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Prevalence of symptoms, sensitization to rats, and airborne exposure to major rat allergen (Rat n 1) and to endotoxin in rat-exposed workers: a cross-sectional study.

OBJECTIVE: To analyse the relation between airborne exposure to major rat allergen and to endotoxins in exclusively rat-exposed workers and the prevalence of rat-related symptoms and sensitization. METHODS: A total of 113 workers answered a standardized questionnaire on their atopy status, occupational exposure to rats, and possible work-related symptoms. Specific IgE against rat urinary proteins (RUP) was measured for 73 subjects. Individual airborne exposure to Rat n 1 and endotoxin were determined with static (n = 256) samplings. Rat n 1 was measured with enzyme-linked immunosorbent assay (ELISA) and endotoxin by the Limulus method. RESULTS: Forty-four of 113 subjects (38.9%) reported at least one rat-related symptom: asthma (4.4%), rhinitis (34%) and conjunctivitis (16%). Twelve per cent were sensitized to RUP (specific IgE > 0.35 KU/L). But only 30.8% of all symptomatic subjects were sensitized to rat allergens. Airborne Rat n 1 levels were not related to symptoms in workers. Symptomatic patients not sensitized to rats were exposed to higher endotoxin levels, but airborne exposure to endotoxins did not significantly protect against or increase sensitization to RUP or rat-related symptoms. CONCLUSION: Most symptomatic workers were not sensitized to rat allergen; but no significant relation between rat-related symptoms and endotoxin levels was found. This suggests that more studies are needed to determine causes other than rat allergens or endotoxins that may be responsible for symptoms in rat-exposed workers.

Adult↗

Effects of sera from Cohen, genetically determined diabetic rats, streptozotocin diabetic rats and sucrose fed rats on in vitro development of early somite rat embryos.

The effects of sera from genetically determined Cohen diabetic rats, streptozotocin (STZ) diabetic rats and non-diabetic control rats fed a 72% sucrose diet on the in vitro development of 9 1/2 day old rat embryos from control rats have been studied. Hyperglycemic sera from diabetic rats had a high teratogenic effect: abnormalities were seen in 41.5% of embryos cultured in serum from Cohen diabetic animals and in 54% of embryos cultured in serum from STZ-diabetic rats. Malformations were seen in 25-27% of embryos cultured in serum from 2 groups of control rats fed a high sucrose diet compared with 10.7% in serum from control rats maintained on regular diet. When embryos from the experimental groups were cultured in serum from control rats on regular diet malformations were seen in 24.7% of embryos from Cohen genetically determined diabetic rats vs 10.9-12.4% in embryos from 2 non-diabetic groups. Only 14% of embryos from STZ-diabetic rats exhibited malformations when cultured in the control serum, but 42% of embryos from the same rats showed abnormalities when grown in serum from STZ-diabetic rats. Normalization of glucose level in the serum of STZ-diabetic rats by prior injection of insulin did not reduce the high incidence of malformations (51%). The high rate of embryonic malformations correlated with the ultrastructural changes of their visceral yolk sac endoderm. We suggest that serum from diabetic rats is teratogenic even at moderate hyperglycemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Reduced urinary noradrenaline excretion during rest, exercise and cold stress in trained rats: a comparison between physically-trained rats, cold-acclimated rats and warm-acclimated rats.

Physically trained rats were compared with cold-acclimated rats. Trained as well as cold-acclimated rats showed cardiac and adrenal hypertrophy. Cardiac noradrenaline (NA) content was increased in both groups of rats but only the trained rats had an increased cardiac NA concentration. The adrenal NA content was increased in both groups but only the trained rats had an increased adrenal content of adrenaline (A). The spleen of trained rats had an increased NA content, while that of cold-acclimated rats had a decreased NA content. The submandibular glands of cold-acclimated rats were enlarged and had an increased NA content. Trained as well as cold-acclimated rats had lower urinary NA excretions during rest, after exercise and during cold stress when compared with controls. However, only the trained rats had a reduced net increment in NA excretion after exercise, whereas there was no difference between the increments of cold-acclimated and control rats. Six months after cessation of training, ex-trained rats still had an increased heart ratio and a reduced urinary NA excretion after exercise. It is suggested that physical training induces "cross tolerance" to cold stress, while cold-acclimation does not lead to "cross tolerance" to acute exercise.

Acclimatization↗

Microsatellite polymorphism analysis allows the individual assignment of the rat 11 beta-hydroxylase gene (Cyp11b1) and the rat aldosterone synthase gene (Cyp11b2) to chromosome 7 using rat x mouse somatic cell hybrids and identifies differences between and within various rat strains.

Mouse hepatoma x rat hepatocyte hybrids that segregate rat chromosomes were used to determine the chromosomal location of the rat genes encoding 11 beta-hydroxylase and aldosterone synthase (Cyp11b1 and Cyp11b2 respectively). By means of species-specific restriction fragments and microsatellite markers both genes were mapped to rat chromosome 7. The Cyp11b1 microsatellite marker was subsequently found to vary in length between and within rat strains. Furthermore, we compared the sequences of Cyp11b1 markers in two genetically hypertensive strains of rat with their normotensive counterparts. Previous studies have indicated that 11 beta-hydroxylase activities in Milan and Lyon hypertensive strains are different from their respective genetic controls. The Cyp11b1 microsatellite regions from Lyon hypotensive and normotensive strains of rat were similar and were both shorter by 15 bases than that of the Lyon hypertensive strain. The Cyp11b1 marker in Milan hypertensive (MHS) and normotensive (MNS) strains differ from all the Lyon strains and from each other. The MHS marker is 12 bases shorter than that of MNS rats. These differences in microsatellite length may provide useful polymorphic markers in cosegregation studies of genetic hypertension in rats.

Animals↗

Different uptake in rat peritoneal macrophages of beta-very low density lipoprotein prepared from Sprague-Dawley rats and hypercholesterolemic rats (ExHC rats).

Rat beta-migrating very low density lipoprotein (beta-VLDL) was obtained from both ExHC rats and Sprague-Dawley rats which had been fed a cholesterol diet for 4 days, and was incubated with peritoneal macrophages from both kinds of rat to compare the cellular uptake of these lipoproteins. ExHC rat beta-VLDL was taken up by the cells three to five times as well as Sprague-Dawley rat beta-VLDL. Uptake depended solely on the lipoproteins used and not on the cells. Both lipoproteins seemed to be slightly different from each other in apolipoprotein composition. This stimulated uptake may explain the aortic lipid deposits found in ExHC rats with dietary hypercholesterolemia.

Animals↗

The Interleukin-6-dependent DNA-binding protein gene (transcription factor 5: TCF5) maps to human chromosome 20 and rat chromosome 3, the IL6 receptor locus (IL6R) to human chromosome 1 and rat chromosome 2, and the rat IL6 gene to rat chromosome 4.

Using two panels of somatic cell hybrids segregating either human or rat chromosomes, the gene encoding the interleukin-6-dependent DNA-binding protein, also called liver activator protein (designated transcription factor 5: TCF5), was assigned to human chromosome 20 and to rat chromosome 3. The TCF5 gene might be identical with the NF-IL6 gene. The locus encoding the IL6 receptor gene (IL6R) was localized to human chromosome 1 and rat chromosome 2. An IL6R-like (IL6RL) locus was also assigned to human chromosome 9. In addition, the rat interleukin-6 (IL6) gene was assigned to rat chromosome 4. These mapping data allow one to extend comparison between the rat, mouse, and human gene maps.

Animals↗

Complexities in ETS-domain transcription factor function and regulation: lessons from the TCF (ternary complex factor) subfamily. The Colworth Medal Lecture.

The ETS-domain transcription factor family can be divided into a series of subfamilies. Elk-1 represents the founding member of the ternary complex factor (TCF) subfamily. By focusing on the TCF subfamily, we can demonstrate the complexities that exist in the function and regulation of ETS-domain transcription factors. This article focuses on Elk-1 in detail and summarizes the functions of other TCFs. The key themes covered include the domain structure of the TCFs, the mechanisms of complex formation with serum response factor, regulation of TCFs by mitogen-activated protein kinase cascades, and transcriptional regulatory properties of the TCFs. Finally, the emerging role of the TCFs in vivo is discussed. A picture is developing indicating that, while these proteins exhibit significant sequence and functional conservation, key differences in their structure and regulation are being identified which may relate to unique functions of these proteins in vivo.

Amino Acid Sequence↗

NTP technical report on the toxicity studies of 1,2-Dichloroethane (Ethylene Dichloride) in F344/N Rats, Sprague Dawley Rats, Osborne-Mendel Rats, and B6C3F1 Mice (Drinking Water and Gavage Studies) (CAS No. 107-06-2).

Thirteen-week studies were conducted to investigate potential differences in rat strain susceptibility to 1,2-dichloroethane toxicity. F344/N rats, Sprague Dawley rats, Osborne-Mendel rats, and B6C3F1 mice (10 animals of each sex) were exposed to 1,2- dichloroethane in drinking water at 0, 500, 1,000, 2,000, 4,000, or 8,000 ppm for 13 weeks. In addition, Groups of 10 F344/N rats of each sex were administered 1,2-dichloroethane in corn oil by gavage to compare toxicity resulting from bolus administration with that of continuous exposure in drinking water. Gavage doses of 1,2-dichloroethane were within the range of daily doses resulting from exposure in drinking water. No compound-related deaths occurred in any of the rat strains exposed to 1,2-dichloroethane in drinking water. Weight gain depression was common in each sex of all three rat strains in the 4,000 and 8,000-ppm groups throughout the studies. Water consumption was decreased by 50%-60% with increasing dose for all exposed male and female rats regardless of strain. Kidney and liver weights were increased in dosed rats of all three strains. No chemical-related lesions were observed except for a dose- related incidence of renal tubular regeneration in female F344/N rats. Nine of 10 female mice exposed to 8,000 ppm 1,2-dichloroethane in drinking water died before the end of the study. Mean body weights of males at 500 ppm or more and females at 1,000 ppm or more were lower than those of controls throughout most of the studies. Kidney weights were significantly increased for dosed males and females. Renal tubular cell regeneration was seen in males at 8,000 ppm; at 4,000 ppm, minimal regeneration was present in 8/10 male mice. All male F344/N rats that received 240 or 480 mg/kg and 9/10 females that received 300 mg/kg 1,2-dichloroethane by gavage died before the end of the studies. Mean body weights of the highest dose males and females were lower than those of vehicle controls throughout the studies. Liver and kidney weights were increased for dosed males and females; however, no compound-related lesions were observed. Necrosis of the cerebellum, hyperplasia, inflammation, and mineralization of the forestomach, and necrosis of the thymus were seen in animals that died or were killed in moribund condition. Rat strain differences in susceptibility to 1,2-dichloroethane toxicity were not apparent at the drinking water concentrations used in these studies; only female F344/N rats exhibited mild chemical related renal lesions. Male B6C3FI mice appeared to be more susceptible than rats to toxicity of 1,2-dichloroethane administered in drinking water; renal tubule regeneration was observed in male mice in the 4,000- and 8,000-ppm groups. The higher toxicity in mice was likely due to higher water consumption, resulting in up to tenfold higher doses to mice than to rats. 1,2-Dichloroethane administered in drinking water resulted in less toxicity to F344/N rats than administration of similar doses by gavage. Synonyms: Freon 150; Brocide; Dutch liquid; Dutch oil. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)

Journal Article↗

Diabetic GK rat plasma but not normal Wistar rat plasma induces insulin-stimulated DNA synthesis in primary cultured smooth muscle cells in GK rat aorta.

We investigated the effect of diabetic plasma on insulin-stimulated DNA synthesis in primary cultured aortic smooth muscle cells (SMC) of the GK rat, a model of non-insulin-dependent diabetes mellitus, and compared it with that of Wistar normal rat plasma. We measured the incorporation of 3H-thymidine into cultured SMC. The diabetic plasma (3%) of GK rat, but neither the plasma (3%) of Wistar normal rat nor the plasma (3%) (not containing both insulin-like growth factor-I (IGF-I) and corticosterone) of Wistar hypophysectomized rat induced insulin-stimulated DNA synthesis in GK rat SMC. The responsiveness of SMC to insulin, not to IGF-I, was decreased remarkably by the diabetic state. The diabetic plasma of GK rat remarkably enhanced and the plasma of Wistar hypophysectomized rat weakly enhanced insulin-stimulated DNA synthesis in Wistar normal rat SMC. Corticosterone (20 nM) increased insulin-stimulated DNA synthesis in GK rat SMC but decreased it in Wistar normal rat SMC, using the plasma of Wistar hypophysectomized rat. Corticosterone levels were lower in GK rat plasma than in normal Wistar rat plasma. These results demonstrate that the enhancement of insulin-stimulated DNA synthesis in diabetic SMC by the diabetic plasma of GK rat may be due to neither IGF-I nor corticosterone but due to other factors.

Animals↗

Difference in exposure to airborne major rat allergen (Rat n 1) and to endotoxin in rat quarters according to tasks.

UNLABELLED: Endotoxins found in occupational settings constitute a risk factor in the severity of respiratory allergic symptoms. OBJECTIVES: To assess the airborne concentrations of major rat allergen (Rat n 1) and endotoxin under various circumstances. METHODS: We took 483 airborne samples from 12 sites: 114 individual samples for endotoxin measurements and 113 for Rat n 1, from 38 workers (nine animal technicians, nine laboratory technicians, nine scientists and 11 students); and 256 static samples in rat rooms and experimental rooms, with or without disturbance, for simultaneous endotoxin and Rat n 1 measurements. Rat n 1 was measured with a two-site monoclonal ELISA and endotoxins with the Limulus method. RESULTS: Airborne Rat n 1 and endotoxin were significantly higher in rat rooms than in experimental rooms. Animal technicians had the greatest exposure to both Rat n 1 and endotoxin. Cage cleaning and rat feeding induced the highest exposure to Rat n 1 and endotoxin. Furthermore, we observed no significant difference in endotoxin exposure between researchers with or without rat contact during the sample period. There was no correlation between the number of rats present and airborne endotoxin concentrations. CONCLUSIONS: Exposure to airborne Rat n 1 and endotoxin is higher during cleaning and feeding tasks than during any other task, we feel that a major source of both is contaminated bedding that becomes airborne during disturbance.

Air Pollutants, Occupational↗

Delayed postnatal behavioral development in spontaneously epileptic rats and tremor rats, and poor operant performance in spontaneously epileptic rats.

Postnatal behavioral development and learning ability of operant performance were examined in spontaneously epileptic rats (SER: zi/zi, tm/tm), and the original tremorous mutant strains of rats, tremor rats (tm/tm) and zitter rats (zi/zi) and their controls. Before the eyes opened, the increase in body weight and the age of achieving the righting reflex on a surface were no significantly different between the SER and their littermates without epileptic seizures (SER-N: zi/zi, tm/+ or zi/zi, +/+), and between tremor rats and the original strain Kyo: Wistar rats. After the eyes opened, the increase in body weight, age of achieving the righting reflex in air and traction performance, and the development of rotarod performance, were delayed in SER and tremor rats in comparison with other groups of rats. The zitter rats were apparently inferior in their development of rotarod performance in comparison with the same zitter homozygous SER-N. Operant performance was more inferior in SER than in SER-N and in tremor rats than in Kyo: Wistar rats. The differences were much more marked between SER and SER-N than between tremor and Kyo: Wistar rats. Thus, homologous tm genes and the coexistence of homologous tm and zi genes have an inhibitory effect on postnatal behavioral development and learning ability.

Animals↗

Action of rat prolactin on plasma somatomedin levels in the rat and on somatomedin release from perfused rat liver.

Rat prolactin at a concentration of 50 ng/ml perfusion medium stimulated the production of somatomedin-like activity (SLA) from the perfused liver of normal rats. The effect was demonstrable in perfusions performed at 11.00 h in which rat prolactin caused a mean (+/- S.E.M.) increase in the uptake of [35S]sulphate into rat costal cartilage in vitro of 64 +/- 14% in comparison with controls, but at 15.00 h no effect was observed. No effect or rat prolactin on hypophysectomized rat liver was detectable at 11.00 h. Hypophysectomized and sham-operated rats were given five intravenous injections of 50 microgram rat prolactin or a similar volume of hormone solvent at 12 h intervals. Plasma somatomedin activity (SMA) and cartilage metabolism, measured by the uptake of radioactive sulphate and thymidine by costal cartilage in vitro, were similar in hypophysectomized animals given rat prolactin or hormone solvent. Sham-operated rats given rat prolactin showed a significant increase of plasma SMA and cartilage metabolism compared with control animals. The production of SLA by rat liver in response to rat prolactin may be related to the density of specific hepatic lactogenic receptors, since these are absent or present only in low numbers in hypophysectomized animals.

Animals↗

Genetic studies in inbred BB/Wor rats. Analysis of progeny produced by crossing lymphopenic diabetes-prone rats with nonlymphopenic diabetic rats.

BB/Wor diabetes-prone (DP) rats are lymphopenic and frequently develop insulin-dependent diabetes. Diabetes-resistant (DR) BB/Wor rats are not lymphopenic and become diabetic rarely and at a significantly younger age. To examine the genetic basis for diabetes, lymphopenia, and age at onset of diabetes among inbred BB/Wor rats, we crossed nonlymphopenic diabetic rats with lymphopenic DP animals and studied F1, F2, and backcross progeny. F1 rats were neither diabetic nor lymphopenic. Diabetes (both types) and lymphopenia reappeared among F2 rats, confirming the permissive association of diabetes and lymphopenia and the recessive nature of both. The absence of diabetes in F1 rats also suggested that the combination of genes responsible for diabetes among lymphopenic and nonlymphopenic rats may be distinct. Nonlymphopenic parental, F1, and F2 rats revealed normal lymphocyte subsets, including CD8+ and RT6+ T-lymphocytes. Lymphopenic parental and F2 rats revealed the absence of CD8+ and RT6+ cells, indicating that these T-lymphocyte abnormalities of lymphopenic DP rats segregate with the lymphopenia gene. The distribution of the ages at onset of diabetes among F2 lymphopenic and F2 intercross rats was significantly earlier than among lymphopenic parental and backcross animals, suggesting that the age of diabetes onset is a heritable trait and that the gene(s) or genetic modifier(s) responsible for the earlier onset of F2 diabetes was acquired from the nonlymphopenic parents. Our genetic studies also confirmed the observations that the 2- and 7-kilobase Bam HI fragments of the MHC class I region do not correlate with diabetes or lymphopenia.

Age Factors↗

Effects of proteolytic enzymes on vitamin B12 uptake by rat intestinal mucosa homogenates and of proteolytic enzymes and anti-rat intrinsic factor antibodies on vitamin B12 absorption in total gastrectomized rats.

Trypsin inhibited 57CoB12-rat IF uptake by rat small intestinal mucosa homogenates in vitro. This tryptic inhibition was inactivated by rat serum and normal human serum, as well as soybean trypsin inhibitor (STI). The effects of trypsin dissolved in distilled water or 0.0025 N HCl, 0.15 M saline extract of rat pancreas and STI on vitamin B12 absorption were studied in vivo, using gastrectomized rats. IF-mediated B12 absorption was significantly decreased by 5 mg of trypsin dissolved either in distilled water or 0.0025 N HCl. However, the inhibition of trypsin was much more remarkable when it was dissolved in 0.0025 N HCl, whereas B12 absorption was insignificantly decreased by administering 10 mg of trypsin dissolved in 0.0025 N HCl. The possibilities of this phenomenon was discussed. The inhibitory effect of 0.5 ml of 0.15 M saline extract of rat pancreas was investigated as well. Soybean trypsin inhibition showed no effect on B12 absorption when it was given with 57CoB12-rat IF at the same time. However, the B12 absorption was significantly increased when STI was given one hour prior to the administration of 57CoB12-rat IF. This suggested that endogenous trypsin bound to rat small intestine had been inactivated and pancreatic secretion had been stimulated by STI. IF-mediated B12 absorption was diminished to almost the same level of 57CoB12 administration alone by simultaneous intubation of both 57CoB12-rat IF and rabbit anti-rat IF serum in total gastrectomized rats.

Animals↗

The hypothalamic-neurohypophysial system of the rat: localization and quantitation of neurophysin by light microscopic immunocytochemistry in normal rats and in Brattleboro rats deficient in vasopressin and a neurophysin.

The cellular distribution of neurophysin was examined in hypothalami and neural lobes of normal Long-Evans rats and Brattleboro rats deficient in vasopressin and a major neurophysin. Tissue sections were treated with antisera to bovine, human, and rat neurophysins, using immunoperoxidase bridge techniques. Antisera to oxytocin (OT) and vasopressin (VP) were applied to adjacent sections. Two distinct cell populations were discernible in both magnocellular nuclei on the basis of the intensity of cytoplasmic staining. About half of the magnocellular neurons in the supraoptic (SON) and paraventricular (PVN) nuclei of homozygous Brattleboro rats with diabetes insipidus (DI) were devoid of immunoreactive neurophysin, OT, and VP. These cells were presumably the defective counterparts of those neurons that produce VP and its associated neurophysin in normal and heterozygous Brattleboro rats. The cells in homozygous DI rats which were stained with immunoreaction products to NP and OT were more concentrated in the dorsal part of the SON and in the periphery of the PVN. Spatial segregation of different neurons was also seen in the neural lobe, where clusters of stained axons were surrounded by bundles of nerve fibers lacking immunoreactive material. In normal rats and heterozygotes nearly all magnocellular neurons reacted immunologically with antiserum to neurophysin but with different intensities, so that "dark" and "light" cells could be distinguished. The darker cells in heterozygous Brattleboro rats had the same pattern of distribution as cells which contained OT. In homozygous DI rats, only some of those cells which contained neurophysin and OT exhibited a positive reaction with antiserum to VP due to slight reactivity with OT. The results obtained in the homozygous Brattleboro rat would suggest that OT and VP and their associated neurophysins are produced in different neurons in both the SON and PVN. However, in normal rats and in heterozygous Brattleboro rats, VP appeared to be present in both OT-positive and OT-negative neurons suggesting that some cells may have the capacity to synthesize two hormones.

Animals↗

Atrial natriuretic peptide in the Milan hypertensive rat and the Milan normotensive rat: plasma concentration and binding to renal glomeruli in young, adult and aged rats.

METHODS: Blood pressures were determined in Milan hypertensive (MHS) and Milan normotensive (MNS) rats at different ages. Mean blood pressure, plasma atrial natriuretic peptide (ANP) concentration and renal glomerular receptors numbers and affinities were determined in young (25-day-old), adult (60- to 80-day-old) and aged (300-day-old) rats. RESULTS: Mean blood pressures, always higher in the MHS than in the MNS rats, increased with age in both strains. Plasma ANP concentrations were similar in the young and aged rats of both strains, but were higher in the adult MHS than in the adult MNS rats. There were no quantitative differences in the ANP receptors between young and old rats of the two strains, but an increase in the maximal binding capacity was observed, in both strains, when adult rats were compared with young rats. Moreover, saturation experiments with [125I]-rat ANP revealed a downregulation of the ANP receptors in the renal glomeruli isolated from the adult MHS rats. In isolated glomeruli the cyclic GMP stimulation by ANP was similar in adult rats of both strains. CONCLUSION: Downregulation in glomeruli of MHS rats, probably involving the clearance receptors for ANP, is concluded to occur.

Aging↗

Long-Evans rats have a larger cortical topographic representation of movement than Fischer-344 rats: a microstimulation study of motor cortex in naïve and skilled reaching-trained rats.

Intracortical microstimulation of the frontal cortex evokes movements in the contralateral limbs, paws, and digits of placental mammals including the laboratory rat. The topographic representation of movement in the rat consists of a rostral forelimb area (RFA), a caudal forelimb area (CFA), and a hind limb area (HLA). The size of these representations can vary between individual animals and the proportional representation of the body parts within regions can also change as a function of experience. To date, there have been no investigations of strain differences in the cortical map of rats, and this was the objective of the present investigation. The effect of cortical stimulation was compared in young male Long-Evans rats and Fischer-344 rats. The overall size of the motor cortex representation was greater in Long-Evans rats compared to Fischer-344 rats and the threshold required to elicit a movement was higher in the Fischer-344 rats. An additional set of animals were trained in a skilled reaching task to rule out the possibility that experiential differences in the groups could account for the result and to examine the relationship between the differences in topography of cortical movement representations and motor performance. The Long-Evans rats were quantitatively and qualitatively better in skilled reaching than the Fischer-344 rats. Also, Long-Evans rats exhibited a relatively larger area of the topographic representation and lower thresholds for eliciting movement in the contralateral forelimb. This is the first study to describe pronounced strain-related differences in the microstimulation-topographic map of the motor cortex. The results are discussed in relation to using strain differences as a way of examining the behavioral, the physiological, and the anatomical organization of the motor system.

Animals↗