Morphological changes in the suprachiasmatic nucleus of aging female marmosets (Callithrix jacchus).

The suprachiasmatic nuclei (SCN) are pointed to as the mammals central circadian pacemaker. Aged animals show internal time disruption possibly caused by morphological and neurochemical changes in SCN components. Some studies reported changes of neuronal cells and neuroglia in the SCN of rats and nonhuman primates during aging. The effects of senescence on morphological aspects in SCN are important for understanding some alterations in biological rhythms expression. Therefore, our aim was to perform a comparative study of the morphological aspects of SCN in adult and aged female marmoset. Morphometric analysis of SCN was performed using Nissl staining, NeuN-IR, GFAP-IR, and CB-IR. A significant decrease in the SCN cells staining with Nissl, NeuN, and CB were observed in aged female marmosets compared to adults, while a significant increase in glial cells was found in aged marmosets, thus suggesting compensatory process due to neuronal loss evoked by aging.

Differential vulnerability of the rat retina, suprachiasmatic nucleus and intergeniculate leaflet to malnutrition induced during brain development.

We investigated in young rats the effects of malnutrition on the main structures of the circadian timing system: retina, hypothalamic suprachiasmatic nuclei (SCN), thalamic intergeniculate leaflet, retinohypothalamic- and geniculohypothalamic tracts. Control rats were born from mothers fed a commercial diet since gestation, and malnourished rats from mothers fed a multideficient diet since gestation (GLA group) or lactation (LA group). After weaning, pups received the same diet as their mothers, and were analysed at postnatal days 27, 30-33 and 60-63. Brain sections were processed to visualise in the SCN neuropeptide Y immunoreactivity and terminal labeling after intraocular tracer injections. Nissl staining was used to assess cytoarchitectonic boundaries of the SCN and cell features in retinal whole mounts. Cell counts, morphometric and densitometric analysis were performed. Compared with controls, the total retinal surface was reduced and the topographical distribution of retinal ganglion cells was altered in malnourished rats, with changes in their density. Alterations were also detected in the SCN dimensions in the GLA and LA groups at one and two postnatal months, as well as in the SCN portion occupied by the retinal input in the GLA group at days 30-33, but not in the NPY-containing geniculohypothalamic tract. The present data point to subtle changes, with a low and differential vulnerability to early malnutrition, of structures involved in circadian timing regulation. Furthermore, the present findings suggest that the altered circadian rhythmicity previously documented in malnourished rats cannot be ascribed to impaired development of the retino- and geniculohypothalamic projections to the SCN.

Postnatal development of neuron number and connections in the suprachiasmatic nucleus of the hamster.

We had previously found a ca. 30% cell death during the prenatal ontogeny of the suprachiasmatic nucleus (SCN) of lambs. The period of neuron death was preceded by the establishment of the retinohypothalamic connections, a major input to this nucleus that allows the entrainment to light of the circadian rhythms generated by the SCN. The present study determined the temporal relationship between the period of ontogenetic neuron death and the establishment of the principal afferent and efferent connections of the SCN in hamsters. We found that during the first 3 postnatal days the SCN volume increases mainly by the addition of cells. After a peak 6140 neurons on each side during the third postnatal day, the SCN underwent an acute decrease of about 40% in neuron number, which led to the final adult complement of neurons, estimated in 3400 neurons per nucleus. The connections of the SCN were studied by placing DiI crystals either into the optic nerve, or into the SCN of brains fixed at different ages. We found, in agreement with previous studies, that retinal axons can be detected after the fifth postnatal day, that is, after the large decrease in neuron number. As for the SCN efferents, they began to invade the appropriate targets during the second postnatal day, followed by a large increase in the density of these efferent projection in the subsequent days. In conclusion, the massive neuronal death in the SCN was preceded by the formation of efferent connections, and followed by the formation of the retinohypothalamic tract.