Immune modulation of learning, memory, neural plasticity and neurogenesis
Cytokine-associated emotional and cognitive disturbances in humans.
- A. Reichenberg, R. Yirmiya, T. Pollmächer
- Medicine, PsychologyArchives of General Psychiatry
- 1 May 2001
In humans, a mild stimulation of the primary host defense has negative effects on emotional and memory functions, which is probably caused by cytokine release, and cytokines represent a novel target for neuropsychopharmacological research.
Brain interleukin-1 mediates chronic stress-induced depression in mice via adrenocortical activation and hippocampal neurogenesis suppression
Elevation in brain IL-1 levels, which characterizes many medical conditions, is both necessary and sufficient for producing the high incidence of depression found in these conditions, and procedures aimed at reducing brain IL -1 levels may have potent antidepressive actions.
A dual role for interleukin-1 in hippocampal-dependent memory processes
Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis
Findings provide direct causal evidence that disturbances in microglial functioning has an etiological role in chronic stress-induced depression, suggesting that microglia stimulators could serve as fast-acting anti-depressants in some forms of depressive and stress-related conditions.
Interleukin-1 (IL-1): A central regulator of stress responses
Depression as a Microglial Disease
Endotoxin produces a depressive-like episode in rats
- R. Yirmiya
- Psychology, BiologyBrain Research
- 4 March 1996
Impaired interleukin‐1 signaling is associated with deficits in hippocampal memory processes and neural plasticity
The results suggest that IL‐1 contributes to the regulation of memory processes as well as short‐ and long‐term plasticity within the hippocampus, which has important implications to several conditions in humans, which are associated with long-term defects inIL‐1 signaling.
The cannabinoid CB1 receptor regulates bone formation by modulating adrenergic signaling
It is demonstrated that traumatic brain injury (TBI), which in humans enhances peripheral osteogenesis and fracture healing, acutely stimulates bone formation in a distant skeletal site and that the sympathetic control of bone formation is regulated through 2‐AG activation of prejunctional CB1.