The effects of carvacrol and p‐cymene on Aβ1‐42‐induced long‐term potentiation deficit in male rats

Abstract

AbstractAimsAlzheimer's disease (AD) is the most common type of dementia in which oxidative stress plays an important role. In this disease, learning and memory and the cellular mechanism associated with it, long‐term potentiation (LTP), are impaired. Considering the beneficial effects of carvacrol (CAR) and p‐cymene against AD, their effect was assessed on in vivo hippocampal LTP in the perforant pathway (PP)‐dentate gyrus (DG) pathway in an Aβ1‐42‐induced rat model of AD.MethodsMale Wistar rats were randomly assigned to five groups: sham: intracerebroventricular (ICV) injection of phosphate‐buffered saline, Aβ: ICV Aβ1‐42 injections, Aβ + CAR (50 mg/kg), Aβ + p‐cymene (50 mg/kg), and Aβ + CAR + p‐cymene. Administration of CAR and p‐cymene was done by gavage daily 4 weeks before and 4 weeks after the Aβ injection. The population spike (PS) amplitude and field excitatory postsynaptic potentials (fEPSP) slope were determined in DG against the applied stimulation to the PP.ResultsAβ‐treated rats exhibited impaired LTP induction in the PP‐DG synapses, resulting in significant reduction in both fEPSP slope and PS amplitude compared to the sham animals. Aβ‐treated rats consumed either CAR or p‐cymene separately (but not their combination), and showed an enhancement in fEPSP slope and PS amplitude of the DG granular cells.ConclusionsThese data indicate that CAR or p‐cymene can ameliorate Aβ‐associated changes in synaptic plasticity. Surprisingly, the combination of CAR and p‐cymene did not yield the same effect, suggesting a potential interaction between the two substances.