Biomedical subjects

R J Pentney

Publications and source records attributed to R J Pentney.

24 records · Page 2Linked to original sources

PubMedDate not supplied

MR imaging of normal rat brain at 0.35 T and correlated histology.

A custom-built small-animal transceiver was used for in vivo imaging of normal rat brain at 0.35 T, with the objective of identifying anatomic components by comparison of images with corresponding histologic sections. The cerebrum, cerebellum, brain stem, ventricles, hippocampus, and subarachnoid space were identified and cerebrospinal fluid (CSF) was differentiated from gray matter and white matter on coronal and transaxial magnetic resonance (MR) images. These images compare favorably with those obtained by others at higher field strengths in regard to delineating major neuroanatomic structures. It is concluded that this technique will be useful for investigating small-animal models of human neurologic disease involving morphologic and morphometric changes in gray matter, white matter, and CSF-filled spaces.

Animals↗

PubMedDate not supplied

Quantitative analysis of dendritic networks of Purkinje neurons during aging.

This study examined quantitative parameters of Golgi-Cox stained Purkinje dendritic networks in Fischer 344 rats of three different ages. Topological patterns of branching, metric parameters of the networks, and spine densities on terminal dendritic branches of the networks were measured and analyzed relative to age of the animals. The data suggested that the networks were topologically stable at all ages, but decreases in spine density on terminal branches, in length per terminal branch, in total length of terminal branches, and in total length of the entire network were shown. Decreases in spine density were found in cells of both older groups of rats; however, decreases in length parameters were significant only in the cells of rats in the intermediate age group.

Aging↗

PubMedDate not supplied

Evidence for nonrandom regression of dendrites of Purkinje neurons during aging.

This study examined dendritic networks of Purkinje neurons for randomness of age-related changes in cerebella from Fischer 344 rats at three ages. Terminal dendritic segments were studied in relation to their distance from the neuronal soma (path length). The data indicated that the terminal dendritic segments furthest from the cell body were preferentially affected during aging and there was a redistribution of the remaining terminal segments in cells from rats of the intermediate age group. The data also suggested that dendritic regrowth occurred in proximal regions of networks from rats in the oldest group.

Age Factors↗

PubMedDate not supplied

Morphometric analyses of Purkinje and granule cells in aging F344 rats.

In this study, the Purkinje neurons and granule neurons in the cerebellar cortex were studied in male Fischer 344 rats at 3, 9, 18, and 27 months of age. The numbers of Purkinje cells (PC) and granule cells (GC) in folia IV, VII, and X of the vermis were quantitated with the disector stereological technique. The numbers of PC and GC and the ratio of PC to GC were stable with advancing age. Measurements of the molecular layer, however, showed that this layer, the site of synaptic contact between GC and PC, decreased in volume with age.

Aging↗

PubMedDate not supplied

Morphometric evidence that the total number of synapses on Purkinje neurons of old F344 rats is reduced after long-term ethanol treatment and restored to control levels after recovery.

Clinical symptoms of alcohol abuse may be confused with symptoms of age-related neuropathologies in human patients. It is important, therefore, to determine the relationships between alcohol abuse and changes in brain structures in well-controlled studies of ageing subjects. Currently there is little well-documented information of this type available. The purpose of this study was to determine whether long-term ethanol treatment during ageing would lead to reductions in synaptic input to cerebellar Purkinje neurons (PN) of old F344 rats that: (1) were more severe than those attributable to ageing alone; (2) might be responsible for an ethanol-related deletion of dendritic segments of PN in old F344 rats shown previously in this laboratory. The total number of synapses per PN dendritic arbor was determined after ethanol treatment of old F344 rats for 40 weeks between 12 and 22 months of age and in similarly treated rats given a subsequent 20-week period of recovery between 22 and 27 months of age. Groups of age-matched rats fed a chow diet and water and rats pair-fed an isocaloric liquid diet lacking ethanol served as controls. The volume of the molecular layer per PN arbor and the numerical density of synapses in the molecular layer was determined from light microscopic preparations of a fixed volume of the cerebellar cortex. Photographic montages of the ultrastructure of the molecular layer of the cerebellum were also prepared from each rat for measurements of synaptic numerical densities. From the volume of the molecular layer per PN arbor and the numerical density of synapses in the molecular layer, the total number of synapses per PN arbor was estimated for each rat. There was a significant reduction in synapses in the old ethanol-treated rats relative to age-matched chow-fed rats. There were also significant interactions between recovery and treatment prior to recovery. During recovery, synaptic numbers in the old, ethanol-treated rats were restored to pre-recovery control levels whereas synaptic numbers in the old, chow-fed rats were significantly reduced during the same period of time. There were no significant diet- or age-related changes in synaptic numbers in the pair-fed control rats during treatment or recovery. The pattern of reduction in synaptic numbers during ethanol treatment and restoration of synaptic numbers during recovery from treatment paralleled the pattern of ethanol-related segment loss and recovery-related segment regrowth noted earlier in PN arbors of old F344 rats, suggesting that reductions in the numbers of synapses and deletion of terminal dendritic segments were causally related in this strain.

Age Factors↗

PubMedDate not supplied

Quantitative measures of mature neuronal morphology after in utero ethanol exposure.

Dendritic networks of neocortical pyramidal cells and cerebellar Purkinje cells of mature adult rats which were exposed to ethanol in utero were analyzed for quantitative deviations from the normal branching patterns present in neurons of unexposed rats. No significant quantitative differences were found between cells of mature ethanol-exposed and control animals. The absence of quantitative deficits in the branching dendrites of these neuronal populations (which do exhibit ethanol-induced maturational retardation when examined at birth) suggests that ethanol treatment confined to the short gestation period in these animals may be of insufficient duration to produce irreversible maturational deficits in the growth pattern of dendrites.

Animals↗