An Examination of the Role of Adrenergic Receptor Stimulation in Mediating the Link Between Early-Life Stress and the Sensitization of Neuroinflammatory-Based Depressive-Like Behavior in Isolated Guinea Pig Pups
Abstract
Early-life stress appears to sensitize neuroinflammatory signaling to increase later vulnerability for stress-related mental disorders. How stress initiates this process is unknown, but sympathetic nervous system activation during the early stress may be key. Isolated guinea pig pups display inflammatory-mediated depressive-like behavior and fever that sensitize on repeated isolation. We assessed whether sympathetic nervous system activity contributed to the sensitization process in guinea pig pups. In Experiment 1, the adrenergic agonist ephedrine, either alone or with cortisol, did not increase depressive-like behavior or fever during an initial isolation the following day. In Experiment 2, both depressive-like behavior and fever sensitized with repeated isolation, but beta-adrenergic receptor blockade with propranolol did not affect either of these responses or their sensitization. Results suggest sympathetic nervous system activation is neither necessary nor sufficient to induce the increased neuroinflammatory signaling underlying sensitization of depressive-like behavioral or febrile responses in developing guinea pigs.
