Midbrain inactivation produces sonar navigation deficits in the echolocating bat, Eptesicus fuscus

Abstract

The contribution of different brain structures to auditory-guided behaviors in echolocating bats is not fully understood. Historically, area-specific inactivation studies have provided insights into the function of brain regions; however, lesioning is permanent and can cause incidental damage to non-target areas, which can compromise the interpretation of behavioral effects. We have established the use of Designer Receptors Exclusively Activated by Designer Drugs (DREADDs) to reversibly inactivate excitatory neurons in the midbrain of the insectivorous bat, Eptesicus fuscus. We targeted the inferior and superior colliculi, two structures implicated in processing returning echoes and coordinating motor responses, including the production of sonar vocalizations. After bilateral infusions in either the IC or SC, bats were trained to fly down a corridor and navigate through an opening in a partition to receive a food reward. Midbrain inactivation dramatically altered performance in the behavioral task. Bats with IC inactivation showed reduced precision in steering through the partition opening, as well as changes in echolocation calls. SC inactivation produced a profound deterioration of the bat's behavior, with the bat unable to fly down the corridor. Our preliminary results open the door to many potential applications of DREADDs to uncover the neural mechanisms supporting navigation through echolocation.