 |
Previous Article | Next Article 
Journal of Neuroscience, Vol 1, 285-291, Copyright © 1981 by Society for Neuroscience
Metabolic effects of unilateral lesion of the substantia nigra
GF Wooten and RC Collins
Regional brain glucose utilization following unilateral lesion of the
substantia nigra in rat was studied by [14C]-2-deoxyglucose
autoradiography. Substantia nigra lesions were performed by perinigral
injections of 6-hydroxydopamine (6-OHDA) . HBr, 6 microgram, in rats
pretreated 30 min earlier with desmethylimipramine (DMI), 25 mg/kg,
subcutaneously. The lesion produced extensive destruction of the
ipsilateral substantia nigra pars compacta and a greater than 99% reduction
in dopamine concentration in the ipsilateral striatum. Pretreatment with
DMI prevented any reduction in the concentration of norepinephrine in
ipsilateral forebrain structures. Glucose utilization was increased in the
ipsilateral globus pallidus at 11, 21, 53, and 104 days after substantia
nigra lesion with the largest increase (about 140% of control) occurring at
21 days post-lesion. In addition, glucose utilization in ipsilateral
lateral habenular nucleus was increased at each of the above time points.
No changes in glucose utilization were noted in frontal cortex, striatum,
subthalamic nucleus, entopeduncularis, or ventral tier nuclei of the
thalamus. These results suggest that lesion of the substantia nigra with
depletion of striatal dopamine content results in disinhibition of some
striatal, and perhaps olfactory cortical, efferents producing increased
metabolism and glucose utilization in terminal fields within the globus
pallidus and lateral habenular nucleus.
This article has been cited by other articles:

|
 |

|
 |
 
T. V. Maia
Reinforcement learning, conditioning, and the brain: Successes and challenges
Cogn Affect Behav Neurosci,
December 1, 2009;
9(4):
343 - 364.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
G. Hasler, S. Fromm, P. J. Carlson, D. A. Luckenbaugh, T. Waldeck, M. Geraci, J. P. Roiser, A. Neumeister, N. Meyers, D. S. Charney, et al.
Neural Response to Catecholamine Depletion in Unmedicated Subjects With Major Depressive Disorder in Remission and Healthy Subjects
Arch Gen Psychiatry,
May 1, 2008;
65(5):
521 - 531.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
T. Hayakawa, M. C. J. Chang, S. I. Rapoport, and N. M. Appel
Selective Dopamine Receptor Stimulation Differentially Affects [3H]Arachidonic Acid Incorporation, a Surrogate Marker for Phospholipase A2-Mediated Neurotransmitter Signal Transduction, in a Rodent Model of Parkinson's Disease
J. Pharmacol. Exp. Ther.,
March 1, 2001;
296(3):
1074 - 1084.
[Abstract]
[Full Text]
|
 |
|

|
 |

|
 |
 
N. Nakao, M. Ogura, K. Nakai, and T. Itakura
Intrastriatal Mesencephalic Grafts Affect Neuronal Activity in Basal Ganglia Nuclei and Their Target Structures in a Rat Model of Parkinson's Disease
J. Neurosci.,
March 1, 1998;
18(5):
1806 - 1817.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
R. S. Menon, S. Ogawa, and J. P. Strupp
Ocular Dominance in Human V1 Demonstrated by Functional Magnetic Resonance Imaging
J Neurophysiol,
May 1, 1997;
77(5):
2780 - 2787.
[Abstract]
[Full Text]
[PDF]
|
 |
|

|
 |

|
 |
 
S. Kim, K Ugurbil, and P. Strick
Activation of a cerebellar output nucleus during cognitive processing
Science,
August 12, 1994;
265(5174):
949 - 951.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
M. S. Buchsbaum, S. G. Potkin, B. V. Siegel Jr, J. Lohr, M. Katz, L. A. Gottschalk, B. Gulasekaram, J. F. Marshall, S. Lottenberg, C. Y. Teng, et al.
Striatal Metabolic Rate and Clinical Response to Neuroleptics in Schizophrenia
Arch Gen Psychiatry,
December 1, 1992;
49(12):
966 - 974.
[Abstract]
[PDF]
|
 |
|

|
 |

|
 |
 
M. I. POSNER
What Is Left of Attention in Schizophrenia?-Reply
Arch Gen Psychiatry,
April 1, 1990;
47(4):
394 - 395.
[Abstract]
[PDF]
|
 |
|
|

|