The Features of Neural Mechanisms Underlying Visceral Pain Processing in the Basolateral Amygdala of Rats with Post-Inflammatory or Stress-Induced Hyperalgesia

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Abstract

Increased intestinal pain sensitivity (intestinal hyperalgesia) may be a consequence of intestinal inflammation or experienced stress. Both conditions are thought to be associated with a dysfunction of the basolateral amygdala (BLA), since they are accompanied by it’s neurochemical and molecular rearrangements. However, the accompanying changes in the neuronal mechanisms of BLA-executed control of visceral nociception and their possible specificity for post-inflammatory and stress-induced hyperalgesia remain unclear. The aim of the study was to compare the changes in the functional properties of visceral pain-responsive BLA neurons and their modulation by the infralimbic area of the medial prefrontal cortex (IL) that occur after intestinal inflammation or stress. The work was performed on male Wistar rats: 1) control, 2) subjected to experimental colitis and 3) subjected to prolonged emotional-painful stress. In animals from different groups, in awake state the intestinal hyperalgesia was assessed by recording the noxious colorectal distension (CRD)-induced visceromotor response, and under general anesthesia the microelectrode recording of the background impulse activity of BLA neurons and their responses to CRD before and after IL electrical stimulation was performed. It was found that rats from the postcolitis and stressed groups demonstrate intestinal hyperalgesia, which is more pronounced after stress. The postcolitis state is associated with a decrease, and the stressed state – with an increase in the background activity frequency of BLA neurons. It was shown for the first time that in both cases the BLA neurons that respond to CRD with excitation or inhibition increase their reactivity to the stimulating action of IL. The postcolitis period is characterized by an increase in the IL activating effect on the CRD-inhibited BLA neurons, whereas the poststress period is characterized by an increase in the IL-induced stimulation of excitated and inhibited nociceptive cells. The neuronal alterations revealed in the BLA may lead to the disturbances in the amygdala-executed control of the sensory and emotional components of visceral pain that are inherent to postinflammatory or stress-induced intestinal hyperalgesia, being thus a specific target for the treatment of such conditions in the clinic.

About the authors

O. A. Lyubashina

Pavlov Institute of Physiology of the Russian Academy of Sciences

Email: lyubashinaoa@infran.ru
St. Petersburg, Russia

D. A. Mehilyainen

Pavlov Institute of Physiology of the Russian Academy of Sciences

St. Petersburg, Russia

I. B. Sivachenko

Pavlov Institute of Physiology of the Russian Academy of Sciences

St. Petersburg, Russia

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