Delivery by cesarean section leads to heavier adult bodyweight in prairie voles (Microtus ochrogaster).

Delivery by cesarean section now makes up 32.1 % of all births in the United States. Meta-analyses have estimated that delivery by cesarean section is associated with a > 50 % increased risk for childhood obesity by 5 years of age. While this association is independent of maternal obesity, breastfeeding, and heritable factors, studies in humans have been unable to test for a causal role of cesarean delivery in this regard. Here, we set out to use an animal model to experimentally test whether delivery by cesarean section would increase offspring weight in adulthood. Delivery by cesarean section may exert neurodevelopmental consequences by impacting hormones that are important at birth as well as during metabolic regulation in later life, such as oxytocin and vasopressin. The prairie vole (Microtus ochrogaster) has long been studied to investigate the roles of oxytocin and vasopressin in brain development and social behavior. Here, we establish that prairie voles tolerate a range of ambient temperatures, including conventional 22° housing, which makes them translationally appropriate for studies of diet-induced obesity. We also studied vole offspring for their growth, sucrose preference, home cage locomotor activity, and food consumption after birth by either cesarean section or vaginal delivery. At sacrifice, we collected measures of weight, length, and adipose tissue to analyze body composition in adulthood. Voles delivered by cesarean section had consistently greater bodyweights than those born vaginally, despite having lower food consumption and greater locomotive activity. Cesarean-delivered animals were also longer, though this did not explain their greater body weights. While cesarean delivery had no effect on vasopressin, it resulted in less oxytocin immunoreactivity within the hypothalamus in adulthood. These results support the case that cesarean section delivery plays a causal role in increasing offspring body weight, potentially by affecting the oxytocin system.

Role of dorsal hippocampal muscarinic receptor activity in acquisition and retention of single- versus multiple-trial contextual fear conditioning in adolescent rats.

The present study examined the effects of the muscarinic acetylcholine receptor (mAChR) antagonist, scopolamine, on standard contextual fear conditioning (sCFC). It compared effects of the drug on acquisition (post-shock freezing) versus 24-hr retention of a context-shock association acquired after one or three pairings of a context with unsignaled shock. During single-trial sCFC, systemic scopolamine (0.5 mg/kg, i.p.) prior to training abolished both post-shock and retention freezing (Experiment 1). This same injection during multiple-trial sCFC also abolished post-shock freezing and impaired 24-hr retention freezing (Experiment 2). These results indicate that cholinergic signaling mediates both acquisition and 24-hr retention of a context-shock association across different trial parameters. Experiment 3 further explored these effects by infusing scopolamine (35 µg per side) into the dorsal hippocampus (dHPC) prior to training in single versus multiple-trial sCFC. This infusion spared post-shock but abolished retention test freezing in single-trial sCFC (Experiment 3A), and had no effect on multiple-trial sCFC (Experiment 3B). The current findings suggest that brain-wide cholinergic signaling mediates acquisition and retention of single-trial sCFC. Despite this, while muscarinic cholinergic signaling in the dHPC does mediate retention of single-trial sCFC, it is not required for acquisition of either variant, or retention of multiple-trial sCFC. These findings also rule out impaired sensory processing of contextual cues as a mechanism of impaired context learning by dHPC scopolamine. The results are discussed in relation to the role of cholinergic function across multiple brain memory systems in elemental versus configural forms of contextual fear conditioning (Fanselow, 2010; Rudy, 2009). (PsycInfo Database Record (c) 2021 APA, all rights reserved).