Anterior olfactory organ removal produces anxiety-like behavior and increases spontaneous neuronal firing rate in basal amygdala.

Some chemical cues may produce signs of anxiety and fear mediated by amygdala nuclei, but unknown is the role of two anterior olfactory epithelial organs, the septal and vomeronasal organs (SO-VNOs). The effects of SO-VNO removal were explored in different groups of Wistar rats using two complementary approaches: (i) the assessment of neuronal firing rate in basal and medial amygdala nuclei and (ii) behavioral testing. Fourteen days after SO-VNO removal, spontaneous activity in basal and medial amygdala nuclei in one group was determined using single-unit extracellular recordings. A separate group of rats was tested in the elevated plus maze, social interaction test, and open field test. Compared with sham-operated and intact control rats, SO-VNO removal produced a higher neuronal firing rate in the basal amygdala but not medial amygdala. In the behavioral tests, SO-VNO removal increased signs of anxiety in the elevated plus maze, did not alter locomotion, and increased self-directed behavior, reflecting anxiety-like behavior. Histological analysis showed neuronal destruction in the accessory olfactory bulb but not anterior olfactory nucleus in the SO-VNO group. The present results suggest the participation of SO-VNO/accessory olfactory bulb/basal amygdala relationships in the regulation of anxiety through a process of disinhibition.

Odors from proximal species reverse the stress-decreased neurogenesis via main olfactory processing.

Unconditioned foot shock followed by restraint in water was used as a stress regimen to induce decreases in neurogenesis in mouse dentate gyrus (DG). Presence of conspecific odors has been known to reverse the stress-induced decrease in DG neurogenesis. In this study, we found that the conspecific odors did not produce these protective effects in mice whose MOE was impaired by nasal zinc sulfate lavage. Moreover, we observed that the presence of odors from rats, hamsters, and guinea pigs throughout the stress procedure reversed the stress-induced decrease in cell proliferation and neurogenesis in mouse dentate gyrus, while these odors alone did not affect mouse dentate cell proliferation or neurogenesis. In contrast, the presence of rabbit, sugar glider, hedgehog, beetle odors did not affect cell proliferation, neurogenesis, the stress-decreased cell proliferation or neurogenesis in DG. Finally, the presence of fox urine odors decreased mouse dentate cell proliferation and neurogenesis but did not affect the stress-induced decrease in cell proliferation or neurogenesis. Taken together, we conclude that olfactory processing via activation of sensory neurons in MOE is responsible for the conspecific odor-produced protective effect against the stress-decreased cell proliferation and neurogenesis. Phylogenetic distances of the odor-generating species and mice might contribute to the odors' protective effects against the stress-induced decreases in cell proliferation and neurogenesis.

Selective enhancement of main olfactory input to the medial amygdala by GnRH.

In male hamsters mating behavior is dependent on chemosensory input from the main olfactory and vomeronasal systems, whose central pathways contain cell bodies and fibers of gonadotropin-releasing hormone (GnRH) neurons. In sexually naive males, vomeronasal organ removal (VNX), but not main olfactory lesions, impairs mating behavior. Intracerebroventricular (i.c.v.)-GnRH restores mating in sexually naive VNX males and enhances medial amygdala (Me) immediate-early gene activation by chemosensory stimulation. In sexually experienced males, VNX does not impair mating and i.c.v.-GnRH suppresses Me activation. Thus, the main olfactory system is sufficient for mating in experienced-VNX males, but not in naive-VNX males. We investigated the possibility that GnRH enhances main olfactory input to the amygdala in naive-VNX males using i.c.v.-GnRH and pharmacological stimulation (bicuculline/D,L-homocysteic acid mixture) of the main olfactory bulb (MOB). In sexually naive intact males there was a robust increase of Fos protein expression in the anteroventral medial amygdala (MeAv) with MOB stimulation, but no effect of GnRH. There was no effect of stimulation or GnRH in posterodorsal medial amygdala (MePd). In naive-VNX animals, GnRH increased Fos in MeAv and MePv. Only combined MOB stimulation and i.c.v.-GnRH produced a significant increase in Fos in the dorsal (reproduction-related) portion of MeP (MePd). When the animals were sexually experienced before VNX, a condition in which GnRH does not enhance mating, i.c.v.-GnRH combined with MOB stimulation suppressed Fos expression in MePd. This suggests a more selective effect of GnRH on olfactory input in MePd than elsewhere in medial amygdala of VNX males.

Behavioral changes of patients after orthognathic surgery develop on the basis of the loss of vomeronasal organ: a hypothesis.

We introduce a hypothesis which presumes that damage to the vomeronasal organ during a Le Fort I osteotomy of the maxilla for the purpose of orthognathic surgical treatment of congenital or acquired jaw deformities affects the patient's social life in terms of the selection of mates and establishment of relationships. The vomeronasal organ is chemosensory for pheromones, and thus registers unconscious olfactory information which might subsequently act on the limbic system of an individual and influence the selection of mates. We believe it is connected to an inhibitory feedback mechanism which is responsible for the exclusion of inappropriate mates. When the vomeronasal organ is removed or damaged during a maxillary osteotomy, the inhibitory function is lost, the patient loses the involuntary ability to exclude inappropriate mates, may become less committed to an existing mate, or even become promiscuous.

Effect of vomeronasal organ removal from male mice on their preference for and neural Fos responses to female urinary odors.

Four experiments were conducted to determine whether vomeronasal organ (VNO) inputs in male mice mediate the rewarding properties of estrous female urinary odors. Sexually naive male mice with either an intact (VNOi) or lesioned (VNOx) VNO preferred to investigate female urine over water in Y-maze tests. Subsequently, VNOi males ran significantly more quickly and remained in nasal contact longer with estrous female urine than with male urine, whereas VNOx males investigated these odors equally. In home-cage habituation-dishabituation tests, VNOi males also investigated female urine significantly longer than did VNOx males, although both groups investigated female urine longer than other non-body odors. Finally, female urinary odors induced Fos in the nucleus accumbens core of VNOi males but not of VNOx males. Our results suggest that female urinary odors retain some incentive value in VNOx males. However, once direct nasal contact is made with female urine, VNO inputs further activate forebrain mechanisms that amplify the reward salience of this stimulus for the male mouse.