Neuroscience Program, Dominican University, River Forest, Illinois 60305.
Neuroscience Program, Dominican University, River Forest, Illinois 60305
eNeuro. 2024 Apr 5;11(4). doi: 10.1523/ENEURO.0516-23.2024. Print 2024 Apr.
Long-term sensitization in is accompanied by a persistent up-regulation of mRNA encoding the peptide neurotransmitter Phe-Met-Arg-Phe-amide (FMRFa), a neuromodulator that opposes the expression of sensitization through activation of the arachidonic acid second-messenger pathway. We completed a preregistered test of the hypothesis that FMRFa plays a critical role in the forgetting of sensitization. received long-term sensitization training and were then given whole-body injections of vehicle (= 27), FMRFa (= 26), or 4-bromophenacylbromide (4-BPB; = 31), a phospholipase inhibitor that prevents the release of arachidonic acid. FMRFa produced no changes in forgetting. 4-BPB decreased forgetting measured 6 d after training [ = 0.55 95% CI(0.01, 1.09)], though the estimated effect size is uncertain. Our results provide preliminary evidence that forgetting of sensitization may be a regulated, active process in , but could also indicate a role for arachidonic acid in stabilizing the induction of sensitization.
长期敏感化伴随着编码肽神经递质苯丙氨酸-甲硫氨酸-精氨酸-苯丙氨酸酰胺(FMRFa)的 mRNA 的持续上调,FMRFa 是一种神经调质,通过激活花生四烯酸第二信使途径来对抗敏感化的表达。我们对 FMRFa 在敏感化遗忘中起关键作用的假设进行了预先登记测试。接受长期敏感化训练的大鼠随后接受全身注射载体(= 27)、FMRFa(= 26)或 4-溴苯乙酰溴(4-BPB;= 31),4-BPB 是一种阻止花生四烯酸释放的磷脂酶抑制剂。FMRFa 对遗忘没有影响。4-BPB 降低了训练 6 天后的遗忘[= 0.55 95% CI(0.01,1.09)],尽管估计的效应大小不确定。我们的结果初步表明,敏感化的遗忘可能是一种受调节的主动过程,但也可能表明花生四烯酸在稳定敏感化诱导中起作用。