Rat Strain Differences
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Rat Strain Differences

Last updated on June 2, 2010

BB

Clostridium piliforme: BB, LE, SHR, Sprague-Dawley rats; ICR mice are susceptible{3577}

BB/Wor

BB/Wor rats are a model for type I diabetes mellitus and autoimmune thyroiditis, and the major diabetogenic gene (Iddm2) is located on chromosome 20. Insulitis and thyroiditis are controlled by a lymphopenia gene on chromosome 4. An MHC class IIa allele appears to protect against insulitis and gives some protection against thyroiditis. Backcrosses with non-lymphopenic MHC congenic strains (PVG.R23) were used to determine gene order.{4064}

BBDP

Model of IDDM, using BBDR as control{4189}

BDII (Berlin Druckrey II)

>90% incidence of endometrial carcinoma in virgin females{4189}

BHE/cdb

Model of NIDDM{4189}

Big Blue

Big Blue mice and rats are transgenic animals used in testing of mutagens. They carry a transgene "shuttle vector" with a reporter gene lac Z and its suppressor locus lac I, coding for bacterial ß-galactosidase. This reporter gene causes no ill effects in the Big Blue animal. A test dose of mutagen is given, the animal's liver DNA is collected and packaged into bacteriophages used to infect an E. coli culture. If the gene was mutated, mutants will appear as blue plaques on a white lawn of E. coli. The MutaMouse is a similar transgenic.{4535}

BUF/Mha

Model of spontaneous tumors{4189}

CRDH

Model of NIDDM{4189}

Diabetes insipidus (di)

Mutation with diabetes insipidus with polyuria, vasopressin resistant{4535}

DSS

Model of hypertension{4189}

Eker rat

Insertional mutation (Tsc2) associated with spontaneous renal cell carcinoma, uterine leiomyoma and hemangioma in heterozygotes; embryonic lethal in homozygotes{4189}

Fatty (fa)

Fatty mutation with obesity, hyperphagia and defective temperature regulation{4535}

FHH (Fawn hooded hypertensive)

Model of hypertension using FHL as control{4189}

Fischer 344

Inbred strain. Less susceptible to severe pulmonary disease caused by Mycoplasma pulmonis than Lewis rats, controlled for age, sex and environment.{4162}

GEPR/3

Model of behavioral and neurological disorders{4189}

GH (Genetic hypertension)

Model of hypertension{4189}

GK

Model of NIDDM{4189}

Hypotrichotic (hairless) rat mutations

There are several mutations in the rat and mouse that cause a hairless phenotype; however, the genetic causes are apparently quite different and are poorly characterized. Rat mutants include Charles River hairless (Crl:CD(SD)-hrBR), naked (n), fuzzy (fz, in which first pelage is sparse with broken hairs and adults are naked, but hair follicles never atrophy), shorn (shn, no histo available), Rowett nude (rnu, epidermis normal, no thymus), hairless Wistar (hW, incomplete dominant, no epidermal abnormalities), Hirosaki hairless (hhr, have large cysts). The hairless mouse (hr/hr) such as rhino (hrrh/hrrh) has been compared with the hairless rat by some authors, but there are significant genetic and morphological differences. Hairless mice develop normal pelage which then all falls out and never comes back; hairless rats are born shiny naked, develop some bristly hair growth and then gradually lose all that. Some considerations for researchers using hairless rats are: hairless rats have an abnormally thick layer of corneoyctes similar to the stratum lucidum found in palmar and plantar skin and footpads, which may affect skin permeability; and prominent hyperplasia of palatine epithelium which may be present elsewhere in the GIT, a possible reason for the 10% lighter weight of the homozygotes. Heterozygotes are normal in appearance.{4598}

Jaundice (j)

Mutation with hyperbilirubinemia and absence of glucuronosyl transferase {4535}

LE (Long Evans)

Clostridium piliforme: BB, LE, SHR, Sprague-Dawley rats; ICR mice are susceptible{3577}

LEC

Model of Wilson's disease {4189} The rats have hereditary hepatitis, and aged rats develop liver cancer. They have abnormal lipid metabolism that is similar to choline-deficient rats, such that the liver fails to transfer triacylglycerols and cholesterol into the plasma. They therefore have low serum lipid levels.{4508}

LETL

Model of IDDM{4189}

LEW (Lewis)

Inbred strain. More susceptible to severe pulmonary disease caused by Mycoplasma pulmonis than F344 rats, controlled for age, sex and environment. Infection persists longer (120 days vs. 28). M. pulmonis may be a B-cell activator in LEW.{4162}

LH (Lyon hypertensive)

Model of hypertension, using LN (Lyon normal) or LL (Lyon low blood pressure) as controls{4189}

MHS (Milano hypertensive)

Model of hypertension, using MNS (Milano normotensive) as control{4189}

MR (Maudsley reactive)

Model of behavioral and neurological disorders using MNR (Maudsley nonreactive) as control{4189}

OLETF

Model of NIDDM{4189}

RHA

Model of behavioral and neurological disorders, using RLA as control{4189}

rdw

Model of congenital hypothyroidism, based on the Wistar-Imamichi strain. Maintained by breeding heterozygotes because homozygotes are infertile.{3722}

Rowett nude (rnu)

The Rowett nude rat (rnu) arose as a spontaneous mutation in hooded rats in the 1950s at the Rowett Research Institute in Scotland, but was not recognized until it occurred again in the 1970s. It arose also in New Zealand in the 1970s and was given the designation rnuN. {4162} It is athymic and immunodeficient.{4535}

SBH

Model of hypertension using SBN as control{4189}

SD (Sprague-Dawley)

Outbred strain. Clostridium piliforme3577}. Unlike Lewis, Wistar and F344, develop adverse pregnancy outcomes when they have genital Mycoplasma pulmonis infection, including low birth weight, small litter size, stillbirth and fetal absorption.{4354}

SHHF

Model of NIDDM{4189}

SHR (Okamoto hypertensive)

Model of hypertension, using WKY (Wistar Kyoto) as control. {4189} The SHR rat was derived from the Wistar-Kyoto rat and develops spontaneous hypertension with age, with systolic BP>150mmHg which is more severe in the male. Cardiac output eventually returns to normal, so there is increased peripheral vascular resistance with normal cardiac output.{4509}

Clostridium piliforme: BB, LE, SHR, Sprague-Dawley rats; ICR mice are susceptible{3577}

SHR-SP

Model of stroke{4189}. The stroke-prone SHR rat was derived from the SHR and has a higher incidence of cerebrovascular disease. Systolic BP is up to 250mmHg and correlates with brain lesions. Normal lifespan of these rats is only a year, and is less if they are fed 1% salt.{4509}

SS (Dahl S)

Model of hypertension using SR (Dahl R) as control{4189}. Genetic models of hypertension in rats are SHR, stroke-prone salt-sensitive, and the Dahl salt-sensitive. Experimentally hypertension can be induced by either administration of deoxycorticosterone acetate salt via osmotic minipump, or by a surgical model called Goldblatt hypertension. The Dahl salt-sensitive rat, when given 4-8% salt in the feed, develops high blood pressure and renal insufficiency (glomerular sclerosis and necrosis) with suppression of the circulating renin-angiotensin system. Transplantation of a kidney from a DSS to a DSR rat induces hypertension in the recipient, highlighting the role of the kidneys in hypertension.{4509}

WF/Ztm

Model of behavioral and neurological disorders{4189}

Zitter (zi)

Model of behavioral and neurological disorders{4189}

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©1999, Janet Becker Rodgers, DVM, MS

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