[CITATION][C] Catecholaminergic innervation of the subthalamic nucleus: evidence for a rostral continuation of the A9 (substantia nigra) dopaminergic cell group

RC Meibach, R Katzman - Brain research, 1979 - Elsevier
RC Meibach, R Katzman
Brain research, 1979Elsevier
The recently described deoxyglucose technique for functional anatomical studies has
implicated the subthalamic nucleus in dopaminergic mechanisms. Apomorphine, a
dopamine agonist, increased glucose utilization 26~ in the subthalamic nucleus 3 and
amphetamine increased glucose utilization 67~ in this structure v. Inasmuch as the
subthalamus has not been associated with the dopaminergic system we re-investigated the
distribution of catecholamines within the mes-and diencephalon and observed both cell …
The recently described deoxyglucose technique for functional anatomical studies has implicated the subthalamic nucleus in dopaminergic mechanisms. Apomorphine, a dopamine agonist, increased glucose utilization 26~ in the subthalamic nucleus 3 and amphetamine increased glucose utilization 67~ in this structure v. Inasmuch as the subthalamus has not been associated with the dopaminergic system we re-investigated the distribution of catecholamines within the mes-and diencephalon and observed both cell bodies and terminal varicosities within the subthalamic nucleus of the cat. The Falck-Hillarp histofluorescent technique was employed on 8 young adult cats (2.0-3.0 kg). The animals were deeply anesthetized with Nembutal (Sodium pentobarbital, 100 mg/kg) and their brains were removed and processed for catecholamine fluorescence as described previously 4. A Leitz microspectro-fluorometer modified according to Bjorklund et al. 1 was used for differentiating between dopamine and norepinephrine. Sections were mounted on quartz slides and were treated with a few drops of xylene before coverslipping with entellan. Standards were prepared with commercially available dopamine. HC1 and norepinephrine. HC1 according to Bjorklund et al. L Sections were scanned utilizing a mercury source and a Ploem epi-illuminator system. Spectra were determined using a xenon light source, an excitation monochromator and a quartz dark-field condenser. On the emission side a 460 nm barrier filter and a monochromator were used. Due to the presence of the barrier filter the 495 nm emission peak of catecholamines was displaced slightly upward by about 10 nm. Spectra were corrected for the intensity of the xenon light source as measured in a rhodamine-containing quantum counter 6. At emission maximum both catecholamine fluorophores have a peak excitation spectrum at 410 nm. When the HC1 is used in place of the free base the peak is shifted to 395 nm. Treatment of the chemical slides in NH4OH for 3 min shifts the curve back to 410 rim. Upon acidification (3-7 min in conc. HC1 fumes) dopamine is converted into its non-quinoidal form which has a peak excitation spectrum at 370 nm. Norepinephrine is converted to 6, 7-dihydroxyisoquinoline which has a maximal peak at 320 nm.
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