Molecular Correlates of Social Dominance: A Novel Role for Ependymin in Aggression

Theoretical and empirical studies have sought to explain the formation and maintenance of social relationships within groups. The resulting dominance hierarchies have significant fitness and survival consequences dependent upon social status. We hypothesised that each position or rank within a group has a distinctive brain gene expression profile that correlates with behavioural phenotype. Furthermore, transitions in rank position should determine which genes shift in expression concurrent with the new dominance status. We used a custom cDNA microarray to profile brain transcript expression in a model species, the rainbow trout, which forms tractable linear hierarchies. Dominant, subdominant and submissive individuals had distinctive transcript profiles with 110 gene probes identified using conservative statistical analyses. By removing the dominant, we characterised the changes in transcript expression in sub-dominant individuals that became dominant demonstrating that the molecular transition occurred within 48 hours. A strong, novel candidate gene, ependymin, which was highly expressed in both the transcript and protein in subdominants relative to dominants, was tested further. Using antibody injection to inactivate ependymin in pairs of dominant and subdominant zebrafish, the subdominant fish exhibited a substantial increase in aggression in parallel with an enhanced competitive ability. This is the first study to characterise the molecular signatures of dominance status within groups and the first to implicate ependymin in control of aggressive behaviour. It also provides evidence for indirect genetic effect models in which genotype/phenotype of an individual is influenced by conspecific interactions within a group. The variation in the molecular profile of each individual within a group may offer a new explanation of intraspecific variation in gene expression within undefined groups of animals and provides new candidates for empirical study

The effects of Δ9-tetrahydrocannabinol on the dopamine system

Δ(9)-tetrahydrocannabinol (THC), the main psychoactive ingredient in cannabis, is a pressing concern to global mental health. Patterns of use are changing drastically due to legalisation, availability of synthetic analogues (‘spice’), cannavaping and aggrandizements in the purported therapeutic effects of cannabis. Many of THC’s reinforcing effects are mediated by the dopamine system. Due to complex cannabinoid-dopamine interactions there is conflicting evidence from human and animal research fields. Acute THC causes increased dopamine release and neuron activity, whilst long-term use is associated with blunting of the dopamine system. Future research must examine the long-term and developmental dopaminergic effects of the drug

Frequency-domain phase-modulation fluorometry: Resolution of complex decays of fluorescence intensity and anisotropy

We used frequency-domain fluorometry to resolve multi-exponential decays of fluorescence intensity and anisotropy. The samples are excited with intensity modulated light, at modulation frequencies ranging from 1 to 200 MHz, and we measure the phase-shifts and demodulation factors. The decay times of a three-component mixture were resolved, 1.2, 4.1 and 7.7 nsec, as well as the two anisotropy decay times of the anisotropic rotator perylene. © 1984

Frequency-domain phase-modulation fluorometry: Resolution of complex decays of fluorescence intensity and anisotropy

We used frequency-domain fluorometry to resolve multi-exponential decays of fluorescence intensity and anisotropy. The samples are excited with intensity modulated light, at modulation frequencies ranging from 1 to 200 MHz, and we measure the phase-shifts and demodulation factors. The decay times of a three-component mixture were resolved, 1.2, 4.1 and 7.7 nsec, as well as the two anisotropy decay times of the anisotropic rotator perylene. © 1984

Quantification of Ethanol's Antipunishment Effect in Humans Using the Generalized Matching Equation

Increases in rates of punished behavior by the administration of anxiolytic drugs (called antipunishment effects) are well established in animals but not humans. The present study examined antipunishment effects of ethanol in humans using a choice procedure. The behavior of 5 participants was placed under six concurrent variable-interval schedules of monetary reinforcement. In three of the six concurrent schedules, punishment, in the form of monetary loss, was superimposed on one alternative. Data were analyzed according to the generalized matching equation which distinguishes between bias (allocation of behavior beyond what matching to relative reinforcer densities would predict) and sensitivity to reinforcement (how well behavior tracks relative reinforcer densities). In addition, participants completed a pencil-tapping test. Under placebo punishment conditions, all participants demonstrated low response rates and a bias against the alternative associated with punishment, despite a resultant loss of available reinforcers. Bias against the punished alternative was dose-dependently reduced in participants shown to be most sensitive to ethanol (0.6, 1.2, and 1.8 g/kg) in measures of overall responding and on the pencil-tapping test. No ethanol-induced change in bias was noted when punishment was not imposed. Sensitivity to reinforcement also decreased for participants shown to be sensitive to ethanol. In addition to extending antipunishment effects to humans, these results also show that antipunishment effects can be quantified via the matching equation