Stress during development alters anxiety-like behavior and hippocampal neurotransmission in male and female rats.

Epidemiological data indicate that early stress increases vulnerability to psychiatric disorders, including anxiety and depression. In the present study we sought to investigate the long-term behavioral and neurochemical consequences of increased and sustained corticosterone levels induced by a 24 h bout of maternal deprivation (DEP) imposed on postnatal day 11 (DEP11). As adults, animals were exposed to the elevated plus maze for assessment of anxiety-like behavior and corticosterone response to this challenge, or decapitated for determination of monoamines and amino acid neurotransmitters content in the hippocampus by HPLC method. The results showed that DEP11 male and female rats displayed increased time in the central hub of the maze and more risk assessment behavior, reflecting increased anxiety-like behavior; in addition, these animals continuously secreted corticosterone in response to the behavioral test until the latest time-point, e.g., 60 min post-stress. In males, maternal deprivation increased aspartate and glutamate levels and reduced taurine levels compared to non-deprived (NDEP) rats. DEP11 females displayed reduced noradrenaline, aspartate and GABA levels compared to NDEP counterparts. These results indicate that maternal deprivation at 11 days of age produced changes in hippocampal neurotransmission that may mediate the increased anxiety-like behavior observed in male and female deprived rats. This article is part of a Special Issue entitled 'Anxiety and Depression'.

Amino acid and monoamine alterations in the cerebral cortex and hippocampus of mice submitted to ricinine-induced seizures.

The alkaloid ricinine isolated from the plant Ricinus communis, when administered to mice at high doses, induces clonic seizures accompanied by electroencephalographic alterations in the cerebral cortex and hippocampus. The lethal nature of ricinine-induced seizures is considered to be a good model for the study of the events that cause death during clonic seizures, particularly those related to respiratory spasms. The initial signs (pre-seizure period) were marked by exophthalmus and decreased locomotor behavior. Animals killed during the preseizure period presented an increased utilization rate (HVA/DA) of dopamine (DA), an increased concentration of noradrenaline (NA), and a decreased concentration of glutamate (Glu), glutamine (Gln), taurine (Tau), and serotonin (5-HT) in the cerebral cortex. The seizure period is characterized by the occurrence of hind limb myoclonus and respiratory spasms, which are followed by death. Alterations in the cerebral cortex concentration of these neurotransmitters persisted during the seizure period. These alterations are only partially observed in the hippocampus, mainly during the seizure period. The present results suggest that an increased release of Glu in the cerebral cortex can be implicated in the genesis of the ricinine-induced seizure and that it triggers many anticonvulsive mechanisms, like the release of Tau, DA, 5-HT, and NA.