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Local cerebral glucose consumption in the rat. II. Effects of unilateral substantia nigra stimulation in conscious and in halothane‐anesthetized animals
Author(s) -
Savaki Helen E.,
Desban Marcel,
Glowinski Jacques,
Besson MarieJo
Publication year - 1983
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902130105
Subject(s) - globus pallidus , subthalamic nucleus , substantia nigra , basal ganglia , stimulation , locus coeruleus , habenula , neuroscience , halothane , striatum , pars compacta , thalamus , brainstem , dorsal raphe nucleus , deep brain stimulation , biology , nucleus , central nervous system , anesthesia , medicine , dopamine , serotonin , parkinson's disease , receptor , disease , serotonergic , dopaminergic
Abstract The energy metabolism of 74 anatomically discrete central nervous structures was investigated by means of the autoradiographic 2‐deoxy‐D‐(1‐ 14 C) glucose method ( 14 C‐DG) in conscious awake, as well as in halothane anesthetized rats, following unilateral substantia nigra (SN) electrical stimulation. All the basal ganglia structures displayed bilateral metabolic activation in conscious animals, with only the contralateral subthalamic nucleus being unaffected. In anesthetized rats only the SN reticulata, globus pallidus, and subthalamic nucleus were affected ipsilaterally whereas anesthesia masked the effects of SN stimulation in SN compacta and striatum ipsilaterally, as well as within‐all the above structures contralaterally. The entopeduncular nucleus was bilaterally activated no matter the state of consciousness. Unilateral SN stimulation also increased glucose utilization within several thalamic regions (ventromedial, ventrolateral, ventroanterior, intralaminar, ventrobasal, and mediodorsal nuclei), the habenular complex, a few mesencephalic, brainstem (locus coeruleus and dorsal raphe) and cerebellar structures, mostly bilaterally and independently of the state of consciousness. Some of the factors suggested to be responsible for the masking effects of halothane‐anesthesia on the metabolic activations elicited by unilateral SN stimulations are the following: (1) absence of movements in anesthetized rats, (2) halothane‐induced depression of polysynaptic pathways mostly mediated through the thalamus, and (3) the stimulatory effect of halothane‐anesthesia itself on metabolic activity in both parts of the SN.