High aggression is often linked to lowered serotonin (5-HT) neurotransmission. Although this may hold for high aggression as a trait characteristic of an individual, serotonergic activity is probably increased during performance of aggressive behavior. To test this hypothesis, first, the 5-HT1A agonist alnespirone and gamma aminobutyric acid-A agonist muscimol were administered into the dorsal raphe nucleus. These treatments, which inhibit 5-HT neuronal activity, were shown to decrease performance of aggressive behavior. Second, after a resident-intruder test, the activation of 5-HT neurons (measured by c-fos expression) was increased in high-aggressive rats, compared with low-aggressive rats or control rats that were not subjected to a social confrontation. Results show that performance of aggressive behavior increases 5-HT neuronal activity and that preventing this activation inhibits expression of aggressive behavior.

. CCK enhances response to gastric distension by acting on capsaicin-insensitive vagal afferents. Am J Physiol Regul Integr Comp Physiol 289: R695-R703, 2005. First published May 19, 2005 doi:10.1152/ajpregu.00809.2004.-Capsaicin treatment destroys vagal afferent C fibers and markedly attenuates reduction of food intake and induction of hindbrain Fos expression by CCK. However, both anatomical and electrophysiological data indicate that some gastric vagal afferents are not destroyed by capsaicin. Because CCK enhances behavioral and electrophysiological responses to gastric distension in rats and people, we hypothesized that CCK might enhance the vagal afferent response to gastric distension via an action on capsaicin-insensitive vagal afferents. To test this hypothesis, we quantified expression of Fos-like immunoreactivity (Fos) in the dorsal vagal complex (DVC) of capsaicin-treated (Cap) and control rats (Veh), following gastric balloon distension alone and in combination with CCK injection. In Veh rats, intraperitoneal CCK significantly increased DVC Fos, especially in nucleus of the solitary tract (NTS), whereas in Cap rats, CCK did not significantly increase DVC Fos. In contrast to CCK, gastric distension did significantly increase Fos expression in the NTS of both Veh and Cap rats, although distension-induced Fos was attenuated in Cap rats. When CCK was administered during gastric distension, it significantly enhanced NTS Fos expression in response to distension in Cap rats. Furthermore, CCK's enhancement of distension-induced Fos in Cap rats was reversed by the selective CCK-A receptor antagonist lorglumide. We conclude that CCK directly activates capsaicin-sensitive C-type vagal afferents. However, in capsaicin-resistant A-type afferents, CCK's principal action may be facilitation of responses to gastric distension.Fos; dorsal vagal complex; C fibers; A fibers VAGAL AFFERENT NEURONS THAT detect gastric distension play an important role in the process of satiation for food and subsequent meal termination (for review, see Ref. 28). However, during ingestion of a normal meal, gastric distension does not occur in the absence of postgastric signals. Rather, gastric distension, intestinal nutrients, and gut hormones all are potential contributors to vagal afferent activation. Therefore, vagal afferents constitute a potential location for integration and modulation of these multiple meal-related signals. Indeed, interactions between gastric distension and other gastrointestinal stimuli have been reported. For example, the gut hormone CCK has been reported to sensitize gastric and duodenal mechanosensitive vagal afferents (7,8). Likewise, CCK and gastric distension appear to interact to reduce food intake in a variety of species, including rats, monkeys, and humans (14,15,17,18,38). Thus there is compelling evidence for cooperation between gastric distension and postgastric signals, such as CCK, in vagal activation and reduction of food intake.Capsaicin has been used successfully as a tool to study the involveme...

We investigated the role of sensory nerves in glucose tolerance in conscious Wistar rats neonatally treated with neurotoxin capsaicin or vehicle. Intravenous glucose tolerance tests (IVGTT, 150, 300 and 450 mg in 30 min) were performed to measure glucose tolerance, and glucose, insulin and glucagon levels were measured. Higher glucose concentration resulted in a greater insulin response in both capsaicin- and vehicle-treated rats. However, glucose-stimulated insulin secretion was attenuated in capsaicin-treated animals, even though glucose levels did not differ. Glucagon levels did not differ between both groups. These results show that capsaicin-sensitive nerves are involved in glucose-stimulated insulin secretion, but are not directly involved in the regulation of blood glucose levels. Moreover, they suggest that capsaicin-sensitive nerves could be involved in the regulation of insulin sensitivity. We hypothesize that sensory afferents could play a role in the aetiology of pathologies where glucohomeostatic mechanisms are disturbed, as is in type 2 diabetes mellitus.

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Several mechanisms involved in ingestive behavior and neuroendocrine activity rely on vagal afferent neuronal signaling. Seemingly contradictory to this idea are observations that vagal afferent neuronal ablation by neonatal capsaicin (CAP) treatment has relatively small effects on glucose homeostasis and long-term regulation of energy balance. It may be proposed that humoral endocrine factors and/or their sensitivities compensate for the loss of vagal afferent information, particularly when subjects face disturbances in ambient fuel levels. Therefore, male adult rats neonatally treated with CAP or with the vehicle (VEH) underwent intravenous glucose tolerance tests (IVGTTs) during which blood fuel levels, and circulating adipose, pancreatic, and adrenal hormones were assessed. CAP rats displayed similar hyperglycemia as VEH rats, but with markedly reduced plasma insulin and corticosterone responses. These results indicate that CAP rats have increased insulin sensitivity during hyperglycemic episodes, and lower plasma levels of corticosterone in CAP rats relative to VEH rats could underlie this effect. After the IVGTT, CAP rats had increased plasma adiponectin and reduced plasma resistin levels, and these alterations in adipose hormones might be relevant for post-ingestive metabolic processes. In a second experiment, anorexigenic efficacies of cholecystokinin and leptin were assessed. While VEH rats, but not CAP rats, responded with reduced food intake to i.p. injected cholecystokinin, only CAP rats responded to i.v. infused leptin with a reduction in food intake. It is concluded that reduced HPA axis activity and/or increased leptin signaling could underlie compensations in fuel handling and energy balance following CAP treatment.