Abstract
The pesticide rotenone inhibits mitochondrial complex I and is thought to cause neurological disorders such as Parkinson’s disease and cognitive disorders. However, little is known about the effects of rotenone on conditioned taste aversion memory. In the present study, we investigated whether intranasal administration of rotenone affects conditioned taste aversion memory in mice. We also examined how the intranasal administration of rotenone modulates synaptic transmission and plasticity in layer V pyramidal neurons of the mouse insular cortex that is critical for conditioned taste aversion memory. We found that the intranasal administration of rotenone impaired conditioned taste aversion memory to bitter taste. Regarding its cellular mechanisms, long-term depression (LTD) but not long-term potentiation (LTP) was impaired in rotenone-treated mice. Furthermore, spontaneous inhibitory synaptic currents and tonic GABA currents were decreased in layer V pyramidal neurons of rotenone-treated mice compared to the control mice. The impaired LTD observed in pyramidal neurons of rotenone-treated mice was restored by a GABAA receptor agonist muscimol. These results suggest that intranasal administration of rotenone decreases GABAergic synaptic transmission in layer V pyramidal neurons of the mouse insular cortex, the result of which leads to impairment of LTD and conditioned taste aversion memory.
Highlights
Rotenone is a highly specific inhibitor of mitochondrial complex I that originates from the roots of plants [1]
We found that the intranasal administration of rotenone impaired conditioned taste aversion memory to bitter taste in mice
We found that the intranasal administration of rotenone impaired GABAergic synaptic transmission and long-term depression (LTD) without affecting glutamatergic synaptic transmission and long-term potentiation (LTP)
Summary
Rotenone is a highly specific inhibitor of mitochondrial complex I that originates from the roots of plants [1]. Rotenone can pass through the blood–brain barrier, reaches the brain, and accumulates in mitochondria where it causes impairment of oxidative phosphorylation by inhibiting complex I and a decrease in energy production, which leads to neuronal death [3]. Evidence has shown that chronic treatment of animals with rotenone-induced selective degeneration of dopaminergic neurons and terminals in the substantia nigra pars compacta and striatum, respectively, motor deficits and postural imbalance reminiscent of Parkinson’s disease (PD) [4,5,6,7]. The neurotoxic effects of rotenone are not specific to the dopaminergic system. The chronic administration of rotenone produces motor deficits including rigidity, postural instability, akinesia/bradykinesia and tremor, and extranigral signs and non-motor symptoms such as gastrointestinal dysfunction, hyposmia, sleep disturbance, circadian dysfunction, cognitive impairment, anxiety, and depression [6,7,9]. There is no study to examine the effects of rotenone on conditioned taste aversion memory
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
