The effect of medial frontal cortex lesions on cardiovascular conditioned emotional responses in the rat.
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.
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, Maywood, IL 60153.
R J
RJ
Frysztak
E J
EJ
Neafsey
D000161:Acoustic Stimulation; D000818:Animals; D001262:Atenolol / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D001931:Brain Mapping; D003213:Conditioning, Psychological; D004597:Electroshock; D004644:Emotions; D005625:Frontal Lobe / Q000187:drug effects / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects; D007263:Infusions, Parenteral; D008032:Limbic System / Q000502:physiology; D008297:Male; D016202:N-Methylaspartate / Q000008:administration & dosage / Q000633:toxicity*; D009498:Neurotoxins / Q000008:administration & dosage / Q000633:toxicity; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors
D009498:Neurotoxins; D001262:Atenolol; D016202:N-Methylaspartate; D001285:Atropine