Novel glutamate- and GABA-independent synaptic depolarization in granule cells of guinea-pig hippocampus.
Novel glutamate- and GABA-independent synaptic depolarization in granule cells of guinea-pig hippocampus.
复制标题
豚鼠海马颗粒细胞中新型谷氨酸和 GABA 独立的突触去极化。
DOI：
10.1111/j.1469-7793.1997.641bd.x
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发表时间：
1997
期刊：
影响因子：
--
通讯作者：
Michelson,HB
中科院分区：
文献类型：
--
作者：
Forti,M;Michelson,HB
1在豚鼠海马横切片上进行颗粒细胞、门部中间神经元和CA 3锥体细胞的双重细胞内记录。在静息膜电位下，在4-氨基吡啶、离子型谷氨酸受体拮抗剂和GABA A受体拮抗剂荷包牡丹碱存在下，颗粒细胞出现与中间神经元同步爆发活动相关的自发大幅度去极化。2在这些条件下，锥体细胞出现与GABA能中间神经元爆发活动同步的大幅度单相GABA B抑制性突触后电位（IPSPs）。颗粒细胞也接受GABA的输入，这是明显的，只有当神经元去极化DC注射。GABAB受体拮抗剂CGP 55845 A（CGP）阻断锥体细胞和颗粒细胞的GABABIPSPs;然而，颗粒细胞的去极化电位不受药物的影响。3在CGP存在下，颗粒细胞的去极化是双相的，并表现出线性电压依赖性，逆转电位约为-40 mV，提示它是由激活混合阳离子电流的突触输入产生的。4在向浴中加入河豚毒素后，颗粒细胞去极化被消除。此外，用低钙溶液灌注切片5（S）-甲基-4-羧基苯甘氨酸、1-（+）-2-氨基-3-膦酰基丙酸、普萘洛尔和阿托品不影响颗粒细胞去极化，表明代谢型谷氨酸受体，β-肾上腺素能受体和毒蕈碱胆碱能受体不参与产生颗粒细胞去极化突触反应。6这些发现表明，在缺乏多巴胺能和GABA能输入的情况下，同步的神经元间活动可以在颗粒细胞中产生去极化突触反应。目前正在研究负责去极化的神经化学物质。
1Dual intracellular recordings of granule cells, hilar interneurons and CA3 pyramidal cells were performed in transverse slices of guinea‐pig hippocampus. At resting membrane potential, in the presence of 4‐aminopyridine, ionotropic glutamate receptor antagonists and the GABAAreceptor antagonist bicuculline, granule cells showed spontaneous, large amplitude depolarizations correlated with synchronous bursting activity of interneurons.2Under these conditions, pyramidal cells exhibited large amplitude monophasic GABABinhibitory postsynaptic potentials (IPSPs) synchronous with the GABAergic interneuron burst discharges. The granule cells also received a GABABinput, which was evident only when the neurons were depolarized by DC injection. The GABABreceptor antagonist CGP 55845A (CGP) blocked the GABABIPSPs in both pyramidal cells and granule cells; however, the depolarizing potential in granule cells was unaffected by the drug.3The granule cell depolarization in the presence of CGP was monophasic and exhibited linear voltage dependence with a reversal potential around −40 mV, suggesting that it was generated by a synaptic input activating a mixed cationic current.4The granule cell depolarization was abolished following the addition of tetrodotoxin to the bath. In addition, perfusing the slice with a low Ca2+‐containing solution (0.5 mmCa2+–10 mmMg2+) also abolished the granule cell depolarization, confirming the synaptic origin of the event.5(S)‐Methyl‐4‐carboxyphenylglycine,l‐(+)‐2‐amino‐3‐phosphonopropionic acid, propranolol and atropine did not affect the granule cell depolarization, indicating that metabotropic glutamate receptors,β‐adrenergic receptors and muscarinic cholinergic receptors were not involved in generating the granule cell depolarizing synaptic response.6These findings indicate that, in the absence of both glutamatergic and GABAergic inputs, synchronous interneuronal activity can produce a depolarizing synaptic response in granule cells. The neurochemical responsible for the depolarization is currently under investigation.