Brown-Norway Rats (brown-norway + rat)

Distribution by Scientific Domains

Selected Abstracts

Pretreatment With Portal Venous Ultraviolet B Irradiated Donor Alloantigen Promotes Donor-Specific Tolerance to Rat Nerve Allografts,

Eric M. Genden MD
Abstract Objective To determine if a single intraportal inoculation of ultraviolet B-irradiated (UVB) donor splenocytes can prevent nerve allograft rejection and confer donor-specific immunotolerance to rat nerve allograft segments. Methods Age-matched, class I and class II major histocompatibility complex (MHC) mismatched Buffalo (RT1b) rats were transplanted with a syngeneic nerve isograft, a Lewis (RT1l) nerve allograft, or a Brown-Norway (RT1n) rat nerve allograft segment. Control Buffalo rats in group I received a 3.0-cm Lewis (RT11) sciatic-posterior tibial interposition nerve allograft without pretreatment;group II Buffalo rats received a syngeneic Buffalo nerve isograft without pretreatment. Group III Buffalo recipients were inoculated with 2.5 107 UVB-irradiated Lewis donor splenocyte cells by portal venous administration 7 days before transplantation with a 3.0-cm sciatic-posterior tibial nerve allograft from a Lewis (RT11) or a third party Brown-Norway rat (RT1n) donor (group IV). Nerve graft regeneration was assessed with walking track analysis, nerve conduction studies, retrograde neural tracing, nerve graft histology, and morphometry. Recipient immune tolerance was assessed through in vitro immunological assessment. Results Pretreatment with UVB-irradiated donor splenocytes 7 days before transplantation prevented nerve allograft rejection. Pretreated animals receiving a nerve allograft recovered limb function, and demonstrated morphological, histological, and electrophysiologic parameters of nerve regeneration similar to that measured in rats receiving a nerve isograft. In vitro immunological assessment by mixed lymphocyte culture (MLC), cytotoxic T lymphocyte (CTL) assay, limiting dilution analysis (LDA) of helper (pTH) and cytotoxic (pCTL) precursor frequencies, and IL-2 production demonstrated a marked donor-specific suppression in allografted animals pretreated with intraportal UVB-irradiated donor splenocytes. These assessments correlated with indefinite acceptance of donor nerve allografts. Conclusions A single pretreatment with a single intraportal dose of UVB-modified donor antigen specifically induces tolerance to peripheral nerve allografts in rats. [source]

Age-dependent enhancement of inhibitory synaptic transmission in CA1 pyramidal neurons via GluR5 kainate receptors

HIPPOCAMPUS, Issue 8 2009
Changqing Xu
Abstract Changes in hippocampal synaptic networks during aging may contribute to age-dependent compromise of cognitive functions such as learning and memory. Previous studies have demonstrated that GABAergic synaptic transmission exhibits age-dependent changes. To better understand such age-dependent changes of GABAergic synaptic inhibition, we performed whole-cell recordings from pyramidal cells in the CA1 area of acute hippocampal slices on aged (24,26 months old) and young (2,4 months old) Brown-Norway rats. We found that the frequency and amplitude of spontaneous inhibitory postsynaptic current (IPSCs) were significantly increased in aged rats, but the frequency and amplitude of mIPSCs were decreased. Furthermore, the regulation of GABAergic synaptic transmission by GluR5 containing kainate receptors was enhanced in aged rats, which was revealed by using LY382884 (a GluR5 kainate receptor antagonist) and ATPA (a GluR5 kainate receptor agonist). Moreover, we demonstrated that vesicular glutamate transporters are involved in the kainate receptor dependent regulation of sIPSCs. Taken together, these results suggest that GABAergic synaptic transmission is potentiated in aged rats, and GluR5 containing kainate receptors regulate the inhibitory synaptic transmission through endogenous glutamate. These alterations of GABAergic input with aging could contribute to age-dependent cognitive decline. 2009 Wiley-Liss, Inc. [source]

Comparison of effects of in vivo nitrogen dioxide exposure starting from different periods on alveolar macrophage activity, assessed by a chemiluminescence technique in Brown-Norway rats

Takashi Kumae
Abstract Nitrogen dioxide (NO2) has been extensively studied for its immune modulating effects on pulmonary cells. Alveolar macrophages (AMs) play an important role in pulmonary immunity. The Brown-Norway (BN) rat has been studied as a high-risk model of allergic diseases. In this study, BN rats were exposed to NO2 from the embryonic or weanling period (EP or WP, respectively). To evaluate the effects of NO2 exposure on pulmonary immunity, the activity levels of rat AMs were assessed as reactive oxygen species-generating capacity, measured by a chemiluminescence (CL) technique, and as cytokine-producing ability. Except for 0.2 ppm of NO2 exposure, the CL responses of AMs obtained from the WP group at 12 weeks old were suppressed significantly. Changes of the cytokine-producing levels suggest that inflammatory reactions are terminated at 12 weeks in the EP group. Correlations between the CL responses and the cytokine levels reveal that NO2 exposure may modulate the direction of AM activation. The CL technique is thought to be useful to evaluate changes in AM activity. In this study, the results suggest that, using the high-risk model of allergic diseases, NO2 exposure from the weanling period has stronger effects on AM activity.Copyright 2006 John Wiley & Sons, Ltd. [source]

Intravitreal treatment with Erythropoietin (EPO) preserves visual function following ocular ischemia in rats

Purpose: Erythropoetin (EPO) is a promising neuroprotective drug. It is known that EPO reduces apoptosis of retinal ganglion cells following axotomy or glaucoma in rats. Until now, functional aspects of this neuroprotective effect have not been addressed. We investigated effects of EPO on retinal and optic nerve function and on the survival of retinal ganglion cells following ocular ischemia. Methods: Ocular ischemia was induced by increase of the IOP to 120mmHg for 55 min in Brown-Norway rats. Animals were treated intravitreally with 4U/eye (n=12) during the time of ischemia, controls (n=16) recieved BSS instead. Visual pathway was investigated by VEP 4 days after ischemia. Potentials were evoked by frequency and luminance modulated flicker stimuli and recorded in awake freely-moving rats. Retinal function was evaluated by ERG 7 days after ischemia. Retinal ganglion cells were labelled retrogradelly 4 days after ischemia and were quantified 6 days later in retinal flatmounts. Results: Both frequency and luminance modulated evoked potentials increased due to the application of EPO from 62% (mean in percent of the non-ischemic eye standard error) in control to 468% in treated animals and from 265% to 696% respectively. EPO increased responses of ischemic eyes from 316,V to 968,V (a-wave) and from 346,V to 11015,V (b-wave). Morphologically, the intravitreal administration of EPO increased the number of surviving ganglion cells from 324% to 9211%. Conclusions: We found a sizable functional benefit of intravitreal injection of EPO following interruption of ocular blood supply. This suggests that administration of EPO is a viable therapeutic option in ischemic retinal diseases. [source]