No abstract

Disorderly resolution of conflict is costly, whereas orderly resolution by consent rules enables quick settlement. However, it is unclear whether non-human animals can make and observe rules to resolve conflict without aggression. Here we report a new behavioral paradigm for mice: a modified two-armed maze that uses wireless electrical brain stimulation as reward. First, the mice were individually operant-trained to initiate and then receive the reward at the signaled arm. Next, two mice were coupled and had to cooperate to initiate reward but then to compete over reward allocation. Mice develop and observe a rule of reward zone allocation that increases the total amount of reward and reward equity between the pair. In the mutual rule-observance behavior, positive reciprocity and tolerance to the other’s violation are also observed. These findings suggest that rodents can learn to make and observe rules to resolve conflict, enhancing long-term benefit and payoff equity.

Absence seizures are caused by abnormal synchronized oscillations in the thalamocortical (TC) circuit, which result in widespread spike-and-wave discharges (SWDs) on electroencephalography (EEG) as well as impairment of consciousness. Thalamic reticular nucleus (TRN) and TC neurons are known to interact dynamically to generate TC circuitry oscillations during SWDs. Clinical studies have suggested the association of Plcβ1 with early-onset epilepsy, including absence seizures. However, the brain regions and circuit mechanisms related to the generation of absence seizures with Plcβ1 deficiency are unknown. In this study, we found that loss of Plcβ1 in mice caused spontaneous complex-type seizures, including convulsive and absence seizures. Importantly, TRN-specific deletion of Plcβ1 led to the development of only spontaneous SWDs, and no other types of seizures were observed. Ex vivo slice patch recording demonstrated that the number of spikes, an intrinsic TRN neuronal property, was significantly reduced in both tonic and burst firing modes in the absence of Plcβ1 . We conclude that the loss of Plcβ1 in the TRN leads to decreased excitability and impairs normal inhibitory neuronal function, thereby disrupting feedforward inhibition of the TC circuitry, which is sufficient to cause hypersynchrony of the TC system and eventually leads to spontaneous absence seizures. Our study not only provides a novel mechanism for the induction of SWDs in Plcβ1 -deficient patients but also offers guidance for the development of diagnostic and therapeutic tools for absence epilepsy.