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The scopolamine induced deficit was not reversed by treatment with 50 mg/kg P. minus.
However, the donepezil, G. biloba and the 100 mg/kg P. minus treated mice did not show a scopolamine induced deficit.
Post-hoc analysis showed a significant increase in path length in the scopolamine treated control mice on days one, two and three (p < 0.05) compared to vehicle treated mice indicating a scopolamine induced deficit in learning.
Application of 5 μM and 10 μM physostigmine into the bath solution immediately prior to the recordings did not rescue the LPS induced deficit in LTP (Additional file 4).
Higher dose of P minus (100 mg/kg) was able to attenuate scopolamine induced deficit in cognition in vivo by a reduction of total path length travelled and total errors prior to finding escape hole and increased duration in target segment during probe trial, indicating improved memory.
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The in vitro data from the present study, demonstrates that the extract has measurable anticholinesterase activity (68%), hence it may be that the extract induced increases in cholinergic tone, additionally providing an explanation for the attenuation of scopolamine induced deficits.
Furthermore, PCP induced deficits in spatial navigation at lower doses in LH than in Wistar rats.
In the current study, localized targeting of VGLUT1 expression within the dorsal hippocampus induced deficits in visual recognition and spatial memory that were actually more marked than those observed in VGLUT1 heterozygotes.
Our results also demonstrated that VAD induced deficits in spatial memory in the water maze.
The scopolamine induced deficits in learning were evidenced by an increase in the number of errors, latency, and path length.
The dose of 100 mg/kg P. minus extract also reversed scopolamine induced deficits in the retention (probe trial) aspect of the task.
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