Abstract
The expression of brain-derived neurotrophic factor (BDNF) mRNA and protein and its primary receptor, TrkB mRNA shows circadian oscillations in adult rats; however it has been unclear if juvenile rats also display a similar pattern in circadian oscillations. We determined the levels of BDNF and TrkB mRNA and of BDNF protein at four separate time points during a 24 hperiod in the hippocampus and frontal cortex. The expression of BDNF and TrkB undergoes diurnal oscillation in adult and postnatal day 21 rats, but no significant variation is present in postnatal day 13 rats. Antidepressant drug treatment also is known to influence BDNF and TrkB levels. However, the reported effects of antidepressant drug treatment on BDNF and TrkB are highly variable and may be influenced by multiple factors, including detection method, class of antidepressant drug, and length of administration. BDNF mRNA levels were decreased significantly in the hippocampus after acute desipramine (a tricyclic antidepressant) treatment compared to control. BDNF mRNA and protein levels, as well as TrkB mRNA levels, were unchanged in adult rats after subchronic and chronic treatment with either desipramine or escitalopram (a selective serotonin reuptake inhibitor) and treatment consistent with several reports in the literature. This study defines several important factors that must be taken into account when comparing BDNF and TrkB levels both within and among studies.
Highlights
In the brain, brain-derived neurotrophic factor (BDNF) has been implicated in development, neural regeneration, synaptic transmission, synaptic plasticity and neurogenesis [1,2,3,4,5]
BDNF mRNA levels at 7 p.m. were the highest in both the hippocampus (p
Our results demonstrate that the expression of BDNF and TrkB mRNA is influenced by several factors
Summary
BDNF has been implicated in development, neural regeneration, synaptic transmission, synaptic plasticity and neurogenesis [1,2,3,4,5]. A role for BDNF and its primary receptor, TrkB, in the action of antidepressant treatments have emerged and are supported by several lines of evidence. Behavioral studies have demonstrated that BDNF infused into the midbrain of rats produces an antidepressant-like effect in animal models of depression [10]. Decreased levels of BDNF may contribute to the atrophy of certain limbic structures including the hippocampus and cortex that has been observed in depressed patients. These findings support that increased expression of BDNF and TrkB contribute to the neural adaptations necessary for the action of antidepressant treatment
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