The central pattern generators (CPGs) for locomotion, located in the lumbar spinal cord, are functional at birth in the rat. Their maturation occurs during the last few days preceding birth, a period during which the first projections from the brainstem start to reach the lumbar enlargement of the spinal cord. The goal of the present study was to investigate the effect of suppressing inputs from supraspinal structures on the CPGs, shortly after their formation. The spinal cord was transected at the thoracic level at birth [postnatal day 0 (P0)]. We examined during the first postnatal week the capacity of the CPGs to produce rhythmic motor activity in two complementary experimental conditions. Left and right ankle extensor muscles were recorded in vivo during airstepping, and lumbar ventral roots were recorded in vitro during pharmacologically evoked fictive locomotion. Mechanical stimulation of the tail elicited long-lasting sequences of airstepping in the spinal neonates and only a few steps in sham-operated rats. In vitro experiments made simultaneously on spinal and sham animals confirmed the increased excitability of the CPGs after spinalization. A left-right alternating locomotor pattern was observed at P1-P3. Both types of experiments showed that the pattern was disorganized at P6-P7, and that the left-right alternation was lost. Alternation was restored after the activation of serotonergic 5-HT(2) receptors in vivo. These results suggest that descending pathways, in particular serotonergic projections, control the strength of reciprocal inhibition and therefore shape the locomotor pattern in the neonatal rat.

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Several data have shown that the neural cell adhesion molecule (NCAM) is necessary for long-term memory formation and might play a role in the structural reorganization of synapses. The NCAM, encoded by a single gene, is represented by several isoforms that differ with regard to their content of ␣-2,8-linked sialic acid residues (PSA) on their extracellular domain. The carbohydrate PSA is known to promote plasticity, and PSA-NCAM isoforms remain expressed in the CA3 region of the adult hippocampus. In the present study, we investigated the effect on spatial memory consolidation of a PSA gain of function by injecting a PSA mimetic peptide (termed pr2) into the dorsal hippocampus. Mice were subjected to massed training in the spatial version of the water maze. Five hours after the last training session, experimental mice received an injection of pr2, whereas control mice received PBS or reverse peptide injections in the hippocampal CA3 region. Memory retention was tested at different time intervals: 24 h, 1 wk, and 4 wk. The results showed that the post-training infusion of pr2 peptide significantly increases spatial performance whenever it was assessed after the training phase. By contrast, administration of the control reverse peptide did not affect retention performance. These findings provide evidence that (1) PSA-NCAM is involved in memory consolidation processes in the CA3 hippocampal region, and (2) PSA mimetic peptides can facilitate the formation of long-term spatial memory when injected during the memory consolidation phase.Evidence has been found to suggest that the properties of the memory trace change in a time-dependent manner. The formation of a long-term memory involves the conversion of a labile short-term memory into a long-lasting stable trace (Muller and Pilzecker 1900;McGaugh 2000;Dudai 2004). This process of post-acquisition stabilization of the trace within minutes or hours after the learning is called memory consolidation or, more precisely, cellular or synaptic consolidation (Dudai and Morris 2000). Synaptic consolidation has been described in numerous species and in various long-term memory tasks (see Dudai 2004). Moreover, in function of the type of memories tested, consolidation involves distinct brain regions (Ambrogi Lorenzini et al. 1999). Nevertheless, consolidation of many types of memories and especially of spatial memory depends on hippocampal processing, and memory consolidation correlates with changes in neuronal connectivity pattern in this structure (Andersen and Soleng 1998;Bailey et al. 2000;Martin et al. 2000). This synaptic reorganization depends on the activation of molecular cascades, and considerable evidence suggests that the neural cell-adhesion molecules (NCAMs) are crucial players in these events (Bailey et al. 1992, Doyle et al. 1992aRonn et al. 1995). Two waves of NCAM synthesis are observed, one immediately following training and a second several hours (4-8 h) post-training (Doyle et al. 1992a; Rose, 1995a,b). This second wave of glycoprotein synthesis seems to ...

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