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Authors & Affiliations
Jacek Wróbel, Daniel K. Wójcik, Mark J. Hunt
Abstract
NMDA receptor antagonists, such as MK801, produce hyperlocomotion and affect the dopamine (DA) system by increasing ventral tegmental area (VTA) activity and enhancing DA release in many regions of the rat brain. NMDAR antagonists also enhance the power of high-frequency oscillations (HFO) in cortical and subcortical areas. The olfactory bulb (OB), a generator of NMDAR-enhanced HFO, contains DA receptors (D1R/D2R) and periglomerular DA neurons. However, the role of DA in the OB in the modulation of MK801-enhanced HFO and locomotion is unknown. Selective DA agonists (SKF38393, quinpirole) and antagonists (SCH23390, eticlopride) were injected systemically or infused locally to the OB of rats 30-min. after 0.15 mg/kg MK801 injection. Local field potentials and beam breaks were recorded. A separate group received 10 ng TTX infusion to the VTA after MK801 injection. Local infusion of DA receptor antagonists to the OB dose-dependently reduced MK801-enhanced locomotion. Systemic or local injection of D1R/D2R agonists or antagonists did not substantially affect MK801-enhanced HFO power, although reductions in HFO frequency were observed after D2R agonist administration. Reversible VTA inhibition reduced MK801-enhanced locomotion and HFO power. In summary, reductions in MK801-enhanced locomotion can occur after inhibition of the VTA, or local blockade of OB DA receptors. Increases in aberrant HFO power, in the OB, depend on VTA activity, but since local modulation of DA receptors produced little change in HFO power, this effect on OB rhythm is likely due to VTA’s actions elsewhere in the brain.