Prenatal stress alters spine density and dendritic length of nucleus accumbens and hippocampus neurons in rat offspring.

Prenatal stress alters neuronal morphology of mesocorticolimbic structures such as frontal cortex and hippocampus in the adult offspring. We investigated here the effects of prenatal stress on the spine density and the dendrite morphology of hippocampal pyramidal neurons and medium spiny cells from nucleus accumbens in prepubertal and adult male offsprings. Sprague-Dawley pregnant dams were stressed by restraining movement daily for 2 hours from gestational day 11 until delivery. Control mothers remained free in their home cage without water and food during the stressful event. Male offsprings from immobilized and control rats were left to grow until postnatal day (PD) 35 for the prepubertal group, and until PD 65 for the adult group. Spontaneous locomotor activity was assessed and then brains were removed to study the dendritic morphology by the Golgi-Cox stain method followed by Sholl analysis. Prenatally stressed animals demonstrated increased locomotion and alterations in spine density in the hippocampus and nucleus accumbens at both ages. However, prepubertal males showed an increase in spine density in the CA1 hippocampus with a decrease in CA3 hippocampus, whereas the adult group showed a decrease in the spine density in both of the regions studied. These results suggest that prenatal stress carried out during the middle of pregnancy affect the spine density and basal dendrites of pyramidal neurons of hippocampus, as well as the dendritic morphology of nucleus accumbens which may reflect important changes in the mesocorticolimbic dopaminergic transmission and behaviors associated with the development of psychiatric diseases such as schizophrenia.

Neonatal caffeine administration causes a permanent increase in the dendritic length of prefrontal cortical neurons of rats.

We studied the morphological changes of the dendritic length of the pyramidal neurons of the prefrontal cortex (PFC) induced by the effect of chronic administration of caffeine in the neonatal rat. The caffeine (50 mg/kg, s.c.) was injected from day 1 after birth (P1) to day 12 (P12). The morphology of the pyramidal neurons of layer 3 of the PFC was investigated in these animals at two different ages, before puberty (P35) and after puberty (P70). Before the animals were sacrificed by using overdoses of sodium pentobarbital and being perfused intracardially with 0.9% saline, the locomotor activity in a novel environment was measured. The brains were then removed, processed by the Golgi-Cox stain, and analyzed by the Sholl method. The dendritic morphology clearly showed that the neonatal animals administered caffeine showed an increase in the dendritic length of the pyramidal neurons of the PFC when compared with the control animals at both ages. The present results suggest that neonatal administration of caffeine may in part affect the dendritic morphology of the pyramidal cells of this limbic structure and this effect persists after puberty and may be implicated in several brain processes.

Alteration in dendritic morphology of cortical neurons in rats with diabetes mellitus induced by streptozotocin.

The animal model of streptozotocin-induced diabetes mellitus is used to study the changes produced by an increase in glucemia. The morphology of the pyramidal neurons of the prefrontal cortex, occipital cortex, and hippocampus was investigated in rats. The level of glucose in the blood was evaluated at 2 months, and the animals that exhibited more than 200 mg/dL were used. After 2 months of increasing blood-glucose level, the animals were sacrificed by an overdose of sodium pentobarbital and perfused intracardially with a 0.9% saline solution. The brains were removed, processed by the Golgi-Cox stain method, and analyzed by the Sholl method. Clearly, the rats with diabetes mellitus induced by streptozotocin showed a decrease in the dendritic length of pyramidal cells from all the analyzed regions (20% to 45%). Furthermore, the density of dendritic spines was decreased in all the pyramidal cells from the diabetic animals (36% to 58%). However, the pyramidal neurons of the CA1 hippocampus region were the most affected (58%). In addition, the Sholl analyses showed that the diabetic rats exhibited a decrease in the number of Sholl intersections when compared with the control group. The present results suggest that diabetes mellitus may in part affect the dendritic morphology in the limbic structures, such as prefrontal cortex, occipital cortex, and hippocampus, which are implicated in cognitive disorders.