THE EFFECT OF MEDIAL FRONTAL-CORTEX LESIONS ON CARDIOVASCULAR CONDITIONED EMOTIONAL RESPONSES IN THE RAT

Citation
Rj. Frysztak et Ej. Neafsey, THE EFFECT OF MEDIAL FRONTAL-CORTEX LESIONS ON CARDIOVASCULAR CONDITIONED EMOTIONAL RESPONSES IN THE RAT, Brain research, 643(1-2), 1994, pp. 181-193
Citations number
69
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00068993
Volume
643
Issue
1-2
Year of publication
1994
Pages
181 - 193
Database
ISI
SICI code
0006-8993(1994)643:1-2<181:TEOMFL>2.0.ZU;2-C
Abstract
The effect of ventral medial frontal cortex (MFC) lesions on heart rat e and blood pressure during conditioned emotional responses (CER) was investigated. Male Sprague-DawIey rats were divided into two groups: M FC-lesioned rats (n = 11) sustained bilateral lesions of the infralimb ic and ventral prelimbic regions of the MFC via microinjection of the neurotoxin N-methyl-D-aspartate; Controls (n = 13) received sterile sa line. Following a 2-week recovery period, all animals were trained; on e of two tones served as the conditioned stimulus (CS) and a 2 mA foot shock served as the unconditioned stimulus (US). The CS+ tone was cons istently paired with the US, while the CS- tone was randomly paired wi th the US. Heart rate and blood pressure were recorded during CS+ and CS- presentations before and after administration of the following pha rmacological agents: atropine, atenolol, and atropine + atenolol. All animals responded to the CS+ with increased BP compared to baseline; t he increase was not significantly different between groups. Controls r esponded to the CS+ with increased HR, while MFC-lesioned animals disp layed a bimodal HR response which was not significantly different from baseline, but was significantly different from Controls. Pharmacologi cal blockade of the HR response revealed coactivation of the sympathet ic and parasympathetic nervous systems during the CS+, with a signific ant decrease (52%) in the sympathetic tachycardia component of the CS HR response in MFC-lesioned rats as compared to Controls; the parasym pathetic bradycardia component was not altered by MFC lesions. In all cases, CS- responses were smaller than the CS+ responses. Pharmacologi cal analysis revealed that the CS- HR response was mediated by the sym pathetic component only, which was also significantly reduced in MFC-l esioned 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 impl ies that the MFC is necessary for complete sympathetic activation of c ardiovascular responses to both severely and mildly stressful stimuli. The role of the MFC in emotion is also discussed.