Brain tissue transplantation in neonatal rats prevents a lesion-induced syndrome of adipsia, aphagia and akinesia.
Previous experiments have proven brain tissue transplantation effective in reversing lesion-induced behavioral deficits in mature rats. This study reversed the usual experimental paradigm, so that fetal substantia nigra was transplanted into intact neonatal rats and allowed to mature in the host brain. Upon maturation substantia nigra lesions were made bilaterally to reveal the functional contribution of the transplanted tissue. In control animals these lesions depleted striatal dopamine, producing rigidity, poverty of movement and abnormal posture comparable to Parkinson's disease in the human; cessation of feeding and drinking led to progressive weight loss and death. In contrast, fetal substantia nigra transplanted into the neonatal rat became well-integrated in the host brain and was shown to protect the animal from this syndrome produced by subsequent substantia nigra lesions. We suggest that transplantation in these neonatal rats was performed during a crucial period of synaptogenesis, an environment particularly favorable to host-transplant interaction.
D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D004327:Drinking Behavior / Q000502:physiology*; D001068:Feeding and Eating Disorders / Q000503:physiopathology*; D005260:Female; D008297:Male; D009069:Movement Disorders / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D013378:Substantia Nigra / Q000201:enzymology / Q000502:physiology / Q000637:transplantation*; D013997:Time Factors; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D014446:Tyrosine 3-Monooxygenase