Abstract:ABSTRACT. Previously, we have demonstrated that the alarm pheromone deteriorates sexual behavior in male rats, which was blocked by pretreatment with a corticotrophin-releasing hormone (CRH) antagonist. Studies have shown that an opioid antagonist blocked the deterioration of male sexual behavior following intracerebroventricular administration of CRH. Therefore, possibly, the pheromone effects could also be mediated by the opioid system. In this study, we pretreated rats with naloxone, an opioid receptor anta… Show more
“…In addition, pretreatment with naloxone blocked these effects in the mPVN, vlPAG, and nPGi. Based on these results, we have revised our hypothesis regarding the neural mechanisms underlying the alarm pheromone-induced deterioration in sexual behavior (Kobayashi et al, 2013a , b ) as follows: when a male rat detects the alarm pheromone, the vomeronasal system, including the BNSTp, and the main olfactory system (Inagaki et al, 2014 ) receive information about the pheromone. Information from these 2 olfactory systems activates the pPVN, which subsequently activates opioidergic neurons in the Arc.…”
Section: Discussionmentioning
confidence: 99%
“…Before the sexual behavior test, water samples that contained either the alarm pheromone or a control odor were prepared according to a previously described method (Kiyokawa et al, 2005a ; Kobayashi et al, 2013b ). Adult male Wistar Imamichi rats (aged 12–16 weeks) were anesthetized and 2 intradermal needles (27G) were attached at either the neck or perianal region.…”
Section: Methodsmentioning
confidence: 99%
“…Sexual behavior tests were conducted as described in previous studies (Kobayashi et al, 2011 , 2013a , b ). Briefly, 1 day before the test, male rats were housed individually and acclimatized for 30 min to the experimental room and devices.…”
Section: Methodsmentioning
confidence: 99%
“…Male sexual behavior was analyzed as described in previous studies by a researcher who was blind to the experimental conditions (Kobayashi et al, 2011 , 2013a , b ). The following measures of sexual behavior were recorded: mount latency (pelvic thrusting from the rear of the female rat without penile insertion), intromission latency (deeper pelvic thrusting from the rear of the female rat with penile insertion), latency for tenth intromission (time from the first intromission to tenth intromission), and number of mounts (number of mounts needed for 10 intromissions).…”
Section: Methodsmentioning
confidence: 99%
“…We found that systemic pretreatment with the opioid receptor antagonist naloxone attenuated sexual deterioration in male rats. This suggests that opioids are involved in the neural mechanism (Kobayashi et al, 2013b ). However, regions in which we found increased Fos expression during deterioration (Kobayashi et al, 2013a ), such as the nPGi and several other nuclei, to our knowledge, do not express opioid receptors.…”
Sexual behavior is suppressed by various types of stressors. We previously demonstrated that an alarm pheromone released by stressed male Wistar rats is a stressor to other rats, increases the number of mounts needed for ejaculation, and decreases the hit rate (described as the number of intromissions/sum of the mounts and intromissions). This deterioration in sexual behavior was ameliorated by pretreatment with the opioid receptor antagonist naloxone. However, the neural mechanism underlying this remains to be elucidated. Here, we examined Fos expression in 31 brain regions of pheromone-exposed rats and naloxone-pretreated pheromone-exposed rats 60 min after 10 intromissions. As previously reported, the alarm pheromone increased the number of mounts and decreased the hit rate. In addition, Fos expression was increases in the anterior medial division (BNSTam), anterior lateral division (BNSTal) and posterior division (BNSTp) of the bed nucleus of the stria terminalis, parvocellular part of the paraventricular nucleus of the hypothalamus, arcuate nucleus, dorsolateral and ventrolateral periaqueductal gray, and nucleus paragigantocellularis (nPGi). Fos expression was decreased in the magnocellular part of the paraventricular nucleus of the hypothalamus. Pretreatment with naloxone blocked the pheromone-induced changes in Fos expression in the magnocellular part of the paraventricular nucleus of the hypothalamus, ventrolateral periaqueductal gray, and nPGi. Based on these results, we hypothesize that the alarm pheromone deteriorated sexual behavior by activating the ventrolateral periaqueductal gray-nucleus paragigantocellularis cluster and suppressing the magnocellular part of the paraventricular nucleus of the hypothalamus (PVN) via the opioidergic pathway.
“…In addition, pretreatment with naloxone blocked these effects in the mPVN, vlPAG, and nPGi. Based on these results, we have revised our hypothesis regarding the neural mechanisms underlying the alarm pheromone-induced deterioration in sexual behavior (Kobayashi et al, 2013a , b ) as follows: when a male rat detects the alarm pheromone, the vomeronasal system, including the BNSTp, and the main olfactory system (Inagaki et al, 2014 ) receive information about the pheromone. Information from these 2 olfactory systems activates the pPVN, which subsequently activates opioidergic neurons in the Arc.…”
Section: Discussionmentioning
confidence: 99%
“…Before the sexual behavior test, water samples that contained either the alarm pheromone or a control odor were prepared according to a previously described method (Kiyokawa et al, 2005a ; Kobayashi et al, 2013b ). Adult male Wistar Imamichi rats (aged 12–16 weeks) were anesthetized and 2 intradermal needles (27G) were attached at either the neck or perianal region.…”
Section: Methodsmentioning
confidence: 99%
“…Sexual behavior tests were conducted as described in previous studies (Kobayashi et al, 2011 , 2013a , b ). Briefly, 1 day before the test, male rats were housed individually and acclimatized for 30 min to the experimental room and devices.…”
Section: Methodsmentioning
confidence: 99%
“…Male sexual behavior was analyzed as described in previous studies by a researcher who was blind to the experimental conditions (Kobayashi et al, 2011 , 2013a , b ). The following measures of sexual behavior were recorded: mount latency (pelvic thrusting from the rear of the female rat without penile insertion), intromission latency (deeper pelvic thrusting from the rear of the female rat with penile insertion), latency for tenth intromission (time from the first intromission to tenth intromission), and number of mounts (number of mounts needed for 10 intromissions).…”
Section: Methodsmentioning
confidence: 99%
“…We found that systemic pretreatment with the opioid receptor antagonist naloxone attenuated sexual deterioration in male rats. This suggests that opioids are involved in the neural mechanism (Kobayashi et al, 2013b ). However, regions in which we found increased Fos expression during deterioration (Kobayashi et al, 2013a ), such as the nPGi and several other nuclei, to our knowledge, do not express opioid receptors.…”
Sexual behavior is suppressed by various types of stressors. We previously demonstrated that an alarm pheromone released by stressed male Wistar rats is a stressor to other rats, increases the number of mounts needed for ejaculation, and decreases the hit rate (described as the number of intromissions/sum of the mounts and intromissions). This deterioration in sexual behavior was ameliorated by pretreatment with the opioid receptor antagonist naloxone. However, the neural mechanism underlying this remains to be elucidated. Here, we examined Fos expression in 31 brain regions of pheromone-exposed rats and naloxone-pretreated pheromone-exposed rats 60 min after 10 intromissions. As previously reported, the alarm pheromone increased the number of mounts and decreased the hit rate. In addition, Fos expression was increases in the anterior medial division (BNSTam), anterior lateral division (BNSTal) and posterior division (BNSTp) of the bed nucleus of the stria terminalis, parvocellular part of the paraventricular nucleus of the hypothalamus, arcuate nucleus, dorsolateral and ventrolateral periaqueductal gray, and nucleus paragigantocellularis (nPGi). Fos expression was decreased in the magnocellular part of the paraventricular nucleus of the hypothalamus. Pretreatment with naloxone blocked the pheromone-induced changes in Fos expression in the magnocellular part of the paraventricular nucleus of the hypothalamus, ventrolateral periaqueductal gray, and nPGi. Based on these results, we hypothesize that the alarm pheromone deteriorated sexual behavior by activating the ventrolateral periaqueductal gray-nucleus paragigantocellularis cluster and suppressing the magnocellular part of the paraventricular nucleus of the hypothalamus (PVN) via the opioidergic pathway.
In this chapter, I describe 2 types of olfactory communication in rats, which appear to arouse anxiety and relief, respectively. In alarm pheromonal communication, rats release 4-methylpentanal and hexanal from their perianal region when they are stressed. These molecules activate the anxiety circuit, including the bed nucleus of the stria terminalis, when 4-methylpentanal and hexanal are simultaneously detected by the vomeronasal system and the main olfactory system, respectively. Consequently, recipient rats show a variety of anxiety responses, depending on the threatening stimuli. In appeasing olfactory communication, non-stressed rats release an appeasing olfactory signal, which is detected by the main olfactory system of other rats. When detected, this olfactory signal suppresses activation of the basolateral complex of the amygdala and, as a result, ameliorates stress responses elicited by an auditory conditioned stimulus during social buffering phenomenon. Because social buffering appears to be based on affinity and attachment to accompanying animals, the appeasing olfactory signal may arouse relief in rats. A definition of social buffering is also proposed as we still have no set definition for the term social buffering yet.
The American National Institute for Mental Health (NIMH) has put out a set of research goals that include a long-term plan to identify more reliable endogenous explanations for a wide variety of mental health disorders (Insel, 2013). In response to this, we have identified a major symptom that underlies multiple mental health disorders – social bonding dysfunction. We suggest that endogenous opioid abnormalities can lead to altered social bonding, which is a symptom of various mental health disorders, including depression, schizophrenia and ASD. This article first outlines how endogenous opioids play a role in social bonding. Then we show their association with the body’s inflammation immune function, and review recent literature linking inflammation to mental health ‘immunophenotypes’. We finish by explaining how these immunophenotypes may be caused by alterations in the endogenous opioid system. This is the first overview of the role of inflammation across multiple disorders where we provide a biochemical explanation for why immunophenotypes might exist across diagnoses. We propose a novel mechanism of how the immune system may be causing ‘sickness-type’ behaviours (fatigue, appetite change, social withdrawal and inhibited motivation) in those who have these immunophenotypes. We hope that this novel aetiology can be used as a basis for future research in mental health.
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