Behavioural recovery following transplantation of substantia nigra in rats subjected to 6-OHDA lesions of the nigrostriatal pathway. I. Unilateral lesions

[1]  J. Brobeck,et al.  Hypothalamic Control of Food Intake in Rats and Cats * , 1951, The Yale journal of biology and medicine.

[2]  P. Teitelbaum,et al.  Recovery from the failure to eat produced by hypothalamic lesions. , 1954, Science.

[3]  P. Teitelbaum,et al.  The lateral hypothalamic syndrome: recovery of feeding and drinking after lateral hypothalamic lesions. , 1962, Psychological review.

[4]  U. Ungerstedt,et al.  Is interruption of the nigro-striatal dopamine system producing the "lateral hypothalamus syndrome"? , 1970, Acta physiologica Scandinavica.

[5]  U. Ungerstedt,et al.  Quantitative recording of rotational behavior in rats after 6-hydroxy-dopamine lesions of the nigrostriatal dopamine system. , 1970, Brain research.

[6]  Solomon Kullback,et al.  Information Theory and Statistics , 1970, The Mathematical Gazette.

[7]  U. Ungerstedt Adipsia and aphagia after 6-hydroxydopamine induced degeneration of the nigro-striatal dopamine system. , 1971, Acta physiologica Scandinavica. Supplementum.

[8]  U. Ungerstedt,et al.  Postsynaptic supersensitivity after 6-hydroxy-dopamine induced degeneration of the nigro-striatal dopamine system. , 1971, Acta physiologica Scandinavica. Supplementum.

[9]  U. Ungerstedt Striatal dopamine release after amphetamine or nerve degeneration revealed by rotational behaviour. , 1971, Acta physiologica Scandinavica. Supplementum.

[10]  B. Turner Sensorimotor syndrome produced by lesions of the amygdala and lateral hypothalamus. , 1973, Journal of comparative and physiological psychology.

[11]  S. D. Glick,et al.  Amphetamine-induced changes in striatal dopamine and acetylcholine levels and relationship to rotation (circling behavior) in rats. , 1974, Biochemical pharmacology.

[12]  P. Teitelbaum,et al.  Nigrostriatal bundle damage and the lateral hypothalamic syndrome. , 1974, Journal of comparative and physiological psychology.

[13]  P. Teitelbaum,et al.  Further analysis of sensory inattention following lateral hypothalamic damage in rats. , 1974, Journal of comparative and physiological psychology.

[14]  S D Glick,et al.  Neurochemical Correlate of a Spatial Preference in Rats , 1974, Science.

[15]  A. E. Fisher,et al.  Tail pinch-induced eating, gnawing and licking behavior in rats: Dependence on the nigrostriatal dopamine system , 1975, Brain Research.

[16]  P. Kelly Unilateral 6-hydroxydopamine lesions of nigrostriatal or mesolimbic dopamine-containing terminals and the drug-induced rotation of rats , 1975, Brain Research.

[17]  P. Teitelbaum,et al.  Somnolence, akinesia, and sensory activation of motivated behavior in the lateral hypothalamic syndrome. , 1975, Proceedings of the National Academy of Sciences of the United States of America.

[18]  H. Szechtman,et al.  Tail pinch induces eating in sated rats which appears to depend on nigrostriatal dopamine. , 1975, Science.

[19]  S. Iversen,et al.  Amphetamine and apomorphine responses in the rat following 6-OHDA lesions of the nucleus accumbens septi and corpus striatum , 1975, Brain Research.

[20]  S. Iversen,et al.  Tail-pinch stimulation: sufficient motivation for learning. , 1976, Science.

[21]  T. Ljungberg,et al.  Sensory inattention produced by 6-hydroxydopamine-induced degeneration of ascending dopamine neurons in the brain , 1976, Experimental Neurology.

[22]  C. Marsden,et al.  Stereotyped behaviour patterns and hyperactivity induced by amphetamine and apomorphine after discrete 6-hydroxydopamine lesions of extrapyramidal and mesolimbic nuclei , 1977, Brain Research.

[23]  U. Ungerstedt,et al.  Supersensitivity to apomorphine following destruction of the ascending dopamine neurons: quantification using the rotational model. , 1977, European journal of pharmacology.

[24]  P. Teitelbaum,et al.  New Considerations in the Neuropsychology of Motivated Behaviors , 1977 .

[25]  J. Bureš,et al.  Asymmetry of EEG arousal in rats with unilateral 6-hydroxydopamine lesions of substantia nigra: Quantification of neglect , 1978, Experimental Neurology.

[26]  A. Bjo¨rklund,et al.  Reconstruction of the nigrostriatal dopamine pathway by intracerebral nigral transplants , 1979, Brain Research.

[27]  J. Marshall Somatosensory inattention after dopamine-depleting intracerebral 6-OHDA injections: Spontaneous recovery and pharmacological control , 1979, Brain Research.

[28]  B J Hoffer,et al.  Brain grafts reduce motor abnormalities produced by destruction of nigrostriatal dopamine system. , 1979, Science.

[29]  S. Iversen,et al.  Regulatory impairments following selective kainic acid lesions of the neostriatum , 1980, Behavioural Brain Research.

[30]  A. Björklund,et al.  The aluminum-formaldehyde (ALFA) histofluorescence method for improved visualization of catecholamines and indoleamines. 1. A detailed account of methodology for central nervous tissue using paraffin, cryostat or vibratome sections , 1980, Journal of Neuroscience Methods.

[31]  A. Björklund,et al.  Reinnervation of the denervated striatum by substantia nigra transplants: Functional consequences as revealed by pharmacological and sensorimotor testing , 1980, Brain Research.

[32]  Louis A. Chiodo,et al.  Sensory stimuli alter discharge rate of dopamine (DA) neurons: evidence for two functional types of DA cells in the substantia nigra , 1980, Brain Research.

[33]  A. Björklund,et al.  Functional reactivation of the deafferented neostriatum by nigral transplants , 1981, Nature.