Neonatal cholinergic lesion alters the acoustic structure of infant rat vocalization but not the early cognitive development

Abstract

Cholinergic innervation is critically required for cytoarchitectonic maturation of the cerebral cortex as well as functional assembling of neuronal networks and their behavioral readout. Selective lesion of cortically projecting cholinergic neurons initiated immediately after birth by the immunotoxin 192 IgG-saporin (SAP) led to abnormal wiring of prefrontal-hippocampal networks, yet the neurobehavioral and cognitive consequences of this impairment are still poorly understood. Here, we show that partial cholinergic depletion initiated at birth did not impact the general development of rat pups during the first 2 postnatal weeks, their homing behavior, and the maturation of recognition memory. However, the acoustic structure of infant ultrasonic vocalization was significantly affected by SAP, indicating that early neurobehavioral development relies on intact cholinergic drive. This altered vocalization did not elicit differential maternal care, suggesting that the previously reported SAP-induced behavioral deficits at adulthood are the direct result of cholinergic depletion rather than of abnormal mother-pup interactions.