Abstract
Stress, such as social isolation, is a well-known risk factor for depression, most probably in combination with predisposing genetic factors. Physical exercise on the other hand, is depicted as a wonder-treatment that makes you healthier, happier and live longer. However, the published results on the effects of exercise are ambiguous, especially when it comes to neuropsychiatric disorders. Here we combine a paradigm of social isolation with a genetic rat model of depression, the Flinders Sensitive Line (FSL), already known to have glutamatergic synaptic alterations. Compared to group-housed FSL rats, we found that social isolation further affects synaptic plasticity and increases basal synaptic transmission in hippocampal CA1 pyramidal neurons. These functional synaptic alterations co-exist with changes in hippocampal protein expression levels: social isolation in FSL rats reduce expression of the glial glutamate transporter GLT-1, and increase expression of the GluA2 AMPA-receptor subunit. We further show that physical exercise in form of voluntary running prevents the stress-induced synaptic effects but do not restore the endogenous mechanisms of depression already present in the FSL rat.
Highlights
Depression is a mood disorder characterized by both emotional and cognitive symptoms
We showed that social isolation reduces long-term potentiation (LTP) in the Flinders Sensitive Line (FSL) rats and, remarkably, running can prevent this reduction (Fig 1A2)
We did not observe any effect of social isolation or running on plasticity (LTP) in the Sprague Dawley (SD) rats (Fig 1B1 and 1B2) confirming that the effect synaptic transmission and plasticity that we observe in the FSL rats upon social isolation is associated with their increased vulnerability to stress
Summary
Depression is a mood disorder characterized by both emotional and cognitive symptoms. Despite the intense research in the field, the neurobiology of depression remains elusive, emerging evidences place the glutamatergic system as central to the neurobiology and treatment of the mood disorders [1]. Our understanding of the etiology of the disease is limited to a list of risk factors where genetic predisposition and environmental risk factors, such as stressful life events, are thought to interact. If the stress-induced mechanisms of depression differs from the endogenous (genetic) factors is not clear.
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