Differential effects of muscarinic receptor blockade in prelimbic cortex on acquisition and memory formation of an odor-reward task

Abstract

The present experiments determined the consequences of blocking muscarinic cholinergic receptors of the prelimbic (PL) cortex in the acquisition and retention of an odor-reward associative task. Rats underwent a training test (five trials) and a 24-h retention test (two retention trials and two relearning trials). In the first experiment, rats were bilaterally infused with scopolamine (20 or 5 microg/site) prior to training. Although scopolamine rats showed acquisition equivalent to PBS-injected controls, they exhibited weakened performance in the 24-h retention test measured by number of errors. In the second experiment, rats were injected with scopolamine (20 microg/site) immediately or 1 h after training and tested 24 h later. Scopolamine rats injected immediately showed severe amnesia detected in two performance measures (errors and latencies), demonstrating deficits in retention and relearning, whereas those injected 1 h later showed good 24-h test performance, similar to controls. These results suggest that muscarinic transmission in the PL cortex is essential for early memory formation, but not for acquisition, of a rapidly learned odor discrimination task. Findings corroborate the role of acetylcholine in consolidation processes and the participation of muscarinic receptors in olfactory associative tasks.

Figure 1.

(A) Photomicrograph of Cresyl violet staining at the level of the PL area (AP, 3.50 mm anterior to bregma) showing the cannula track and the microinjector tip of a representative subject. (B,C) Microinjector tip placements for different groups throughout the rostral-caudal extent of the PL (from 3.70 to 2.70 mm anterior to bregma) in experiments 1 (B) and 2 (C). Reprinted with permission from Elsevier © 1997, Paxinos and Watson (1997). (●) n = 1, (*) n = 2, (+) n = 3. (Cg1) Cingulated cortex area 1; (fmi) forceps minor of the corpus callosum; (IL) infralimbic cortex; (PL) prelimbic cortex.

Figure 2.

Pre-acquisition scopolamine injections in the prelimbic cortex. (A) Latency to make the correct response (±SEM) over the three first acquisition trials (Acq123), the two last acquisition trials (Acq45), the two first 24-h test trials (Retention), and the two last 24-h test trials (Relearning). All groups show similar performance both in acquisition and 24-h test. (B) Number of errors before making the correct response (±SEM) over the three first acquisition trials (Acq123), the two last acquisition trials (Acq45), the two first 24-h test trials (Retention) and the two last 24-h test trials (Relearning). All groups show similar performance in the acquisition, but both SCOP groups commit more errors than the control group in the retention phase, and the SCOP20 group in the relearning the phase. (**) P ≤ 0.001, (*) P < 0.05.

Figure 3.

Latency to find the buried cookie (±SEM) in the olfactory perception test. SCOP groups show similar latencies to the control group.

Figure 4.

Post-acquisition scopolamine injections (immediately or 1 h after) in the prelimbic cortex. (A) Latency to make the correct response (±SEM) over the three first acquisition trials (Acq123), the two last acquisition trials (Acq45), the two first 24-h test trials (Retention), and the two last 24-h test trials (Relearning). The SCOP-Immed group demonstrates more latency to nose-poking than VEH-Immed and SCOP-1h both in retention and relearning. (B) Number of errors before making the correct response (±SEM) over the three first acquisition trials (Acq123), the two last acquisition trials (Acq45), the two first 24-h test trials (Retention), and the two last 24-h test trials (Relearning). The SCOP-Immed group commit more errors than the VEH-Immed group both in retention and relearning and also the SCOP-1h group in retention. The SCOP-Immed group significantly impaired performance from Acq45 to Retention, indicated by higher latencies and more errors. (***) P < 0.0001; (**) P ≤ 0.01; (*) P < 0.05.