Location: Livestock Behavior ResearchTitle: Effects of selective serotonin antagonism on central neurotransmission Author
|Cheng, Heng Wei|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/19/2011
Publication Date: 4/1/2012
Citation: Dennis, R.L., Cheng, H. 2012. Effects of selective serotonin antagonism on central neurotransmission. Poultry Science. 91,817-822. Interpretive Summary: Aggressive and cannibalistic behaviors greatly impact the welfare of laying hens while reducing the profitability of the industry. Beak trimming has been used to control these abnormal behaviors. However, the beak trimming procedure itself is also a potential stressor, causing acute and probably chronic pain. Breeders have attempted to breed birds with less aggressive and cannibalistic behaviors, but have been met with limited success. Understanding of the heritable mechanisms regulating aggression in laying hens could lead to more effective selection against these harmful behaviors. In the present study we investigated the heritable differences in two neurotransmitter regulation of aggression. The results showed that aggression is regulated differently through these systems in hens from high aggressive strains compared to hens of a low aggressive strain. The heritable differences in aggression between the lines suggest that neurotransmitters can be used as selection indicators in order to more efficiently select for low aggressive and cannibalistic hens. The data from the present study can be used by producers in management practices and other scientists when planning or interpreting their studies.
Technical Abstract: Serotonergic and dopaminergic mediation of aggression has been evidenced in numerous studies. However, these studies have met with varying and sometimes conflicting results. Here we test the hypothesis that hens with genetic propensity for high and low aggressiveness exhibit distinctly different aggressive mediation via serotonin (5-HT) 1A and 1B and dopamine (DA) D1 and D2 receptor pathways. In the present study, we utilized two high aggressive (DXL and LGPS) and one low aggressive strain (HGPS) of laying hens. Hens were pair housed and the subordinate hen within each pair was treated with D1 agonist, D2 agonist, or saline controls. Dominate hens from different pairs was treated with 5-HT1A agonist, 5-HT1B agonist or saline control (n=12). Aggressive behaviors and central neurotransmitter response were measured. Aggression was increased in all strains in response to D1 agonism (P<0.05), but D2 agonism only increased aggression in the less aggressive HGPS hens (P<0.05). Although HGPS hens showed no effect of 5-HT1A or 1B agonism on aggressiveness (P>0.05), decreased aggression was seen in DXL and LGPS hens following 5-HT1A agonism (P<0.05) and DXL hens treated with 5-HT1B agonism (P<0.05). Central 5-HT and 5-HIAA (a metabolite of 5-HT) were also altered by agonist treatment. Agonism of D1 receptor in the high aggressive strain reduced 5-HIAA concentration in the raphe nucleus (P<0.05), while D2 agonism in the less aggressive strain increased raphe nucleus 5-HIAA (P<0.05). Serotonin concentrations were elevated in the DXL hens following treatment with 5¬HT1A and 1B agonist (P<0.05), and in HGPS hens following 5-HT1B agonism (P<0.05). Our data show evidence for distinct neurotransmitter regulation of aggression in high and low aggressive strains of hens through different receptor systems.