Proximal colon distension induces Fos expression in oxytocin-, vasopressin-, CRF- and catecholamines-containing neurons in rat brain

Abstract

Little is known about the chemical coding of the brain neuronal circuitry activated by nociceptive signals of visceral origin. We characterized brain nuclei activated during isovolumetric phasic distension of the proximal colon (10 ml, 30 s on/off for 10 min) in conscious male rats, using Fos as a marker of neuronal activation and dual immunohistochemistry to visualize co-localization of Fos expression and oxytocin (OT), arginine-vasopressin (AVP), corticotrophin-releasing factor (CRF) or tyrosine hydroxylase (TH). Proximal colon distension, compared with sham distension, induced a robust increase in Fos-like immunoreactive (IR) neurons in the paraventricular nucleus (PVN), supraoptic nucleus (SON) and accessory neurosecretory nuclei of the hypothalamus, nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM), and to a lower extent, in the locus coeruleus (LC) and Barrington nucleus. Fos-like immunoreactivity in the PVN after colon distension of identified in 81% of OT-IR, 18% AVP-IR and 18% CRF-IR neurons, while in the SON it represented 36% of OT-IR and 16% AVP-IR. Catecholaminergic cell groups in the pons (LC) and medulla (VLM, NTS) were also activated by proximal colon distension. Of the TH-IR neurons in VLM and NTS, 74% and 42% respectively were double labeled. These results indicate that colon distension stimulates OT-, AVP- and CRF-containing hypothalamic neurons, likely involved in the integration of colonic sensory information to modulate autonomic outflow and pain-related responses. Activation of medullary catecholaminergic centers might reflect the afferent and efferent limbs of the functional responses associated to visceral pain.

The role of catecholaminergic neurons in the hypothalamus and medullary visceral zone in response to restraint water-immersion stress in rats

“…Fos-IR nuclei in the VLM were found in the entire rostral-caudal column including the C1/A1 cell groups, and the number of the Fos-IR nuclei was significantly different in nonstressed rats and rats exposed to RWIS for 1 h, in agreement with results for proximal colon distension in rats [20].…”

“…Many previous studies have found that CA-neurons of the MVZ were involved in processing and conducting visceral nociceptive information. Proximal colon distension induced Fos in approximately 74 and 42% of CA-neurons in the VLM and the NTS, respectively [20]. RWIS induced substantial Fos protein expression in noradrenergic neurons of the MVZ (A1/A2 cell groups) [43].…”

“…Osmotic stimulus (i.p. hypertonic saline) or immobilization [19] and proximal colon distension [20] evoked Fos protein expression in CA neurons in specific brain nuclei. The PVN contains a dense network of CA terminals originating in the medullary visceral zone CA-cell groups, for example the NTS, the ventrolateral medulla (VLM), and locus coeruleus (LC) [15,16,21,22].…”

Lactobacillus reuteri ingestion prevents hyperexcitability of colonic DRG neurons induced by noxious stimuli

“…This deduction is consistent with the results published by others who found no evidence of an increase in MPO levels or histological damage or inflammatory infiltrate after 1-h repetitive CRD at 60 mmHg in rat (22) or mouse (24) colon. Similarly, Wang et al (48) reported that repeated CRD in healthy rats at 78 -100 mmHg activated certain hypothalamic brain nuclei 1 h after CRD cessation; no inflammation was reported that might have evoked the brain activity.…”

The Irritable Bowel Syndrome: How Stress Can Affect the Amygdala Activity and the Brain-Gut Axis

“…The use of C-Fos expression as a marker of neuronal activation has shown that somatovisceral Sinniger, et al 2004;2005), and visceral (Wang, et al 2009) pain as well as stress-or abdominal surgery-induced GI disturbances (Bonaz and Tache 1994a;1994b;1997;Bonaz and Rivest 1998) and colitis ) induced the activation of the amygdala. In addition, the amygdala is one of the central areas from where digestive sensations are elicited in epileptic patients (Mulak, et al 2008) during intracerebral electrical stimulations.…”