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Pain. 2001 May;92(1-2):19-27.

Vagal afferent signaling of a gastric mucosal acid insult to medullary, pontine, thalamic, hypothalamic and limbic, but not cortical, nuclei of the rat brain.

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  • 1Department of Experimental and Clinical Pharmacology, University of Graz, Universit√§tsplatz 4, A-8010, Graz, Austria.


Although gastric acid is a factor in upper abdominal pain, the signaling and processing of a gastric mucosal acid insult within the brain are not known. This study examined which nuclei in the rat brain respond to challenge of the gastric mucosa by a noxious concentration of hydrochloric acid (HCl) and whether the central input is carried by vagal afferent neurons. Activation of neurons in the brain was mapped by in situ hybridization autoradiography of messenger ribonucleic acid (mRNA) for the immediate early gene c-fos 45 min after intragastric administration of saline or HCl. Following intragastric HCl (0.5 M) challenge, many neurons in the nucleus tractus solitarii, lateral parabrachial nucleus, thalamic and hypothalamic paraventricular nucleus, supraoptic nucleus, central amygdala and medial/lateral habenula expressed c-fos mRNA as compared to intragastric treatment with saline (0.15 M). However, c-fos transcription in the insular cortex was not enhanced by the gastric acid insult. Hypertonic saline (0.5 M) caused only a minor expression of c-fos mRNA in the hypothalamus and amygdala. The acid-evoked c-fos induction in subcortical nuclei was depressed by at least 80% five days after bilateral subdiaphragmatic vagotomy. Collectively, these observations indicate that vagal afferent input from the acid-threatened gastric mucosa does not reach the insular cortex but leads to activation of subcortical brain nuclei that are involved in emotional, behavioral, neuroendocrine, autonomic and antinociceptive reactions to a noxious stimulus.

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