The AMOG/beta 2 subunit of Na,K-ATPase is not necessary for long-term survival of telencephalic grafts

TY - JOUR

T1 - The AMOG/beta 2 subunit of Na,K-ATPase is not necessary for long-term survival of telencephalic grafts

AU - Isenmann, S

AU - Molthagen, M

AU - Brandner, S

AU - Bartsch, U

AU - Kühne, G

AU - Magyar, J P

AU - Sure, U

AU - Schachner, M

AU - Aguzzi, A

PY - 1995/12

Y1 - 1995/12

N2 - Adhesion molecule on glia (AMOG) represents the beta 2-subunit of murine Na,K-ATPase. Mice carrying a targeted deletion of the AMOG/beta 2 gene exhibit tremor and limb paralysis at postnatal day (P) 15 and die 2 days after the onset of symptoms. The brains of these mice show edema and swelling of astrocytic end feet. However, the cause of death has remained unclear. To identify long-term consequences of AMOG/beta 2 deficiency, we have grafted parts of the embryonic telencephalic anlage of AMOG/beta 2-deficient mice into the caudoputamen of wild-type mice and analyzed the grafts up to 500 days after transplantation. Histological, immunocytochemical, and in situ hybridization techniques were applied to examine histoarchitecture, proliferation, differentiation, and long-term survival of grafts. AMOG/beta 2-deficient telencephalic grafts develop normally and form solid neural tissue that cannot be distinguished from control grafts by morphological features or with immunocytochemical stains for neuronal and glial markers. No signs of degeneration can be found. Expression analysis, however, revealed that no AMOG/beta 2 protein of possible host origin can be detected in AMOG/beta 2-deficient grafts. Graft-borne astrocytes express neither the AMOG/beta 1 nor the AMOG/beta 2 subunit of Na,K-ATPase as examined with immunocytochemistry and in situ hybridization. These findings indicate that AMOG/beta 2 is not necessary for long-term survival of telencephalic graft tissue.

AB - Adhesion molecule on glia (AMOG) represents the beta 2-subunit of murine Na,K-ATPase. Mice carrying a targeted deletion of the AMOG/beta 2 gene exhibit tremor and limb paralysis at postnatal day (P) 15 and die 2 days after the onset of symptoms. The brains of these mice show edema and swelling of astrocytic end feet. However, the cause of death has remained unclear. To identify long-term consequences of AMOG/beta 2 deficiency, we have grafted parts of the embryonic telencephalic anlage of AMOG/beta 2-deficient mice into the caudoputamen of wild-type mice and analyzed the grafts up to 500 days after transplantation. Histological, immunocytochemical, and in situ hybridization techniques were applied to examine histoarchitecture, proliferation, differentiation, and long-term survival of grafts. AMOG/beta 2-deficient telencephalic grafts develop normally and form solid neural tissue that cannot be distinguished from control grafts by morphological features or with immunocytochemical stains for neuronal and glial markers. No signs of degeneration can be found. Expression analysis, however, revealed that no AMOG/beta 2 protein of possible host origin can be detected in AMOG/beta 2-deficient grafts. Graft-borne astrocytes express neither the AMOG/beta 1 nor the AMOG/beta 2 subunit of Na,K-ATPase as examined with immunocytochemistry and in situ hybridization. These findings indicate that AMOG/beta 2 is not necessary for long-term survival of telencephalic graft tissue.

KW - Adenosine Triphosphatases

KW - Animals

KW - Brain Tissue Transplantation

KW - Cation Transport Proteins

KW - Cell Adhesion Molecules, Neuronal

KW - Cell Division

KW - Graft Survival

KW - Immunohistochemistry

KW - In Situ Hybridization

KW - Mice

KW - Mice, Inbred C57BL

KW - Rats

KW - Sodium-Potassium-Exchanging ATPase

KW - Telencephalon

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1002/glia.440150403

DO - 10.1002/glia.440150403

M3 - SCORING: Journal article

C2 - 8926033

VL - 15

SP - 377

EP - 388

JO - GLIA

JF - GLIA

SN - 0894-1491

IS - 4

ER -