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Serotonin in Adolescence: Role in Behavioral Inhibition

机译：血清素在青春期：在行为抑制中的作用

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Background: Adolescents are impulsive and novelty seeking, normal behaviors that engage the adolescents in the world outside the home but also increase involvement in risky behaviors. Immaturity of frontal cortex circuits involved in executive function may be the main reason for this behavioral profile. As serotonergic innervation of the frontal cortex is critical for behavioral inhibition, we investigated the hypothesis that immaturity in serotonergically-mediated behavioral inhibition contributes to the adolescent behavioral profile.Design: To investigate the role of serotonergic innervation, we evaluated the behavioral and neurochemical effects of fluoxetine in adolescent (PN 28) and adult male rats (PN 70). Rats were treated with fluoxetine (0, 10 mg/kg) and tested in the light/dark anxiety test. In addition, the ability of fluoxetine (0, 2.5, 5 and 10 mg/kg at hourly intervals) to increase extracellular serotonin in the prefrontal cortex was measured using microdialysis. Finally, the ability of fluoxetine (10 mg/kg) to activate the immediate early gene c-fos relative to vehicle control was determined to investigate downstream effects of the increase in extracellular serotonin.Results: Fluoxetine did not inhibit behavior in the light/dark anxiety test in adolescents relative to vehicle control, but it did so in adults. However, the neurochemical effects of fluoxetine were comparable in adolescents and adults: fluoxetine elicited comparable increases in extracellular 5-HT in adolescents and adults. To examine the contribution of postsynaptic mechanisms, we evaluated the behavioral effects of the 5 HT1a agonist 8-OHDPAT and the 5 HT2 agonist mCPP. mCPP (0.5 or 1 mg/kg) produced comparable behavioral inhibition relative to vehicle control in adolescents and adults, but 8-OHDPAT (0.25, 0.5 mg/kg) did not. To determine if neural circuit activation by postsynaptic mechanisms was functional in adolescents, we tested the ability of fluoxetine (10 mg/kg) and 8-OHDPAT (0.5 mg/kg) to activate C-fos. Neither drug activated C-fos in amygdala or PVN of the hypothalamus.Conclusions: These results suggest that cortical inhibition of stress circuitry is immature in adolescents.
机译：背景：青少年是冲动和寻求新奇的，正常的行为，这种行为使世界各地的青少年不在家中，但也增加了对危险行为的参与。执行功能所涉及的额叶皮层回路的不成熟可能是这种行为特征的主要原因。由于额叶皮质的血清素能神经支配对于行为抑制至关重要，因此我们研究了血清素介导的行为抑制的不成熟有助于青春期行为特征的假说。设计：为了研究血清素能神经支配的作用，我们评估了行为和氟西汀对青少年（PN 28）和成年雄性大鼠（PN 70）的神经化学作用。用氟西汀（0，10 mg / kg）治疗大鼠，并在明/暗焦虑测试中进行测试。此外，使用微透析法测定了氟西汀（每小时间隔为0、2.5、5和10 mg / kg）增加额叶前额叶皮层中细胞外血清素的能力。最后，确定氟西汀（10 mg / kg）激活相对于运载体对照的立即早期基因c-fos的能力，以调查细胞外血清素增加的下游影响。相对于媒介物对照，青少年进行了明/暗焦虑测试，但成年人进行了。然而，氟西汀的神经化学作用在青少年和成年人中是可比的：氟西汀在青少年和成年人中引起细胞外5-HT的可比增加。若要检查突触后机制的贡献，我们评估了5 HT1a激动剂8-OHDPAT和5 HT2激动剂mCPP的行为效果。与青少年和成人的媒介物对照相比，mCPP（0.5或1 mg / kg）产生了可比的行为抑制作用，但8-OHDPAT（0.25，0.5 mg / kg）却没有。为了确定通过突触后机制激活的神经回路在青少年中是否起作用，我们测试了氟西汀（10 mg / kg）和8-OHDPAT（0.5 mg / kg）激活C-fos的能力。结论：这些结果表明，皮质对应激回路的抑制在青少年中尚不成熟。这两种药物均未激活杏仁核或下丘脑PVN中的C-fos。

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