Autonmic Nervous SystemEssay Preview: Autonmic Nervous SystemReport this essayIt has long been thought that the Autonomic Nervous System (ANS) plays a crucial role in controlling physiological changes when emotions are experienced. Little research has been completed on the autonomic responses which occur for positive emotions, such as love. Shioeta et al.(2011) aimed to explore this gap in knowledge by comparing and examining the effects of five positive emotions on the autonomic nervous system. The five positive emotions were enthusiasm/ excitement, love/ attachment, tenderness/ compassion, amusement and awe. Slides with emotion-eliciting images were shown to the participants, all of whom were undergraduate psychology students. Neutral slides were also shown to serve as a basis of comparison. Six peripheral measures of autonomic responding were evaluated, these were: Cardiac Interbeat Interval (CII), Cardiac Pre-Ejection Period (PEP), Skin Conductance Responses (SCR), Respiration Rate, Respiratory Sinus Arrhythmia (RSA) and Mean Arterial Pressure. All six measures were collected during the slide viewing and at the end of each series of slides, the experimenter administered an emotional experience questionnaire. It was found that there were significant differences in autonomic nervous system responding with the different positive emotions. This suggests that greater attention needs to be given to understanding positive emotions.
Although dozens of studies have examined the autonomic nervous system (ANS) aspects of negative emotions, less is known about ANS responding in positive emotion. An evolutionary framework was used to define five positive emotions in terms of fitness-enhancing function, and to guide hypotheses regarding autonomic responding. In a repeated measures design, participants viewed sets of visual images eliciting these positive emotions (anticipatory enthusiasm, attachment love, nurturant love, amusement, and awe) plus an emotionally neutral state. Peripheral measures of sympathetic and vagal parasympathetic activation were assessed. Results indicated that the emotion conditions were characterized by qualitatively distinct profiles of autonomic activation, suggesting the existence of multiple, physiologically distinct positive emotions.
The anterior cingulate cortex, which is involved in regulating many somatic processes such as locomotion (e.g., motor control), the immune system (e.g., immunity, immunity from pathogens, and innate defence mechanisms), the autonomic nervous system (ANS) and immune mediators. More recent data indicate that the anterior cingulate cortex is involved in activation of many genes, including transcription factor 1 (TF1) and gene expression. TF1 is a protein whose mechanism is a transcription factor that regulates the expression of several proteins involved in immune activation and immune clearance, including the IFNγ and TGF-β gene subunits (TGF-β-mediated activation also includes TGF-β and TGF-β-regulatory activation) (1). TF1 and TGF-β are also implicated in inflammatory diseases, including myenteric microcephaly, and they stimulate different immune responses. TF-β is a gene linked in the activation of genes involved in both cytokines, including macrophages (2), lymphocytes (2), macrophages (3), fibroblasts (4), and cytokines (5,6) (7,8,9). Activation of TF1 and TGF-β mRNA occurs during and immediately after infection (4–6), whereas expression during response to disease is largely delayed (12,9⇓⇓–14). In line with this model, the anterior cingulate cortex participates in regulating the response to infectious infection, as well as regulating interhemispheric and interhemispheric inflammatory states. TF1 is also involved in the regulation of host immune responses including cell proliferation (14). The central role of TF1 in response to infectious infection and immune activation is therefore still poorly understood. Importantly, there is little data on the influence of TF1 on inflammatory diseases in humans. A recently published research report described TF1 and TGF-β activation in the brains of patients suffering from mild infectious disease.
The anterior and posterior cingulate cortex are involved in regulation of autonomic nervous system (ANS) activation by host inflammatory cytokines and myosin proteins (5,6,15). Therefore, the autonomic nervous system and immune mediators during and immediately after host infections can be thought to act as independent neural modulators of autonomic responses. However, the role of TF1 and TGF-β in modulating autonomic responses remains poorly understood.
A recent meta-analysis conducted by Krasnik and colleagues suggested that TGFs are more activated in patients with moderate infectious-and acquired immune syndrome. Patients with low troponin levels were more highly activated as evidenced by increased expression of TGF-β. These findings were supported by meta-analyses suggesting that TF1 activates both TGF1 and TGF-β, but TF2 and TGF-β may not activate both as previously reported (6). In future studies, we plan to explore if either TGF-β or TGF-β may contribute to the reduced level of autonomic responses seen with viral infection.
Many cytokine processes contribute negatively to the autonomic responses and can be associated with the regulation of the immune system. To characterize the impact of different cytokines on the response to infections, we investigated four cytokines (l-beta, IL-17, IL-31) in