Frysztak R J, Neafsey E J
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, Maywood, IL 60153.
Brain Res. 1994 Apr 18;643(1-2):181-93. doi: 10.1016/0006-8993(94)90024-8.
The effect of ventral medial frontal cortex (MFC) lesions on heart rate and blood pressure during conditioned emotional responses (CER) was investigated. Male Sprague-Dawley rats were divided into two groups: MFC-lesioned rats (n = 11) sustained bilateral lesions of the infralimbic and ventral prelimbic regions of the MFC via microinjection of the neurotoxin N-methyl-D-aspartate; Controls (n = 13) received sterile saline. Following a 2-week recovery period, all animals were trained; one of two tones served as the conditioned stimulus (CS) and a 2 mA footshock served as the unconditioned stimulus (US). The CS+ tone was consistently paired with the US, while the CS- tone was randomly paired with the US. Heart rate and blood pressure were recorded during CS+ and CS- presentations before and after administration of the following pharmacological agents: atropine, atenolol, and atropine + atenolol. All animals responded to the CS+ with increased BP compared to baseline; the increase was not significantly different between groups. Controls responded to the CS+ with increased HR, while MFC-lesioned animals displayed a bimodal HR response which was not significantly different from baseline, but was significantly different from Controls. Pharmacological blockade of the HR response revealed coactivation of the sympathetic and parasympathetic nervous systems during the CS+, with a significant decrease (52%) in the sympathetic tachycardia component of the CS+ HR response in MFC-lesioned rats as compared to Controls; the parasympathetic bradycardia component was not altered by MFC lesions. In all cases, CS- responses were smaller than the CS+ responses. Pharmacological analysis revealed that the CS- HR response was mediated by the sympathetic component only, which was also significantly reduced in MFC-lesioned animals as compared to Controls. This significant reduction in the sympathetically mediated HR component of both the reinforced CER (CS+) and the unreinforced CER (CS-) following ventral MFC lesions implies that the MFC is necessary for complete sympathetic activation of cardiovascular responses to both severely and mildly stressful stimuli. The role of the MFC in emotion is also discussed.
研究了腹内侧前额叶皮质(MFC)损伤对条件性情绪反应(CER)期间心率和血压的影响。将雄性Sprague-Dawley大鼠分为两组:MFC损伤组(n = 11)通过微量注射神经毒素N-甲基-D-天冬氨酸对MFC的下缘和腹侧前边缘区域进行双侧损伤;对照组(n = 13)注射无菌生理盐水。经过2周的恢复期后,对所有动物进行训练;两种音调之一作为条件刺激(CS),2 mA的足部电击作为非条件刺激(US)。CS+音调始终与US配对,而CS-音调随机与US配对。在给予以下药物制剂之前和之后,在呈现CS+和CS-期间记录心率和血压:阿托品、阿替洛尔以及阿托品+阿替洛尔。与基线相比,所有动物对CS+的反应均表现为血压升高;两组之间的升高无显著差异。对照组对CS+的反应表现为心率升高,而MFC损伤动物表现出双峰心率反应,与基线无显著差异,但与对照组有显著差异。对心率反应的药理学阻断显示,在CS+期间交感神经系统和副交感神经系统共同激活,与对照组相比,MFC损伤大鼠CS+心率反应的交感心动过速成分显著降低(52%);副交感心动过缓成分未因MFC损伤而改变。在所有情况下,CS-反应均小于CS+反应。药理学分析显示,CS-心率反应仅由交感成分介导,与对照组相比,MFC损伤动物的该成分也显著降低。腹侧MFC损伤后,强化CER(CS+)和未强化CER(CS-)的交感介导心率成分均显著降低,这意味着MFC对于心血管系统对严重和轻度应激刺激的反应进行完全交感激活是必要 的。还讨论了MFC在情绪中的作用。