大麻二酚（cannabidiol, CBD）為大麻的主要成份之一，其不會產生酬賞效果，也不會造成精神症狀。此外，大麻二酚的毒性和造成死亡比率皆很低，因此具備臨床治療諸多疾病之潛力。舉例來說，先前研究指出大麻二酚可以減緩癌症、藥物濫用、創傷後壓力症候群（post-traumatic stress disorder, PTSD）、憂鬱、焦慮和癲癇。美國食品藥物管理局（Food and Drug Administration, FDA）於 2018 年正式批准大麻二酚做為合法治療雷葛氏症候群（Lennox-Gastaut syndrome）和卓飛症候群（Dravet syndrome）兩種兒童常見癲癇的藥物。此外，過去有文獻指出大麻二酚可以防止癲癇、利血平（reserpine）、腦膜炎或敗血症所引發的記憶損害。然而，過去多數研究大麻二酚對於恐懼記憶的作用都是使用情境恐懼制約（contextual fear conditioning, CFC）作業，鮮少使用抑制性逃避行為（inhibitory avoidance, IA）作業來檢視大麻二酚如何調節不同的嫌惡記憶歷程。因此，本研究旨在探討大麻二酚對抑制性逃避記憶再穩固化及穩固化歷程之調節。首先，我們發現大麻二酚依使用劑量不同而損害抑制性逃避記憶的再穩固化歷程，此一損害效果會被 Trk 受體拮抗劑（K252a）反轉。在記憶重新激活後給予大麻二酚注射會顯著地降低海馬回中腦源性神經營養因子前體蛋白（proBDNF）的表現量，但不影響腦源性神經營養因子（mature BDNF）。接著，我們發現有效損害記憶再穩固化之大麻二酚劑量並不影響抑制性逃避記憶之穩固化歷程。儘管如此，大麻二酚反轉了茴香黴素（anisomycin, ANI） 對記憶穩固化所造成的損害效果，而使用 K252a 可以阻斷大麻二酚反轉茴香黴素的損害效果。除此之外，茴香黴素顯著性地降低了海馬回中的 mature BDNF 表現量， 這個現象亦可被大麻二酚反轉。因此，我們的結果暗示了大麻二酚對於抑制性逃避記憶再穩固化的損害效果與降低海馬回的 proBDNF 的表現量有關；然而大麻二酚反轉茴香黴素所引發記憶穩固化的損害效果與反轉茴香黴素降低海馬回的 mature BDNF 表現量有關。總結上述實驗結果，大麻二酚調節抑制性逃避記憶再穩固化和記憶穩固化分別與 proBDNF 和 BDNF 訊息傳遞路徑相關。因此，大麻二酚作為記憶相關疾病的臨床治療之應用需更謹慎看待。

Cannabidiol (CBD) is one of the major ingredients of marijuana. CBD is not rewarding and does not induce psychoactive effects. Moreover, CBD causes very low toxicity and fatality and thus has great potential for development as a therapeutic strategy for many diseases. For example, prior researches suggest that CBD can alleviate cancers, drug abuse, post-traumatic stress disorder (PTSD), depression, anxiety, and seizure. The Food and Drug Administration (FDA) in the United States approves CBD as a prescription medicine to treat seizures associated with Lennox-Gastaut syndrome and Dravet syndrome, in 2018. Moreover, CBD has been shown to prevent memory impairment induced by seizure, reserpine, pneumococcal meningitis, or sepsis. While most studies have examined CBD's effect on fear memory in the contextual fear conditioning test, few studies investigated how CBD modulates different memory processes in the inhibitory avoidance (IA) task. Therefore, this study aimed to investigate the modulatory effects of CBD on IA memory reconsolidation and consolidation processes. We first showed that CBD dose-dependently impaired IA memory reconsolidation, which was reversed by the Trk receptor antagonist K252a. CBD administered after the memory reactivation significantly decreased the proBDNF protein levels without changing the mature BDNF protein levels in the hippocampus. Second, we found that the effective dose of CBD for IA memory reconsolidation did not affect IA memory consolidation. Nevertheless, CBD reversed the ANI-induced impairment of IA memory consolidation, which was also blocked by K252a. ANI significantly decreased the hippocampal mature BDNF protein levels, which was reversed by CBD. Therefore, our results suggest that CBD's impairing effect of IA memory reconsolidation is correlated with the decrease of the proBDNF protein levels, while CBD's reversing effect on the ANI-induced deficit of memory consolidation is correlated with the reversing effect on the ANI-reduced mature BDNF protein levels in the mouse hippocampus. In summary, CBD may modulate IA memory reconsolidation and IA memory consolidation through the proBDNF and BDNF signaling pathways. Hence, the clinical application of CBD as a therapeutic strategy for memory-associated disorders requires discretion.

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