A mathematical non cumulative damage model for the secretion of glutamate and dopamine due to the stress effect in terms of ketamine

Based on the distribution of damage, caused by a shock affecting a system, the intervals with small, intermediate and large damage are introduced. The initial homogeneous Poisson process is split into three homogeneous Poisson processes and studied independently. Several criteria of failure are considered, based on the assumption that shocks with small level of damage are harmless for a system, shocks with a large level of damage results in the system's failure and shocks with an intermediate level of damage can result in the system's failure only with some probability. Ketamine (18 mg/kg, s.c.) evoked a significant release of glutamate and DA, although the glutamate response was slower in onset compared with DA. Pretreatment with either systemic (3 mg/kg s.c.) or local (1 μ M, in the probe) LY379268 blocked ketamine-evoked glutamate, but not DA, release. When applied directly to the mPFC via the dialysis probe, ketamine (1 μ M in the probe) had no effect on glutamate release but did significantly enhance the release of DA. Local ketamine, on the other hand, does not increase glutamate but does increase DA release. This suggests that ketamine acts outside of the mPFC to enhance glutamate, but within the mPFC to enhance DA release. The origin of the ketamine effect on mPFC glutamate is currently not known.