Skip to main content
. Author manuscript; available in PMC: 2012 Mar 4.
Published in final edited form as: Cell. 2011 Mar 4;144(5):810–823. doi: 10.1016/j.cell.2011.02.018

Figure 6. Disruption of MCT2 expression impairs long-term memory.

Figure 6

Mean %, n, latency and detailed statistic are reported in Table S5.

(A) Examples and densitometric analysis of MCT2, MCT1 and MCT4 quantitative western blots of extracts from dorsal hippocampal punches taken around the needle placement from trained rats that received hippocampal MCT2- or SC2-ODN injections and were euthanized 12 h after training (n=4/group). Data are expressed as mean percentage ± SEM of trained-SC2-ODN (100%) mean values. All MCTs values were normalized to those of actin.

(B-D) Acquisition (acq) and retention are expressed as mean latency ± SEM (in seconds, sec).

(B) Hippocampal injections of MCT2-ODN 1 hr before training did not affect short-term memory tested 1 hr later (n=8/group).

(C) Hippocampal injections of MCT2-ODN disrupted long-term memory. MCT2- or SC2-ODN were injected 1 hr before training. Rats were tested 24 hr after training (Test 1) and 6 days later (Test 2). The memory disruption persisted at Test 2, and memory did not recover following a reminder foot shock (Test 3). The amnesic rats that received the MCT2-ODN showed normal retention after re-training (Test 4) (n = 8/group).

(D) Neither L-lactate nor glucose rescued the memory impairment induced by MCT2 disruption (n = 6-8/group). MCT2- or SC2-ODN were injected 1 hr before training. Llactate, glucose or vehicle (PBS) were injected 15 min before training. Rats were tested 24 hr after training (Test 1) and 6 days later (Test 2). * p < 0.05.