The striatum is innervated by histaminergic fibers and expresses a high density of histamine H₃ receptors (H₃Rs), present on medium spiny neurons (MSNs) and corticostriatal afferents. In this study, in sagittal slices from the rat dorsal striatum, excitatory postsynaptic potentials (EPSPs) were recorded in MSNs after electrical stimulation of corticostriatal axons. The effect of H₃R activation and blockers of calcium and potassium channels was evaluated with the paired-pulse facilitation protocol. In the presence of the H₃R antagonist/inverse agonist clobenpropit (1 μM), the H₃R agonist immepip (1 μM) had no effect on the paired-pulse ratio (PPR), but in the absence of clobenpropit, immepip induced a significant increase in PPR, accompanied by a reduction in EPSP amplitude, suggesting presynaptic inhibition. The blockade of Ca_V2.1 (P/Q-type) channels with ω-agatoxin TK (400 nM) increased PPR and prevented the effect of immepip. The Ca_V2.2 (N-type) channel blocker ω-conotoxin GVIA (1 μM) also increased PPR, but did not occlude the immepip action. Functional K_IR3 channels are present in corticostriatal terminals, and in experiments in which immepip increased PPR, the K_IR3 blocker tertiapin-Q (30 nM) prevented the effect of the H₃R agonist. These results indicate that the presynaptic modulation by H₃Rs of corticostriatal synapses involves the inhibition of Ca_v2.1 calcium channels and the activation of K_IR3 potassium channels.

纹状体由组胺能纤维支配，并表达高密度的组胺 H ₃受体 (H ₃ Rs)，存在于中等棘神经元 (MSN) 和皮质纹状体传入神经上。在这项研究中，在大鼠背侧纹状体的矢状切片中，在对皮质纹状体轴突进行电刺激后，在 MSN 中记录了兴奋性突触后电位 (EPSP)。使用配对脉冲促进方案评估H _{3 R 激活和钙和钾通道阻滞剂的效果。}在 H ₃ R 拮抗剂/反向激动剂 clobenpropit (1 μM) 存在下，H ₃R 激动剂 immepip (1 μM) 对双脉冲比 (PPR) 没有影响，但在没有 clobenpropit 的情况下，immepip 诱导 PPR 显着增加，同时 EPSP 幅度降低，表明突触前抑制。用 ω-agatoxin TK (400 nM)阻断 Ca _V 2.1（P/Q 型）通道可增加 PPR 并阻止 immepip 的作用。Ca _V 2.2 (N-type) 通道阻滞剂 ω-芋螺毒素 GVIA (1 μM) 也增加了 PPR，但没有阻断 immepip 作用。功能性 K _IR 3 通道存在于皮质纹状体末端，在 immepip 增加 PPR 的实验中，K _IR 3 阻滞剂 tertiapin-Q (30 nM) 阻止了 H _3的作用R激动剂。这些结果表明H ₃ Rs 对皮质纹状体突触的突触前调节涉及Ca _{v 2.1 钙通道的抑制和K IR} 3 钾通道的激活。