Aging to 24 months increased C57BL/6J mouse social sniffing and hippocampal Neto1 levels, and impaired female spatial learning.

Understanding how natural aging impacts rodent performance in translational behavior tests is critical to teasing apart impairments due to age-related decline from neurodegenerative disorder modeling. Reduced neuropilin and tolloid-like 1 (NETO1), an accessory protein of ionotropic glutamate receptors involved in synaptic plasticity, was associated with Alzheimer's disease, yet aging effects on Neto1 remain unclear. For these reasons, our goal was to characterize how Neto1 expression corresponded with social, repetitive, and spatial learning behaviors and stress response across the C57BL/6J mouse lifespan. We measured social preferences in three-chamber tests, and motor stereotypies by marble burying. Cognitive flexibility is typically assessed in the Morris water maze (MWM), wherein C57BL/6J mice exhibit deficits with age. However, fatigue or locomotor impairment may confound interpretation of MWM performance. Therefore, we used a less arduous water T-maze (WTM) to compare spatial learning flexibility in 2, 9-15, and 24-month-old male and female mice to test the hypothesis that deficits would emerge with age. In both sexes, 9-15-month-olds made more chamber entries during social preference tests, while 2-month-olds did less social sniffing than aged mice. No age or sex differences emerged in marble burying or serum corticosterone measurements. In 24-month-olds hippocampal Neto1was increased relative to 2-month-olds, and male cognitive flexibility was strong, while spatial learning and reversal learning of 24-month-old females was impaired in WTM irrespective of Neto1 expression. The WTM is a useful alternative assessment for cognitive flexibility deficits in aged mice, and the role of hippocampal Neto1 in promoting social sniffing is of interest.

Fins of Fury or Fainéant: Fluoxetine impacts the aggressive behavior of fighting fish (Betta splendens).

While an extensive literature has demonstrated that the selective serotonin reuptake inhibitor (SSRI) antidepressant fluoxetine, disrupts aggressive behavior in male Betta splendens the behavioral mechanisms underlying this disruption remain unknown. To elucidate the behavioral mechanism underlying fluoxetine, male fish were acutely exposed to a 10 µmol (0.0034578 µg/L) concentration of fluoxetine for 25 days using an ABA design. Male Betta splendens are naturally aggressive fish with well-studied and patterned behavioral responses. Importantly, aggressive behavior in this species can be conditionally primed allowing for examination of motivational components of behavior in addition to motor performance. The present study focused on using female fish as an ecologically relevant prime for eliciting aggressive behavior as a means of examining the motivational and motoric effects of fluoxetine. We found that male courtship with a female was strongly correlated with aggressive responding against a mirror. However, despite the strong correlation male fish were not found to have different levels of aggression or changes in aggressive responding when compared to males not primed with a female. Also, latency was not different between the no female prime and female prime males for either the excitatory mirror condition or inhibitory white wall condition, of which the fish had no preference. However, fluoxetine was found to have profound effects on all males in the study regardless of prime type, with increases in latency for the mirror and white wall and decreases in aggressive responding to the mirror. These results support the hypothesis that fluoxetine impairs aggressive motivation and movement in Betta splendens.

Assessment of autism-relevant behaviors in C57BKS/J leptin receptor deficient mice.

Gestational diabetes mellitus (GDM) was associated with greater autism risk in epidemiological studies. Disrupted leptin signaling may contribute to their coincidence, as it is found in both disorders. Given this we examined leptin receptor (Lepr) deficient (BKS.Cg-Dock7m +/+ Leprdb/J diabetic (db)) heterozygous (db/+) mice for autism-relevant behaviors. BKS db/+ females are lean with normal blood glucose, but they develop GDM while pregnant. We hypothesized BKS db/+ offspring might exhibit physiological and behavior traits consistent with autism. Adolescent body weight, fasting blood glucose, serum corticosterone, social preferences, self-grooming, marble burying, social dominance and cognitive flexibility of BKS db/+ mice was compared to C57BLKS/J (BKS) and C57BL/6J (BL6) mice. Male db/+ weighed more and had higher blood glucose and corticosterone relative to BL6, but not BKS mice. Also, male db/+ lacked social interaction preference, explored arenas less, and buried more marbles than BL6, but not BKS males. Male and female db/+ were more dominant and made more mistakes in water T-mazes locating a sunken platform after its position was reversed than BL6, but not BKS mice. Overall BKS db/+, particularly males, exhibited some autism-like social deficits and restrictive-repetitive behaviors relative to BL6, but BKS strain contributions to BKS db/+ behaviors were evident. Since BKS db/+ and BKS behavioral and physiological phenotypes are already so similar, it will be difficult to use these models in studies designed to detect contributions of fetal GDM exposures to offspring behaviors.