Biomedical subjects

Anton Reiner

Publications and source records attributed to Anton Reiner.

22 records · Page 2Linked to original sources

PubMed2002

Cellular localization and development of neuronal intranuclear inclusions in striatal and cortical neurons in R6/2 transgenic mice.

The cellular localization and development of neuronal intranuclear inclusions (NIIs) in cortex and striatum of R6/2 HD transgenic mice were studied to ascertain the relationship of NIIs to symptom formation in these mice and gain clues regarding the possible relationship of NII formation to neuropathology in Huntington's disease (HD). All NIIs observed in R6/2 mice were ubiquitinated, and no evidence was observed for a contribution to them from wild-type huntingtin; they were first observed in cortex and striatum at 3.5 weeks of age. In cortex, NIIs increased rapidly in size and prevalence after their appearance. Generally, cortical projection neurons developed NIIs more rapidly than cortical interneurons containing calbindin or parvalbumin. Few cortical somatostatinergic interneurons, however, formed NIIs. In striatum, calbindinergic projection neurons and parvalbuminergic interneurons rapidly formed NIIs, but they formed more gradually in cholinergic interneurons, and few somatostatinergic interneurons developed NIIs. Striatal NIIs tended to be smaller than those in cortex. The early accumulation of NIIs in cortex and striatum in R6/2 mice is consistent with the early appearance of motor and learning abnormalities in these mice, and the eventual pervasiveness of NIIs at ages at which severe abnormalities are evident is consistent with their contribution to a neuronal dysfunction underlying the abnormalities. That cortex develops larger NIIs than striatum, however, is inconsistent with the preferential loss of striatal neurons in HD but is consistent with recent evidence of early morphological abnormalities in cortical neurons in HD. That calbindinergic and parvalbuminergic striatal neurons develop large NIIs is consistent with a contribution of nuclear aggregate formation to their high degree of vulnerability in HD.

Aging↗

PubMed2002

Selective loss of striatal preprotachykinin neurons in a phenocopy of Huntington's disease.

Phenocopies of Huntington's disease (HD) are individuals with a family history, clinical symptoms, and occasionally pathological evidence of HD but without an expanded CAG repeat within the HD gene. We report on an HD phenocopy with selective loss of preprotachykinin (PPT) neurons, dysfunction of surviving PPT neurons, preservation of preproenkephalin (PPE) neurons within the striatum, and greater loss of immunohistochemical staining for substance P in terminals of striatal neurons projecting to the substantia nigra, than in those projecting to the internal pallidal segment. This case demonstrates the existence of one type of striatal lesion that may produce a clinical picture similar to HD, and raises the possibility of a rare hereditary disease that mimics HD.

Aged↗

PubMed2002

Temporal relationship of choroidal blood flow and thickness changes during recovery from form deprivation myopia in chicks.

When form deprived, young chicks rapidly develop axial myopia, from which they recover if the treatment is ceased at a sufficiently early age. The increased axial growth of the eye is accompanied by choroidal thinning and decreased choroidal blood flow (ChBF). In contrast, during the early part of the recovery process, the choroid thickens, shifting the retina towards the new plane of focus. Little information is available about ChBF during recovery from myopia. Because of the possibility that choroidal thickening during recovery from myopia might be driven by an increase in ChBF, the temporal relationship of ChBF and choroidal thickness changes was examined during such recovery. White Leghorn chicks were form deprived from 3 days of age for 2-3 weeks using detachable plastic diffusers. Axial ocular dimensions, including choroidal thickness, were then measured by high frequency A-scan ultrasonography at various times after the diffusers were removed up to 240 hr. ChBF was measured transclerally immediately following the A-scan ultrasonography, using laser Doppler flowmetry. In the chicks measured immediately after diffuser removal, the vitreous chamber was 29.9% longer, the choroid was 6.4% thinner and ChBF was 13.7% less in the treated than in the non-treated control eyes. These changes are characteristic of myopic chick eyes and are reversible in young eyes. Thus, in chicks examined 7 hr after diffuser removal, the ChBF in recovering eyes was now greater than that in control eyes. This ChBF increase peaked about 19 hr after the diffusers were removed. The mean increase in ChBF in treated eyes for the 7-30 hr monitoring period was 187%, relative to control eyes. ChBF in the treated eyes gradually returned to the control level after this time. By contrast to the early, transient increase in ChBF, significant choroidal thickening was not observed in treated eyes until 30 hr after diffuser removal, and continued to increase relative to control eyes over the remainder of the monitoring period, reaching a final mean value of 182%. This study demonstrates, in chick eyes recovering from form deprivation myopia, large increases in ChBF that preceded increases in choroidal thickness and were also more transient than the latter. These results raise the possibility that the increase in ChBF may trigger or even drive the subsequent onset of choroidal expansion, perhaps by facilitating the filling of the choroidal lymphatic lacunae that are well developed in the avian eye.

Animals↗

PubMedDate not supplied

Functional circuitry of the avian basal ganglia: implications for basal ganglia organization in stem amniotes.

Histochemical, pathway tracing, and neuropeptide/neurotransmitter localization studies in birds, reptiles and mammals during the 1970s and 80s clearly showed that the telencephalon in all amniotes consists of a prominent ventrally situated subpallial region termed the basal ganglia, and a large overlying region involved in higher order information processing termed the pallium or cortex. These studies also showed that the basal ganglia in all extant amniote groups possessed neurochemically and hodologically distinct striatal and pallidal territories. More recently, studies of the localization of genes controlling regional brain development have confirmed the homology of the basal ganglia among amniotes. In our ongoing studies, we have identified several aspects of the functional organization of the basal ganglia that birds also share with mammals. These include: (1) an extensive glutamatergic "cortico"-striatal input and distinctive, cell-type specific localization of glutamate receptor subtypes; (2) an extensive, presumptively glutamatergic intralaminar thalamic input to striatal neurons; (3) an extensive dopaminergic input from the midbrain targeting both substance P (SP) type and enkephalin (ENK) type striatal projection neurons, with SP-type striatal neurons seemingly richer in the D-1 type dopamine receptor; and (4) SP+ and ENK+ striatal outputs giving rise to functionally distinct so-called direct and indirect motor output pathways, with the direct pathway having a pallido-thalamo-motor cortex loop and the indirect pathway relaying back to the direct circuit via the subthalamic nucleus. These findings suggest that the major aspects of the cellular organization and functional circuitry of the basal ganglia in stem amniotes were already as observed in living amniotes, as therefore presumably was its key role in movement control. Because the organization of the basal ganglia of anamniotes is clearly less elaborate than in amniotes, and because the basal ganglia and cortex in amniotes are clearly extensively interconnected structures, it seems likely that stem amniotes were characterized by a major step forward in the grade of telencephalic organization of both the basal ganglia and the pallium.

Afferent Pathways↗