Memory impairment in early sensorimotor deprived rats is associated with suppressed hippocampal neurogenesis and altered CREB signaling.

Sensorimotor function is important for cognitive development; however, little experimental evidence exists to support this assumption. In this study we tested the hypothesis that altered cAMP response element binding (CREB) protein induction and activity-regulated cytoskeletal-associated gene (Arc) expression may underlie the suppression of hippocampal neurogenesis and memory impairment associated with early sensorimotor deprivation. Associated memory was evaluated in sensorimotor deprived (T) and sham operated (C) rats using a contextual fear-conditioning task. Hippocampal dentate gyrus (DG) neurogenesis was assessed by Brdu and NeuN labeling. Hippocampal DG CREB signaling was examined by measuring protein and mRNA levels of CREB and activity-regulated cytoskeletal-associated gene (Arc). Contextual freezing responses in the 1-day recall test were significantly lower in 25- and 35-day-old group T compared to C rats (P<0.01), indicating that hippocampal-dependent memory impairment was caused by early sensorimotor deprivation. Furthermore, group T rats exhibited significantly decreased CREB and Arc activation in the hippocampal DG at 25 and 35 days compared to in group C rats (P<0.01 for both). These changes may underlie decreased neurogenesis and impaired memory. No significant between groups differences were apparent in 45- and 60-day-old rats. These results suggest that early sensorimotor deprivation may alter CREB signaling, decrease Arc activation, suppress neurogenesis and ultimately impair memory.

The immunologic effect of TGF-beta1 chitosan nanoparticle plasmids on ovalbumin-induced allergic BALB/c mice.

Studies suggested that an increased transforming growth factor-beta (TGF-beta) level in the intestinal tract helps to alleviate symptoms of food allergy. An efficient method for in vivo delivery of TGF-beta is yet to be developed. In this report, we investigated some DNA-based therapeutic strategies. Our results demonstrate that a sustainable increase of TGF-beta protein in mouse intestinal tissue can be induced after oral administration by gavage of a TGF-beta expressing DNA vector that was packed in chitosan nanoparticles. Concomitantly, a significant amelioration of ovalbumin-induced food allergy symptoms was observed. Thus, our study supports this therapy being perhaps a better alternative to the previously reported protein-based strategies.

The influence of forepaw palmar sensorimotor deprivation on learning and memory in young rats.

This study examined the effects of early palmar forepaw sensorimotor deprivation on learning and memory in rats. Sensorimotor deprivation was performed on 18-day-old male rats. Controls were sham operated. Studies were performed on rats aged 18, 25, 35, 45 and 60 days. Morris water maze testing was used to assess learning and memory. Long-term potentiation (LTP) was assessed by electrophysiological means in slices obtained from the hippocampal Schaffer collateral pathway. Nissl staining was performed to assess pyramidal cell number in hippocampal CA1 and CA3 regions. Hippocampal N-methyl-d-aspartate receptor 1 (NMDAR1) mRNA and protein levels were assessed. Learning and short-term memory were significantly depressed in 25 and 35 day old sensorimotor deprived rats (P<0.01). LTP was also significantly depressed in sensorimotor deprived rats at these ages, while hippocampal CA1 pyramidal cell counts were significantly decreased (P<0.05). CA3 cell numbers were significantly lower in 25-day-old sensorimotor deprived rats (P<0.05). Both NMDAR1 mRNA and protein levels were significantly lower in sensorimotor deprived rats aged 25 and 35 days (P<0.05). These findings indicate that palmar surface forepaw sensorimotor deprivation impairs subsequent learning and memory in young rats. Decreased hippocampal pyramidal cell numbers and altered NMDAR1 expression may underlie this impairment.