.


Assuntos
Acetilcolina/metabolismo , Adenosina/metabolismo , Células do Corno Anterior/metabolismo , Sinalização do Cálcio/fisiologia , Exocitose/fisiologia , Junção Neuromuscular/metabolismo , Terminações Pré-Sinápticas/metabolismo , Ranidae/metabolismo , Adenosina/farmacologia , Animais , Células do Corno Anterior/citologia , Células do Corno Anterior/efeitos dos fármacos , Cálcio/metabolismo , Sinalização do Cálcio/efeitos dos fármacos , Relação Dose-Resposta a Droga , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/fisiologia , Estimulação Elétrica , Potenciais Pós-Sinápticos Excitadores/efeitos dos fármacos , Potenciais Pós-Sinápticos Excitadores/fisiologia , Exocitose/efeitos dos fármacos , Soluções Hipertônicas/farmacologia , Inibição Neural/efeitos dos fármacos , Inibição Neural/fisiologia , Junção Neuromuscular/citologia , Junção Neuromuscular/efeitos dos fármacos , Terminações Pré-Sinápticas/efeitos dos fármacos , Terminações Pré-Sinápticas/ultraestrutura , Ranidae/anatomia & histologia , Regulação para Cima/efeitos dos fármacos , Regulação para Cima/fisiologia
10.
J Neurophysiol ; 87(3): 1222-33, 2002 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-11877496

RESUMO

Transmitter release at Cs(+)-loaded autaptic terminals was selectively activated by the subthreshold concentration of external K+, and Ca(2+) channel types and transmitter pools involved in synchronous and asynchronous exocytosis were studied. When a neuron was depolarized to +30 mV by applying a current through a pipette containing Cs(+) for >30 s, a rapid external K+ jump to 3.75-10 mM, otherwise ineffective, produced an outward current (K10 response). K10 responses were initially graded (type-1) and then became a spike and plateau-shape with (type-2) or without a latency (type-3). On repolarization to -60 mV, a high K+ jump induced inward currents (called also K10 response) similar to those at +30 mV, whose shape changed from that of type-3, then type-2 and finally type-1 over 30 min. During a period favorable for inducing a type-3 response, a current similar to this response was generated by a voltage pulse (+ 80 or 90 mV, 20 or 30 ms) to the cell soma. Currents similar to K10 responses were rarely induced by a high K+ jump without a conditioning depolarization except for some cells, but consistently produced when 3 mM Cs(+) and 50 microM 4-aminopyridine were externally applied for tens of minutes. Picrotoxin, 6-cyano-7-nitroquinoxaline-2,3-dione with 3-[(RS)-2-carboxypiperazin-4-yl]-propyl-1-phosphonic acid or Cd(2+) in, or Ca(2+) removal from, a high-K+ solution blocked all the K10 responses, while a plateau remaining after a high K+ jump was not blocked by Ca(2+) removal immediately after the K+ jump. Thus Cs(+) loading and decreased K+ concentration in autaptic terminals by a conditioning depolarizing current selectively sensitize the terminals to a subthreshold high K+ jump for depolarization to activate synchronous or asynchronous transmitter release. Nicardipine (5-10 microM) blocked type-1 and -2 responses but not type-3 responses, while omega-conotoxin (10 microM) blocked all the types of K10 response in the presence of nicardipine. Increasing the interval of high K+ jumps biphasically increased the magnitude of K10 response, preferentially in the postjump fraction reflecting purely the asynchronous activation of exocytotic machinery, and decreased the reduction of miniature postsynaptic current frequency after a K10 response. These results suggest the roles of N(P/Q)-type Ca(2+) channels in synchronous exocytosis at the terminals, L-type Ca(2+) channels in initiating a Ca(2+) action potential at the parent axon and both types in asynchronous exocytosis and also suggest the different releasable pools of transmitter for two modes of exocytosis in cultured hippocampal neurons.


Assuntos
Césio/farmacologia , Exocitose/fisiologia , Neurônios/metabolismo , Potássio/farmacocinética , Terminações Pré-Sinápticas/metabolismo , Animais , Bloqueadores dos Canais de Cálcio/farmacologia , Canais de Cálcio/metabolismo , Células Cultivadas , Estimulação Elétrica , Antagonistas de Aminoácidos Excitatórios/farmacologia , Exocitose/efeitos dos fármacos , Feminino , Antagonistas GABAérgicos/farmacologia , Hipocampo/citologia , Magnésio/farmacologia , Potenciais da Membrana/efeitos dos fármacos , Potenciais da Membrana/fisiologia , Neurônios/citologia , Picrotoxina/farmacologia , Canais de Potássio/metabolismo , Gravidez , Terminações Pré-Sinápticas/efeitos dos fármacos , Ratos , Ratos Wistar , Vesículas Sinápticas/metabolismo
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