CEBPβ regulation of endogenous IGF-1 in adult sensory neurons can be mobilized to overcome diabetes-induced deficits in bioenergetics and axonal outgrowth.

Aberrant insulin-like growth factor 1 (IGF-1) signaling has been proposed as a contributing factor to the development of neurodegenerative disorders including diabetic neuropathy, and delivery of exogenous IGF-1 has been explored as a treatment for Alzheimer's disease and amyotrophic lateral sclerosis. However, the role of autocrine/paracrine IGF-1 in neuroprotection has not been well established. We therefore used in vitro cell culture systems and animal models of diabetic neuropathy to characterize endogenous IGF-1 in sensory neurons and determine the factors regulating IGF-1 expression and/or affecting neuronal health.

Exercise and fluoxetine treatment during adolescence protect against early life stress-induced behavioral abnormalities in adult rats.

Depression is a psychiatric disorder with several comorbidities that has a complicated pathophysiology. Multiple mechanisms such as abnormal hypothalamic-pituitary adrenal (HPA) axis activity, neurotransmission (namely serotonin), and immune-inflammatory responses are involved in the pathophysiology of disease. In this study, we hypothesized that applying exercise (running wheel (RW) and treadmill (TM)) or fluoxetine (FLX) during adolescence could protect adult rats against the negative impact of early-life stress.

Clozapine attenuates mitochondrial dysfunction, inflammatory gene expression, and behavioral abnormalities in an animal model of schizophrenia.

Beyond abnormalities in the neurotransmitter hypothesis, recent evidence suggests that mitochondrial dysfunction and immune-inflammatory responses contribute to the pathophysiology of schizophrenia. The prefrontal cortex (PFC) undergoes maturation and development during adolescence, which is a critical time window in life that is vulnerable to environmental adversities and the development of psychiatric disorders such as schizophrenia. Applying eight weeks of post-weaning social isolation stress (PWSI) to rats, as an animal model of schizophrenia, we decided to investigate the effects of PWSI on the mitochondrial function and expression of immune-inflammatory genes in the PFC of normal and stressed rats.