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L J Quackenbush

Publications and source records attributed to L J Quackenbush.

At least 19 recordsLinked to original sources
PubMed1993

Models for growth, decline and regrowth of the dendrites of rat Purkinje cells induced from magnitude and link-length analysis.

This study examines Purkinje neurons of rats aged 1, 10, 18 and 28 months to investigate growth and decline in the magnitude of the dendritic tree, i.e. the number of exterior links (terminal segments) per cell. Growth in the mean number of exterior links was observed from 1 to 10 months, decline at 18 months and regrowth at 28 months. At 10, 28, and especially at 18 months, the cell size frequency distribution indicates two groups of cells, one of small and the other of large sized cells. The study also examines the relationship of age to lengths of topologically defined links of various types. For each age group we find that exterior links are longer than interior links (non-terminal or intermediate segments). Analysis of the geometric mean lengths of subtypes of exterior and interior links at maturity (10 months) indicates that they follow a Fibonacci series of link lengths, such that mean lengths of topologically defined types of mean exterior links are either about 13 or 8 microns long, while interior links are about 5 microns long. A sequential growth model for adding exterior links is suggested to illustrate a style of growth which could account for the various mean link lengths and the Fibonacci ratio (1.618) between their lengths. Interior link lengths are also dependent on the generation of exterior links from the sides of pre-existing interior links. If the Strahler branching ratio, Rb, should increase owing to growth of terminals from interior links, then mean interior link length would decline. During a period of regression, mean exterior link lengths become shorter and mean interior link lengths become longer. Changes in mean interior link length are much less affected by changes in Rb during regression than is the situation during growth. Finally, the changes in link lengths dictate that the ratio of mean exterior to mean interior link length increases during growth phases from 1 to 10 and 18 to 28 months, and declines during regression from 10 to 28 months. The lowest values of the ratio of mean exterior to mean interior lengths are found at 1 month. This is the period of most intense growth. During this period, the rate of development of new exterior links outbalances the rate at which the links increase in length.

Aging↗
PubMed1991

Effects of long durations of ethanol treatment during aging on dendritic plasticity in Fischer 344 rats.

Twelve-month-old Fischer 344 rats were fed a liquid diet containing 35% ethanol until they were 18 or 24 months old. Pair-fed and chow-fed control rats were matched to each ethanol-fed rat for concurrent treatment. Cerebellar Purkinje cell networks were measured in half of the rats at the end of the ethanol treatment and in the remaining rats after a subsequent 2-month recovery period. Chronic ethanol consumption resulted in significant elongation of terminal segments in the networks, and the unpaired terminal segments were the predominant sites of this growth. An increase in the duration of ethanol consumption from 24 to 48 weeks caused significantly greater segment elongation in the ethanol-fed rats in spite of the fact that circulating blood levels of ethanol declined markedly with the increased duration of treatment. During the same period of time, a pattern of terminal segment regression followed by terminal segment regrowth characterized age-induced changes in these networks. Thus the effects of long-term ethanol consumption were distinct from effects of concurrent aging processes in the Purkinje cell networks. There were significant interactions between the diets and the longer duration of treatment, such that as segments elongated in the ethanol-fed rats, they shortened in the pair-fed rats, and between the diets and the recovery period, such that as segments elongated during recovery in the pair-fed rats, they shortened in the ethanol-fed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMed1990

Dendritic hypertrophy in Purkinje neurons of old Fischer 344 rats after long-term ethanol treatment.

Metric parameters of Purkinje cell dendritic networks in 24- to 26-month-old Fischer 344 rats were determined after 48 weeks of chronic ethanol intake. Measurements included the total number and length of all segments/network, the total number and length of segments within topologically defined segment categories, and the mean length of segments in each category. A main effect of ethanol was expressed as a significant increase in cumulative length within one category of terminal segments. This increase was the result of a significant increase in mean length/segment in that category. Metric changes in other segment categories were not significant, showing that changes in the networks during ethanol treatment were not distributed randomly. Recovery after ethanol treatment was associated with further nonrandom remodeling of these networks. Significant differences in lengths of terminal segments were no longer present, but internal segments in networks of both pair-fed and ethanol-fed rats were significantly longer. Only one category of internal segments showed this change during recovery. The data showed that long term ethanol treatment in old rats, at a time when effects of aging processes were prominent in Purkinje cell networks, was associated with remodeling of those networks through dendritic extension. This effect was interpreted as compensatory growth in surviving networks following ethanol-related neuronal loss and/or damage to the surrounding neuropil. Recovery from dietary treatment produced further internal remodeling of those networks that was not related specifically to ethanol. It could be shown, however, that the restructuring processes that resulted in longer internal segments after dietary recovery were different in the pair-fed and the ethanolfed rats.

Alcoholism↗
PubMed1989

In vitro proliferation of murine spleen cells: genetic control of proliferative responses induced by phorbol ester and calcium ionophore A23187.

Proliferative responses of normal (not immunized intentionally) spleen cells from inbred strains of mice to co-stimulation with phorbol ester (PMA) and calcium ionophore A23187 were studied. Striking differences in the magnitude of the responses of spleen cells and splenic T cells from various strains were observed. It appeared that these differences reflected mainly differences in the inducibility of the expression of the gene for the alpha chain of the IL2 receptor (IL2R) by phorbol ester. Formal genetic analysis suggested that the differences in response to phorbol ester and calcium ionophore are controlled by two independent genes with the alleles controlling good response being dominant. The differences in the inducibility of the IL2R gene seemed to be controlled by alleles of a single gene. At least one of the putative genes may be a regulatory element affecting the gene for the alpha chain of IL 2R. The results may have a practical significance for devising more efficient procedure(s) to generate LAK cells used for tumor immunotherapy.

Animals↗
PubMed1989

Length changes in dendritic networks of cerebellar Purkinje cells of old rats after chronic ethanol treatment.

Dendritic networks of cerebellar Purkinje neurons from aging ethanol-treated Fisher 344 rats were analyzed for metric changes in terminal and internal segments of the networks. Mean lengths of three categories of dendritic segments were determined. No significant metric changes in segment lengths were detectable immediately at the termination of 24 weeks of ethanol treatment, but significant changes were apparent after 8 weeks of recovery from ethanol treatment. Return to a diet of standard laboratory chow was associated with a period of dendritic extension in networks from pair-fed control rats but not in those from the ethanol-treated rats. The resulting significant differences in mean segment length were restricted to the paired terminal segments at the peripheral tips of the bifurcating networks. Unpaired terminal segments and internal segments of the networks showed no significant changes in length during the recovery period.

Age Factors↗
PubMed1989

In vitro proliferation of murine spleen cells. Strain variation of proliferative responses induced by recombinant IL-2.

Proliferative responses of normal (not immunized intentionally) spleen cells from inbred mouse strains to human recombinant interleukin 2 (L-2) were studied. It was shown that inbred strains vary in their responses to IL-2. The differences were observed for various doses of IL-2 and at various times after stimulation. Experimental data suggested that the strain differences in the magnitude of proliferative responses may result from an interplay of several interrelated factors such as differences in the frequency of the IL-2-responsive cells, differences in inducibility of the expression of the gene for the alpha-chain of the IL-2R, and genetic control of the responses. The latter was found to be exerted by two independent genes with the dominant alleles determining good responses to IL-2. The magnitude of the responses to IL-2 correlated with the magnitude of responses to concanavalin A, but seemed to have no effect on the interferon production or on the primary response to sheep red blood cells. The described phenomenon may have a practical significance in studies aimed at improving tumor immunotherapy with lymphokine-activated killer cells.

Animals↗
PubMed1989

In vitro proliferation of murine spleen cells: I. Strain variation of response to medium from cultures of EL-4 cells.

Proliferative responses of murine lymphoid cells were elicited in vitro with supernatant fluid from cultures of EL-4 thymoma cells stimulated with phorbol ester. It was demonstrated that such responses depend on IL-2 contained in the supernatant fluid, but reflect co-stimulation with IL-2 and phorbol ester. Striking differences in the magnitude of proliferative responses of spleen, splenic T lymphocytes, thymus and bone marrow cells from various strains were observed. Three classes of responders could be identified. The differences in responsiveness, at least in part, reflected differences in the frequency of responsive cells and were genetically controlled by codominant alleles of two independent somatic genes.

Animals↗
PubMed1986

Anti-Thy-1 response of H-2f/H-2r heterozygotes: an unusual case of genetic control.

Anti-Thy-1 responsiveness of H-2r homozygous and H-2f/H-2r heterozygous mice was studied. Good responsiveness appeared to be independent of H-2 phenotype of responder but was influenced by the phenotype of the donor. These results were incompatible with the concept of Ir-Thy-1 genes controlling the response to cell-free Thy-1 in these mice. In contrast the results were indicative of the response to the cell-bound form of the Thy-1 antigen. It is proposed that good anti-Thy-1 response may reflect the presence of clones capable of recognizing the Thy-1 antigen in the context of or in association with incompatible class I H-2 molecules.

Animals↗
PubMed1985

Search for I-A trans-complementation affecting the anti-thy-1 response in mice: a final report.

Twenty-nine different F1 hybrids were tested for the possible effect of the H-2 (I-A) heterozygosity purportedly mediated by I-A trans-complementation, on the magnitude of the anti-Thy-1 response. Although the hybrids tested responded well to immunization with Thy-1 disparate thymocytes from donors H-2 compatible with one of the parents they responded poorly when immunized with thymocytes from donors H-2 incompatible with both parents. Preliminary data suggest that H-2 heterozygosity may exert a small but definite effect in H-2r/H-2f hybrids.

Animals↗
PubMed1985

Strain differences in the response of normal murine spleen cells to interleukin-2 (IL-2).

Susceptibility of normal spleen cells from various murine strains to IL-2 was assessed. The strains could be classified as highly susceptible (C57BL/6Kh, B6.PL(74NS), AKR.B6, and AKR.M) and moderately susceptible (C3H.B10 and C3H.A). These differences were demonstrable when cells were grown in the presence of relatively high concentrations of crude or highly purified IL-2 preparations, but were undetectable in low concentrations. The susceptibility appears to be genetically determined by multiple dominant or codominant genes that most likely control quantitative and/or qualitative differences in the composition of T-cell population residing in the normal spleen. From a practical point of view, the results suggest a need for testing experimental mice for their susceptibility to IL-2 prior to designing specific experiments.

Animals↗
PubMed1984

HLA-DR7-specific monoclonal antibodies and a chimpanzee anti-DR7 serum detect different epitopes on the same molecule.

We describe here two monoclonal antibodies with HLA-DR7 serologic specificity. The antibodies, SFR16-DR7M, a cytotoxic rat IgM antibody of high affinity, and SFR16-DR7G, a noncytotoxic antibody of the rat IgG 2a class, react with only DR7-positive cells in radioimmunoassay. The cytotoxic activity of SFR16-DR7M correlates completely with the presence of the DR7 specificity, and segregates with the DR7-bearing haplotype in a family. SFR16-DR7M precipitates a class II molecule with the electrophoretic characteristics of DR molecules from LG-10, an HLA-DR7 homozygous cell line. SFR16-DR7G completely inhibits the cytotoxicity of SFR16-DR7M, but only partially inhibits the cytotoxicity of a chimpanzee antiserum with DR7 specificity, Gay/Swei. In binding-inhibition studies, binding of SFR16-DR7M to LG-10 cells is only partially inhibited by the chimpanzee antiserum and vice versa. Both SFR16-DR7M and Gay/Swei reciprocally deplete the same class II molecules from a 35S-methionine-labeled detergent-solubilized membrane preparation of the LG-10 cell line. The chimpanzee serum Gay contains antibodies reactive with epitopes on separated DR7 beta chains, while both SFR16-DR7M and SFR16-DR7G bind only to DR7 alpha-beta complexes. These data suggest that at least two allogenic epitopes exist which result in the same serologic specificity, and that these epitopes differ in their requirement for alpha-beta complex formation.

Animals↗