Further, micro-infusion of CGP44532 directly into the ventral tegmental area elevated ICSS thresholds similarly in saline- and nicotine-treated rats.
Micro-infusion of strychnine (0.5 µgin 0.25 µlaCSF) within the superficial laminae of the MDH (n = 7) significantly increased the firing responses of Sp5O WDR neurons to brushing (Figure 3).
Micro-infusion of strychnine (0.5 µg in 0.25 µl aCSF) in the Sp5O significantly increased firing responses of WDR neurons to brushing (n = 9), without altering their basal firing and this effect lasted for 29±3 minutes (Figure 2).
We performed a similar experiment as in Figure 1A, except that the mice received a footshock at Reactivation (Training-2) at 5 s after they entered the dark compartment and then received micro-infusions of drugs immediately after Training-2.
The mice received a footshock in the reactivation (Training-2) session at 5 s after they entered the dark compartment and then received micro-infusions of drugs immediately after Training-2.
Interestingly, micro-infusions of β-lac into the amygdala, mPFC, or hippocampus blocked the enhancement of IA memory, indicating that activating proteasome-dependent protein degradation in these brain regions is required for the enhancement of IA memory.
In contrast, micro-infusion of ANI into the hippocampus or mPFC did not affect additional training.
In contrast, micro-infusion of ANI into the hippocampus or mPFC blocked the enhancement, but not the underlying performance.
Micro-infusion of AMPAR antagonist CNQX 30 min before the taste learning did not affect the incidental form of the appetitive taste memory (T (14) = 0.335, p=0.743).
Micro-infusion of ANI into the amygdala blocked IA memory as seen by the reduction in performance between Reactivation and PR-LTM.
(E and F ) Effects of micro-infusion of ANI (62.5 μg) or β-lac (9.6 ng) into the hippocampus immediately after training on IA memory.
