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J P Adèr

Publications and source records attributed to J P Adèr.

9 recordsLinked to original sources
PubMed1987

[AIDS; current status].

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Acquired Immunodeficiency Syndrome↗
PubMed1980

Bilaterally diverging axon collaterals and contralateral projections from rat locus coeruleus neurons, demonstrated by fluorescent retrograde double labeling and norepinephrine metabolism.

Evans Blue (EB) and a mixture of 4'-6'-diamidino-2-phenylindol 2 HCl and primuline (DAPI-Pr), fluorescing at different wave-lengths were injected into the rat hippocampus, frontal cortex or lateral part of the thalamus. After unilateral injection either of the two substances was retrogradely transported not only to ipsilateral but also to contralateral locus coeruleus (LC) neurons. Moreover after simultaneous injections of EB and DAPI-Pr respectively into the opposite brain structures of individual animals double-labeled neurons were observed in the bilateral LC. Unilateral electrical stimulation of the LC induced significant decreases of norepinephrine and increases of 3-methoxy-4-hydroxyphenylethylene-glycol in both the ipsi- and contralateral frontal cortex and whole forebrain, respectively. These ipsi- and contralateral alterations of the amine and its metabolite correlated highly significantly. These results indicate that several LC neurons have both contralateral and bilateral projections to the brain areas mentioned above.

Animals↗
PubMed1979

Contribution of the locus coeruleus to the adrenergic innervation of the rat spinal cord: a biochemical study.

The possible existence and magnitude of a noradrenergic innervation from the locus coeruleus (LC) to the spinal cord was investigated in the rat with various techniques. Horseradish peroxidase, injected into the lumbar spinal cord produced heavy labelling of presumably noradrenaline (NA)-containing neurons in the ventral region of the LC, while cells in the dorsal region of the LC were only lightly labelled. The effects of electrothermic destruction and electrical stimulation of the LC on levels of NA in various parts of the spinal cord, the cerebral cortex and the hippocampus were studied. Fourteen days after unilateral destruction of the LC there were decreases in NA levels of about 85% in the cerebral cortex and hippocampus and of about 15% in the cervical and thoracic segments of the spinal cord (ipsilateral versus contralateral). Fourteen days after bilateral lesioning of the LC significant decreases (about 25%) in NA levels were observed in all spinal cord segments. Unilateral stimulation in or near the LC induced decreases of NA levels in all areas of the central nervous system investigated. In this experiment the levels of NA in the spinal cord were significantly lowered in the ipsilateral cervical (16%), thoracic (12%) and lumbar/sacral (15%) segments of the spinal cord. These findings together indicate that a small part (no more than 30%) of the NA levels in the rat spinal cord are dependent upon the integrity and activity of NA-containing neurons of the predominantly ipsilaterally localized LC.

Animals↗
PubMed1979

Origin of free 3-methoxy-4-hydroxyphenylethyleneglycol.

The origin of free 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG, a major metabolite of norepinephrine) in rat cerebrospinal fluid (CSF) was investigated using brain and spinal cord perfusions with artificial CSF, electrical stimulation of the locus coeruleus (LC) and the technique of retrograde cell labelling with horseradish peroxidase (HRP). The rates of appearance of MHPG into ventricular-cisternal and lumbar-cisternal perfusates were about 12.4 and 19.2 ng/hour respectively. Probenecid (200 mg/kg i.p.) did not alter the MHPG output in either preparation. Intravenous administration of 3 micrograms MHPG did not substantially enhance the outflow of the metabolite in the ventricular-cisternal perfusate, indicating that MHPG found in the perfusate is of central origin. Maximal activation of central norepinephrine (NE)-containing neurons of the LC by electrical stimulation induced a 50% increase of MHPG levels in the ventricular-cisternal perfusate. In addition HRP was found to be retrogradely transported from the lateral ventricle to these LC-neurons. These findings indicate that MHPG in CSF originates, at least in part from NE of nerve terminals adjacent to the cerebral ventricles, which have their origin in the LC. We calculated that the fraction of MHPG formed in the central nervous system, that was released into the CSF was about 34%. It is concluded that MHPG in CSF is a measure for changes in central NE turnover and that a considerable portion is dependent upon the activity of LC neurons.

Animals↗