REGULATION OF GLUTAMATE AND ASPARTATE RELEASE FROM SLICES OF THE HIPPOCAMPAL CA1 AREA - EFFECTS OF ADENOSINE AND BACLOFEN
REGULATION OF GLUTAMATE AND ASPARTATE RELEASE FROM SLICES OF THE HIPPOCAMPAL CA1 AREA - EFFECTS OF ADENOSINE AND BACLOFEN
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DOI：
10.1111/j.1471-4159.1988.tb01123.x
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发表时间：
1988-11-01
影响因子：
4.7
通讯作者：
NADLER, JV
中科院分区：
文献类型：
--
作者：
BURKE, SP;NADLER, JV
谷氨酸和/或天冬氨酸可能是从大鼠海马结构CA 1区CA 3衍生的Schaffer侧支、连合和同侧联合纤维的突触终末释放的递质。使用CA 1区域的切片来测试腺苷和γ-腺苷的作用。氨基丁酸（GABA）相关化合物对谷氨酸和天冬氨酸从该投射中释放的影响。在这些实验的条件下，50 mM K+诱发的谷氨酸和天冬氨酸的释放是90%以上的Ca 2+依赖性的，并且主要来源于CA 3-衍生途径。腺苷减少K+诱发释放谷氨酸和天冬氨酸的最大约60%，但不影响释放GABA。该作用被1 μ M 8-苯基茶碱逆转。腺苷类似物的效力顺序如下：L-N6-苯基异丙基-腺苷> N6-环己基腺苷> D-N6-苯基异丙基腺苷。2-氯腺苷>腺苷. mchgt. 5“-N-乙基羧酰胺腺苷。8-苯茶碱（10 μ M）本身增强谷氨酸/天冬氨酸释放，而单独的双嘧达莫抑制释放。这些结果支持的观点，腺苷抑制传输Schaffer侧副连合同侧关联突触主要是通过减少发射器的释放，这些影响涉及激活A1受体。腺苷、L-N6-苯基异丙基腺苷、8-苯基异丙基腺苷和8-苯基茶碱都不影响由10 μ M藜芦啶诱发的谷氨酸或天冬氨酸的释放。腺苷化合物对K+和藜芦碱引起的释放的不同影响表明，A1受体激活抑制Ca 2+通过电压敏感性通道流入或干扰一个步骤后，Ca 2+进入耦合到电压敏感性Ca 2+通道在一个强制性的方式。无论是巴氯芬还是任何其他对GABAB或GABAA受体有活性的药物都不会影响由升高的K+或藜芦碱引起的谷氨酸或天冬氨酸释放。因此，或者巴氯芬不会通过抑制递质释放来抑制这些突触的传递，或者巴氯芬以一种当使用化学去极化剂时无法检测到的方式来抑制传递。
Glutamate and/or aspartate is the probable transmitter released from synaptic terminals of the CA3-derived Schaffer collateral, commissural, and ipsilateral associational fibers in area CA1 of the rat hippocampal formation. Slices of the CA1 area were employed to test the effects of adenosine and .gamma.-aminobutyrate (GABA)-related compounds on the release of glutamate and aspartate from this projection. Under the conditions of these experiments, the release of glutamate and aspartate evoked by 50 mM K+ was more than 90% Ca2+-dependent and originated predominantly from the CA3-derived pathways. Adenosine reduced the K+-evoked release of glutamate and aspartate by a maximum of about 60%, but did not affect the release of GABA. This action was reversed by 1 .mu.M 8-phenyltheophylline. The order of potency for adenosine analogues was as follows: L-N6-phenylisopropyl-adenosine > N6-cyclohexyladenosine > D-N6-phenylisopropyladenosine .simeq. 2-chloroadenosine > adenosine .mchgt. 5''-N-ethylcarboxamidoadenosine. 8-Phenyltheophylline (10 .mu.M) by itself enhanced glutamate/aspartate release, whereas dipyridamole alone depressed release. These results support the view that adenosine inhibits transmission at Schaffer collateral-commissural-ipsilateral associational synapses mainly by reducing transmitter release and that these effects involve the activation of an A1 receptor. Neither adenosine, L-N6-phenylisopropyladenosine, nor 8-phenylisopropyladenosine, nor 8-phenyltheophylline affected the release of glutamate or aspartate evoked by 10 .mu.M veratridine. The differing effects of adenosine compounds on release evoked by K+ and veratridine suggest that A1 receptor activation either inhibits Ca2+ influx through the voltage-sensitive channels or interferes with a step subsequent to Ca2+ entry that is coupled to the voltage-sensitive Ca2+ channels in an obligatory fashion. Neither baclofen nor any other agent active at GABAB or GABAA receptors affected glutamate or aspartate release evoked by elevated K+ or veratridine. Therefore, either baclofen does not inhibit transmission at these synapses by depressing transmitter release or else it does so in a way that cannot be detected when a chemical depolarizing agent is employed.