We first verified that our 12-arm radial maze test enabled demonstration of memory deficits in rats treated with the muscarinic antagonist scopolamine hydrobromide (0.5 mg/kg, i.p.). We then investigated whether a systemically-injected quaternary-ammonium derivate of this antagonist (scopolamine methylbromide; MBR), which poorly crosses the blood–brain barrier (BBB), altered maze performance after a 45-min exposure to 2.45 GHz electromagnetic field (EMF; 2 μs pulse width, 500 pps, whole-body specific energy absorption rate [SAR] of 2.0 W/kg, ±2 dB and brain averaged SAR of 3.0 W/kg, ±3 dB); if observed, such an alteration would reflect changes in BBB permeability. The drug was injected before or after exposure. Controls were naïve rats (no experience of the exposure device) and sham-exposed rats (experience of the exposure device without microwaves). In a final approach, rats were subjected to i.v. injections of Evans blue, a dye binding serum albumin, before or after EMF exposure. Whether scopolamine MBR was injected before or after exposure, the exposed rats did not perform differently from their naïve or sham-exposed counterparts. Thus, EMFs most probably failed to disrupt the BBB. This conclusion was further supported by the absence of Evans blue extravasation into the brain parenchyma of our exposed rats.