Data from: Escitalopram and NHT normalized stress-induced anhedonia and molecular neuroadaptations in a mouse model of depression

Anhedonia is defined as a diminished ability to obtain pleasure from
otherwise positive stimuli. Anxiety and mood disorders have been
previously associated with dysregulation of the reward system, with
anhedonia as a core element of major depressive disorder (MDD). The aim of
the present study was to investigate whether stress-induced anhedonia
could be prevented by treatments with escitalopram or novel herbal
treatment (NHT) in an animal model of depression. Unpredictable chronic
mild stress (UCMS) was administered for 4 weeks on ICR outbred mice.
Following stress exposure, animals were randomly assigned to
pharmacological treatment groups (i.e., saline, escitalopram or NHT).
Treatments were delivered for 3 weeks. Hedonic tone was examined via
ethanol and sucrose preferences. Biological indices pertinent to MDD and
anhedonia were assessed: namely, hippocampal brain-derived neurotrophic
factor (BDNF) and striatal dopamine receptor D2 (Drd2) mRNA expression
levels. The results indicate that the UCMS-induced reductions in ethanol
or sucrose preferences were normalized by escitalopram or NHT. This
implies a resemblance between sucrose and ethanol in their
hedonic-eliciting property. On a neurobiological aspect, UCMS-induced
reduction in hippocampal BDNF levels was normalized by escitalopram or
NHT, while UCMS-induced reduction in striatal Drd2 mRNA levels was
normalized solely by NHT. The results accentuate the association of stress
and anhedonia, and pinpoint a distinct effect for NHT on striatal Drd2
expression.