Fujiwara-Tsukamoto Y, Isomura Y, Nambu A, Takada M
Department of System Neuroscience, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan.
Neuroscience. 2003;119(1):265-75. doi: 10.1016/s0306-4522(03)00102-7.
GABA, which generally mediates inhibitory synaptic transmissions, occasionally acts as an excitatory transmitter through intense GABA(A) receptor activation even in adult animals. The excitatory effect results from alterations in the gradients of chloride, bicarbonate, and potassium ions, but its functional role still remains a mystery. Here we show that such GABAergic excitation participates in the expression of seizure-like rhythmic synchronization (afterdischarge) in the mature hippocampal CA1 region. Seizure-like afterdischarge was induced by high-frequency synaptic stimulation in the rat hippocampal CA1-isolated slice preparations. The hippocampal afterdischarge was completely blocked by selective antagonists of ionotropic glutamate receptors or of GABA(A) receptor, and also by gap-junction inhibitors. In the CA1 pyramidal cells, oscillatory depolarizing responses during the afterdischarge were largely dependent on chloride conductance, and their reversal potentials (average -38 mV) were very close to those of exogenously applied GABAergic responses. Moreover, intracellular loading of the GABA(A) receptor blocker fluoride abolished the oscillatory responses in the pyramidal cells. Finally, the GABAergic excitation-driven afterdischarge has not been inducible until the second postnatal week. Thus, excitatory GABAergic transmission seems to play an active functional role in the generation of adult hippocampal afterdischarge, in cooperation with glutamatergic transmissions and possible gap junctional communications. Our findings may elucidate the cellular mechanism of neuronal synchronization during seizure activity in temporal lobe epilepsy.
γ-氨基丁酸(GABA)通常介导抑制性突触传递,但即使在成年动物中,它偶尔也会通过强烈激活GABA(A)受体而充当兴奋性递质。这种兴奋作用源于氯离子、碳酸氢根离子和钾离子梯度的改变,但其功能作用仍然是个谜。在此,我们表明这种GABA能兴奋参与了成熟海马CA1区癫痫样节律同步化(后放电)的表达。在大鼠海马CA1区分离脑片标本中,高频突触刺激诱发了癫痫样后放电。海马后放电被离子型谷氨酸受体或GABA(A)受体的选择性拮抗剂以及缝隙连接抑制剂完全阻断。在CA1锥体细胞中,后放电期间的振荡性去极化反应很大程度上依赖于氯离子电导,其反转电位(平均-38 mV)与外源性GABA能反应的反转电位非常接近。此外,GABA(A)受体阻滞剂氟化物的细胞内加载消除了锥体细胞中的振荡反应。最后,直到出生后第二周,GABA能兴奋驱动的后放电才能够被诱发。因此,兴奋性GABA能传递似乎在成年海马后放电的产生中与谷氨酸能传递和可能的缝隙连接通讯协同发挥积极的功能作用。我们的发现可能阐明颞叶癫痫发作活动期间神经元同步化的细胞机制。