|Cheng, Heng Wei|
Submitted to: Poultry Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: September 24, 2010
Publication Date: November 1, 2011
Citation: Dennis, R.L., Cheng, H. 2011. The dopaminergic system and aggression in laying hens. Poultry Science. 90(11): 2440-2448. Interpretive Summary: Dopamine is a primary neurotransmitter involved in mediating behaviors, including aggression and feather pecking. In the present study we investigated the role of two distinct dopamine receptors (D1 and D2) in regulating aggression in high and low aggressive strains of birds. Our data show that when the D1 receptor is stimulated with a pharmaceutical agonist, aggression is increased in all strains, however, when it is inhibited with a pharmaceutical antagonist aggression is only reduced in high aggressive birds. Alternately, when the D2 receptor is inhibited all strains studied showed reduced aggression, while only the low aggressive strain increased aggressiveness in response to stimulation of this receptor pathway. Our results show clear evidence of distinct dopamine regulation in high versus low aggressive strains of birds. These data suggest that biomarkers for aggressiveness may exist in the dopaminergic system on which breeders could select for more docile phenotypes to reduce social stress.
Technical Abstract: The dopaminergic system regulates aggression in humans and other mammals. To investigate if birds with genetic propensity for high and low aggressiveness may exhibit distinctly different aggressive mediation via dopamine (DA) D1 and D2 receptor pathways, two high aggressive (DXL and LGPS) and one low aggressive strain (HGPS) of laying hens were used in the study. HGPS and LGPS lines were diversely selected for high and low group production and survivability in multiple-bird cages; and DXL (DeKalb XL) was a commercial line. The birds were pair housed and characterized based on their aggressiveness. In experiment I, the subordinate birds were treated with D1 agonist, D2 agonist, or saline controls (n=12). In experiment II, the dominant birds from a separate flock were treated with D1 antagonist, D2 antagonist or saline controls (n=12). Treatment-associated changes in aggressive behaviors and central neurotransmitters were measured. Aggression was increased in all strains in response to D1 agonism, but in only the less aggressive HGPS birds with D2 agonism. Central 5-HT and 5-HIAA (5-Hydroxyindoleacetic acid, a metabolite of 5-HT) were also altered by agonist treatment. Agonism of the D1 receptor reduced 5-HIAA concentrations in the raphe nucleus of the high aggressive strain, DXL, while D2 agonism increased raphe nucleus 5-HIAA in the less aggressive strain, HGPS. Aggression was decreased and hypothalamic serotonin (5-HT) and epinephrine were elevated in birds from all strains treated with D2 receptor antagonist. D1 receptor antagonism elicited different behavioral and neurotransmitter responses based on the aggressive phenotype of the genetic strains. Aggressive strains DXL and LGPS decreased aggressiveness following antagonism of the D1 receptor. The data show evidence for distinct neurotransmitter regulation of aggression in high and low aggressive strains of hens through different receptor systems. These chicken lines could provide new animal models for the biomedical investigation of genetic basis of aggression.