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The present study was undertaken to investigate the effect of prenatal protein deprivation on the postnatal development of the mossy fiber plexus of the hippocampal formation on postnatal (P) days 15, 30, 90, and 220. Although there is extensive information about the effects of malnutrition on cell body and dendrite morphology, little attention has been paid to axons or axon plexuses. The mossy fiber plexus represents the dentate gyrus granule cell axonal projection to areas CA4 and CA3 of the hippocampal formation and is readily demonstrated with Timm's heavy metal stain. With the use of this stain, the plexus was measured at 13 levels throughout the hippocampal complex. There was no effect of the diet on the anatomical distribution of the plexus. The current study, however, does show significant effects of prenatal protein malnutrition on postnatal development of the mossy fiber plexus that are age dependent. The prenatally malnourished rats show significant deficits in the total rostro-caudal extent and volume of the plexus on P15, P90, and P220, with the most marked dietary effect on P220. There was no significant diet effect on P30 in either extent or volume.

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This study examined how chronic protein malnutrition (6% casein diet) affected the electrocorticogram (ECoG) in young rats following 24 h of sleep deprivation. Baseline (basal day) ECoG-polygraphic recordings were obtained in Sprague-Dawley rats after which animals were sleep-deprived for 24 h by means of a slowly rotating cylinder. ECoG recordings were subsequently obtained for a further three days of recovery. Body weight was significantly reduced in malnourished rats from postnatal day 4 until 34. On basal day, malnourished rats showed a significant increase of slow wave sleep (SWS) during the light and dark phases of the circadian period, and over the 24 h of recording in comparison to control rats. Also, rapid eye movement sleep (REMS) was significantly increased in these rats during the 12-h dark phase of basal day, but wake ECoG activity was significantly reduced during both light and dark phases and over the 24 h of recording, as a result of sleep increases. After sleep deprivation, young malnourished rats failed to show any significant SWS rebound and, unlike control rats, they did not regain pre-deprivation SWS levels within the 3-day post-deprivation recovery period. Further, malnourished rats also failed to have a significant REMS rebound, especially during the dark phase. These results show an important alteration produced by protein malnutrition in the homeostatic and circadian control of vigilance states before and after sleep deprivation.