Lalonde Robert, Strazielle Catherine
Laboratory of Stress, Immunity, Pathogens (EA7300), Medical School, University of Lorraine, 54500, Vandœuvre-les-Nancy, France.
CHRU Nancy, Vandœuvre-les-Nancy, France.
Behav Genet. 2022 May;52(3):158-169. doi: 10.1007/s10519-022-10102-1. Epub 2022 Apr 28.
First described by Boissier and Simon in (Ther Recreat J 17:1225-1232, 1962), the hole-board has become a recognized test of anxiety and spatial memory. Benzodiazepines acting at the GABA-BZD site increase hole-pokes in rats and mice, indicating a loss in behavioral inhibition concordant with the behavior of mutant mice deficient in the GABA transporter. Hole-poking also depends on arousal mechanisms dependent on dopaminergic transmission, as indicated by drug and null mutant studies. In addition, the behavior is modified in natural and null mutants affecting the cerebellum as well as null mutants affecting neuropeptides, growth factors, cell adhesion, and inflammation. Further research is required to determine convergences between genetic and pharmacological effects.
博伊斯尔和西蒙于1962年（《治疗与康复杂志》17:1225 - 1232）首次描述了空板试验，该试验已成为一种公认的焦虑和空间记忆测试方法。作用于GABA - BZD位点的苯二氮䓬类药物会增加大鼠和小鼠的探洞次数，这表明行为抑制能力丧失，与GABA转运体缺陷的突变小鼠的行为一致。药物和基因敲除突变研究表明，探洞行为还依赖于多巴胺能传递的唤醒机制。此外，在影响小脑的天然突变体和基因敲除突变体以及影响神经肽、生长因子、细胞黏附及炎症的基因敲除突变体中，该行为都会发生改变。需要进一步研究以确定遗传效应和药理效应之间的共同作用机制。
