Motor learning induces astrocytic hypertrophy in the cerebellar cortex.

Motor skill learning, but not mere motor activity, is associated with an increase in both synapse number and glial cell volume within the cerebellar cortex. The increase in synapse number has been shown to persist for at least 4 weeks in the absence of continued training. The present experiment similarly examined how a prolonged interruption in training affects the training-induced increase in astrocytic volume. Adult female rats were randomly allocated to either an acrobatic motor learning condition (AC) or a motor control condition (MC). The AC animals were trained to traverse a complex series of obstacles and each AC animal was pair matched with an MC animal that traversed an obstacle-free runway. These groups were further assigned to one of three training conditions. Animals in the early condition were trained for 10 consecutive days, animals in the delay condition received the same 10 days of training followed by a 28-day period without training, and animals in the continuous condition were trained for the entire 38 days. Unbiased stereological techniques were used to determine that AC animals had a significantly greater volume of astrocytes per Purkinje cell in the cerebellar paramedian lobule than the MC animals, a difference which was reduced (and not statistically detectable) among animals in the delay condition. These findings demonstrate that learning triggers the hypertrophy of astrocytic processes and furthermore that, unlike learning-induced synaptogenesis, astrocytic growth is reduced in the absence of continued training.

Geometry and cell density of rat craniofacial sutures during early postnatal development and upon in vivo cyclic loading.

Cranial sutures are unique to skull bones and consist of multiple connective tissue cell lineages such as mesenchymal cells, fibroblast-like cells, and osteogenic cells, in addition to osteoclasts. Mechanical modulation of intramembranous bone growth in the craniofacial suture is not well understood, especially during postnatal development. This study investigated whether in vivo mechanical forces regulate sutural growth responses in postnatal rats. Cyclic compressive forces with a peak-to-peak magnitude of 300 mN and 4 Hz were applied to the maxilla in each of 17-, 23-and 32-day-old rats for 20 min/day over 5 consecutive days. Computerized histomorphometric analysis revealed that cyclic loading significantly increased the average geometric widths of the premaxillomaxillary suture (PMS) to 86 +/- 7 microm, 99 +/- 12 microm, and 149 +/- 30 microm, representing 32%, 50%, and 39% increases for P17, P23, and P32 in comparison with age-matched sham controls. For the nasofrontal suture (NFS), cyclic loading significantly increased the average sutural widths to 88 +/- 15 microm, 92 +/- 10 microm, and 100 +/- 14 microm, representing 33%, 24%, and 32% increases for P17, P23, and P32 relative to age-matched controls. The average PMS cell density upon cyclic loading was 10182 +/- 132 cells/mm(2), 9752 +/- 661 cells/mm(2), and 9521 +/- 628 cells/mm(2), representing 62%, 35%, and 30% increases for P17, P23, and P32 in comparison with age-matched controls. For the NFS, cyclic loading increased the average cell density to 9884 +/- 893 cells/mm(2), 9818 +/- 1091 cells/mm(2), 9355 +/- 661 cells/mm(2), representing 44%, 46% and 40% increases at P17, P23, and P32 respectively. Osteoblast-occupied sutural bone surface was significantly greater in cyclically loaded sutures for P17, P23, and P32 than corresponding controls for both the PMS and NFS. On the other hand, cyclic loading elicited significantly higher sutural bone surface populated by osteoclast-like cells by P17 and P23 days, but not P32 days, for the PMS. For the NFS, sutural osteoclast surface was significantly higher upon cyclic loading for P23 and P32 days, but not P17. The present data demonstrate that cyclic forces are potent stimuli for modulating postnatal sutural development, potentially by stimulating both osteogenesis and osteoclastogenesis. Cyclic loading may have clinical implications as novel mechanical stimuli for modulating craniofacial growth in patients suffering from craniofacial anomalies and dentofacial deformities.