D-025
Sex-specific effects of daytime disturbances on sleep and adenosine receptor expression in zebrafish.
Luisa Gaydou1,2, Rocío Schumacher1, Cora Stoker1,2, Guillermina Canesini1,3, Pamela Fernández1,3, María Florencia Rossetti1, Jorge Guillermo Ramos1,2, Ana Paula García1
  1. Instituto de Salud y Ambiente del Litoral (ISAL), UNL-CONICET, Santa Fe, Argentina.
  2. Departamento de Bioquímica Clínica y Cuantitativa, FBCB-UNL, Santa Fe, Argentina.
  3. Cátedra de Nutrición en Situaciones Patológicas, FBCB-UNL, Santa Fe, Argentina.
Presenting Author:
Ana Paula García
anhapaulag@gmail.com
Adenosine is a key mediator of sleep homeostasis, linking energy metabolism with sleep pressure and acting mainly through adora1 (A1R) and 2 (A2AR) receptors that regulate excitatory circuits. While its role in mammalian sleep has been widely studied, its contribution in zebrafish remains poorly understood. Sleep regulation is also strongly influenced by environmental challenges, yet little is known about how daytime disturbances affect subsequent sleep and activity in this model. Adult zebrafish (male and female) were exposed to daytime disturbances for two days (5min vibration every15min from 13:00-19:00hs) and compared to a control group (n=8-12). Locomotor activity, nocturnal sleep, and the expression of adenosine receptors in the whole brain by RT-PCR were assayed. Baseline recordings revealed a clear sexual dimorphism in nocturnal sleep, with males awakening earlier than females. Daytime disturbance increased locomotor activity during the stimulation period. However, after two consecutive days of disturbances, only females showed a significant reduction in sleep during the first two hours of the night, without changes in total nocturnal sleep. Notably, females also exhibited increased A1R expression compared to controls. In conclusion, our findings identify a sex- specific vulnerability to daytime disturbances, with females being uniquely affected. The upregulation of A1R may represent a compensatory mechanism enhancing adenosine signaling following reduced sleep.