BIC administration changed MG-132 ic50 the shape of the SF tuning curve of the spike response from band-pass to low-pass. We took the tuning curve obtained under the BIC condition as an estimated excitatory contribution to the control tuning curve and then estimated the difference between tuning curves recorded with and without BIC as the tuning curve of the estimated GABAergic inhibitory contribution.

The SF tuning profile of estimated inhibition (Estimated-Inh) varied widely from cell to cell, as did estimated excitation (Estimated-Ex). Nonetheless, the relationship that Estimated-Inh exhibited more low-pass tuning than did Estimated-Ex was well conserved in the majority of cells, and the relationship refined the SF tuning of Estimated-Ex toward the band-pass tuning of the geniculate output. Lowering the stimulus contrast decreased the response magnitude, but did not change the degree of band-pass tuning. The GABAergic refinement of the SF tuning was also observed at low stimulus contrast, but was weaker than at high contrast, suggesting that GABAergic inhibition is regulated in coordination with excitatory

inputs to keep the degree of the band-pass tuning constant. We therefore concluded that the degree of band-pass tuning selleck inhibitor is conserved contrast invariantly in the lateral geniculate nucleus on the basis of the dynamic regulatory action of GABAergic inhibition. “
“Three experiments were conducted to contrast the hypothesis others that hippocampal N-methyl-d-aspartate (NMDA) receptors participate directly in the mechanisms of hippocampus-dependent learning with an alternative view that apparent impairments of learning induced by NMDA receptor antagonists arise because of drug-induced neuropathological and/or sensorimotor disturbances. In Experiment 1, rats given a chronic i.c.v. infusion of d-AP5 (30 mm) at 0.5 μL/h were selectively impaired, relative to aCSF-infused animals, in place but not cued navigation learning

when they were trained during the 14-day drug infusion period, but were unimpaired on both tasks if trained 11 days after the minipumps were exhausted. d-AP5 caused sensorimotor disturbances in the spatial task, but these gradually worsened as the animals failed to learn. Histological assessment of potential neuropathological changes revealed no abnormalities in d-AP5-treated rats whether killed during or after chronic drug infusion. In Experiment 2, a deficit in spatial learning was also apparent in d-AP5-treated rats trained on a spatial reference memory task involving two identical but visible platforms, a task chosen and shown to minimise sensorimotor disturbances. HPLC was used to identify the presence of d-AP5 in selected brain areas. In Experiment 3, rats treated with d-AP5 showed a delay-dependent deficit in spatial memory in the delayed matching-to-place protocol for the water maze.