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van Bockstaele, Elisabeth J.; Colago, Eric E.O.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<483::AID-CNE1>3.0.CO;2-0pmid: 8761923
The regional and cellular distribution of the different classes of excitatory amino acid receptors with respect to the noradrenergic neurons of the nucleus locus coeruleus (LC) are unknown. We therefore combined immunoperoxidase labeling for the R1 subunit of the N‐methyl‐D‐aspartate (NMDA) receptor with immunogold‐silver localization of the catecholamine synthesizing enzyme, tyrosine hydroxylase (TH), in single sections through the rat LC to determine the subcellular localization of this glutamate receptor subtype with respect to the noradrenergic neurons. At the light microscopic level, there was light to moderate labeling for the NMDA‐R1‐like (li) receptor in the caudal pole of the LC and dense labeling in the dorsolateral aspect of the LC adjacent to the superior cerebellar peduncle. In the rostral pole of the LC which is enriched with noradrenergic dendrites, significant overlap between both immunoreactivities could be observed. At the ultrastructural level, immunoperoxidase labeling for NMDA‐R1 was selectively distributed in astrocytic processes and within presynaptic axon terminals but was rarely seen in catecholamine‐containing somata or dendrites. Peroxidase labeling for NMDA‐R1, however, was occasionally observed in dendrites in the rostral pole of the LC. Most of these dendrites lacked detectable levels of TH, although TH immunoreactivity was apparent in the neuropil. Dendrites containing NMDA‐R1‐li immunoreactivity often received asymmetric (excitatory‐type) contacts from unlabeled terminals. NMDA‐R1‐li‐immunoreactive axon terminals usually contained small clear, as well as large dense‐core vesicles and were often apposed to unlabeled dendrites, axon terminals and/or glial processes. These results provide the first ultrastructural evidence that NMDA‐R1‐li immunoreactivity is selectively distributed within astrocytic processes and presynaptic axon terminals within the LC. © 1996 Wiley‐Liss, Inc.
Moore, Jean K.; Osen, Kirsten K.; Storm‐Mathisen, Jon; Ottersen, Ole Petter
doi: 10.1002/(SICI)1096-9861(19960610)369:4<497::AID-CNE2>3.0.CO;2-#pmid: 8761924
Previous studies of the cochlear nuclei in cat, rat, and guinea pig have demonstrated neural structures that are enriched in the inhibitory neurotransmitter amino acids γ‐aminobutyric acid (GABA) and glycine. In these mammals, inhibitory terminals are widely distributed throughout the nuclear complex, but somata of inhibitory neurons are concentrated in the dorsal cochlear nucleus, in granule cell regions, and in the cap area. Because these are the subdivisions that undergo the most pronounced phylogenetic changes in primates, we wanted to see whether the inhibitory systems are influenced by changes in cytoarchitecture. Therefore, we applied light microscopic postembedding immunostaining and optical densitometry to the cochlear nuclei of an anthropoid primate, the Senegalese baboon (Papio anubis). Our results demonstrate that, in baboon 1) glycinergic neurons and axons in the ventral cochlear nucleus seem to form a commissural system similar to that of other mammals; 2) the tuberculoventral system appears to be unchanged in morphology but exhibits a higher level of colocalization of GABA with glycine; 3) there is a reduction of the granule/cartwheel cell system, which is reflected in lesser numbers of inhibitory cartwheel, Golgi, and molecular layer stellate cells; 4) the cap area is larger than in rodents and carnivores and contains many neurons that colocalize GABA and glycine; and 5) throughout the nuclear complex, a higher proportion of the inhibitory terminals colocalize GABA and glycine. We conclude that modulation of the ascending auditory pathway in baboon is likely to differ from that in rodents and cat. © 1996 Wiley‐Liss, Inc.
Schmidt, Matthias; Lehnert, Gesa; Baker, Robert G.; Hoffmann, Klaus‐Peter
doi: 10.1002/(SICI)1096-9861(19960610)369:4<520::AID-CNE3>3.0.CO;2-6pmid: 8761925
The distribution and dendritic morphology of neurons in the cat pretectal nuclear complex were analyzed with respect to their projection to the ipsilateral dorsal lateral geniculate nucleus (LGNd) and the ipsilateral inferior olive (IO). Single and double retrograde tracing techniques were combined with intracellular injections of either horseradish peroxidase into electrophysiologically identified pretectal neurons or Lucifer Yellow into retrogradely labeled somata.
El Manira, A.; Shupliakov, O.; Fagerstedt, P.; Grillner, S.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<533::AID-CNE4>3.0.CO;2-5pmid: 8761926
The sensory control of lamprey dorsal fin motoneurons was studied by using paired intracellular recordings combined with a morphological analysis. Dorsal cells innervating the skin of the dorsal fin and fin motoneurons were retrogradely labeled by injecting fluorescein‐coupled dextran amines into the dorsal fin. Labeled motoneurons and dorsal cells showed close appositions, suggesting that the dorsal cells innervating the fin region make monosynaptic connections with fin motoneurons. By using conventional electrophysiological criteria, monosynaptic excitatory connections were found between fin dorsal cells and fin motoneurons. In addition, Lucifer yellow injection followed by confocal three‐dimensional (3‐D) reconstructions of monosynaptically connected pairs, revealed close apposition between dorsal cell axons and the distal dendrites of fin motoneurons. Each fin motoneuron received monosynaptic excitatory input from at least four different afferents. The amplitude of the monosynaptic excitatory postsynaptic potential (EPSP)s was reduced by administration of the N‐methyl‐D‐aspartate (NMDA) receptor antagonist DL,2 amino‐5‐phosphovaleric acid (APV). Sensory stimulation could also elicit di‐ or oligosynaptic inhibitory postsynaptic potential (IPSP)s, which were blocked by the glycine antagonist strychnine, resulting in the appearance of large monosynaptic EPSPs, which could induce action potentials. © 1996 Wiley‐Liss, Inc.
Clatterbuck, Richard E.; Price, Donald L.; Koliatsos, Vassilis E.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<543::AID-CNE5>3.0.CO;2-4pmid: 8761927
Ciliary neurotrophic factor is a cytokine that has effects on neuronal survival and phenotype in vitro and in vivo. Ciliary neurotrophic factor has also been shown to have effects on microglia and oligodendrocytes in vitro and in vivo. In this study, we demonstrate in vivo effects of ciliary neurotrophic factor on astrocytes in both the injured and uninjured central nervous system. Ciliary neurotrophic factor increases the expression of glial fibrillary acidic protein and induces concomitant morphological changes in central nervous system astrocytes. Messenger RNA for both ciliary neurotrophic factor and the α‐component of the ciliary neurotrophic factor receptor is demonstrated in the optic nerve, an essentially pure population of central nervous system glia. We also report here that the promoter region of the glial fibrillary acidic protein gene contains sequences thought to confer direct ciliary neurotrophic factor modulation of glial fibrillary acidic protein gene transcription. Although it is thought that astrocytes are a source of endogenous ciliary neurotrophic factor in the central nervous system and that neurons express the α‐component of the ciliary neurotrophic factor receptor, the results of the present investigation suggest that astrocytes themselves respond to ciliary neurotrophic factor and that ciliary neurotrophic factor may also be important in glial cell‐cell interactions. © 1996 Wiley‐Liss, Inc.
Lynn, Richard B.; Hyde, Thomas M.; Cooperman, Robin R.; Miselis, Richard R.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<552::AID-CNE6>3.0.CO;2-3pmid: 8761928
Bombesin is a peptide neurotransmitter/neuromodulator with important autonomic and behavioral effects that are mediated, at least in part, by bombesin‐containing neurons and nerve terminals in the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus (DMV). The distribution of bombesin‐like immunoreactive nerve terminals/fibers and cell bodies in relation to a viscerotopically relevant subnuclear map of this region was studied by using an immunoperoxidase technique. In the rat, bombesin fiber/terminal staining was heavy in an area that included the medial subnucleus of the NTS and the DMV over their full rostral‐caudal extent. Distinctly void of staining were the gelatinous, central, and rostral commissural subnuclei and the periventricular area of the NTS, regions to which gastric, esophageal, cecal, and colonic primary afferents preferentially project. The caudal commissural and dorsal subnuclei had light bombesin fiber/terminal staining, as did the intermediate, interstitial, ventral, and ventrolateral subnuclei. With colchicine pretreatment, numerous cell bodies were stained in the medial and dorsal subnuclei, with fewer neurons in the caudal commissural, intermediate, interstitial, ventral, and ventrolateral subnuclei. Bombesin‐like immunoreactive neurons were found in numerous other areas of the brain, including the ventrolateral medulla, the parabrachial nucleus, and the medial geniculate body. In the human NTS/DMV complex, the distribution of bombesin fiber/terminal staining was very similar to the rat. In addition, occasional bombesin‐like immunoreactive neurons were labeled in a number of subnuclei, with clusters of neurons labeled in the dorsal and ventrolateral subnuclei. Double immunofluorescence studies in rat demonstrated that bombesin colocalizes with tyrosine hydroxylase in neurons in the dorsal subnucleus of the NTS. Bombesin does not colocalize with tyrosine hydroxylase in any other location in the brain. In conclusion, the distribution of bombesin in the NTS adheres to a viscerotopically relevant map. This is the anatomical substrate for the effects of bombesin on gastrointestinal function and satiety and its likely role in concluding a meal. The anatomic similarities between human and rat suggest that bombesin has similar functions in the visceral neuraxis of these two species. Bombesin coexists with catecholamines in neurons in the dorsal subnucleus, which likely mediate, in part, the cardiovascular effects of bombesin. © 1996 Wiley‐Liss, Inc.
Nie, Feng; Wong‐Riley, Margaret T.T.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<571::AID-CNE7>3.0.CO;2-1pmid: 8761929
One of the hallmarks of the primate striate cortex is the presence of cytochrome oxidase (CO)‐rich puffs and CO‐poor interpuffs in its supragranular layers. However, the neurochemical basis for their differences in metabolic activity and physiological properties is not well understood. The goals of the present study were to determine whether CO levels in postsynaptic neuronal compartments were correlated with the proportion of excitatory glutamate‐immunoreactive (Glu‐IR) synapses they received and if Glu‐IR terminals and synapses in puffs differed from those in interpuffs. By combining CO histochemistry and postembedding Glu immunocytochemistry on the same ultrathin sections, the simultaneous distribution of the two markers in individual neuronal profiles was quantitatively analyzed. As a comparison, adjacent sections were identically processed for the double labeling of CO and GABA, an inhibitory neurotransmitter. In both puffs and interpuffs, most axon terminals forming asymmetric synapses (84%)—but not symmetric ones, which were GABA‐IR—were intensely immunoreactive for Glu. GABA‐IR neurons received mainly Glu‐IR synapses on their cell bodies, and they had three times as many mitochondria darkly reactive for CO than Glu‐rich neurons, which received only GABA‐IR axosomatic synapses. In puffs, GABA‐IR neurons received a significantly higher ratio of Glu‐IR to GABA‐IR axosomatic synapses and contained about twice as many darkly CO‐reactive mitochondria than those in interpuffs. There were significantly more Glu‐IR synapses and a higher ratio of Glu‐ to GABA‐IR synapses in the neuropil of puffs than of interpuffs. Moreover, Glu‐IR axon terminals in puffs contained approximately three times more darkly CO‐reactive mitochondria than those in interpuffs, suggesting that the former may be synaptically more active. Thus, the present results are consistent with our hypothesis that the levels of oxidative metabolism in postsynaptic neurons and neuropil are positively correlated with the proportion of excitatory synapses they receive. Our findings also suggest that excitatory synaptic activity may be more prominent in puffs than in interpuffs, and that the neurochemical and synaptic differences may constitute one of the bases for physiological and functional diversities between the two regions. © 1996 Wiley‐Liss, Inc.
Chen, Er‐yun; Mufson, Elliott J.; Kordower, Jeffrey H.
doi: 10.1002/(SICI)1096-9861(19960610)369:4<591::AID-CNE8>3.0.CO;2-#pmid: 8761930
The prenatal development of the neurons immunoreactive for high‐affinity tropomycin‐related kinase (trk) receptor (pan trk which recognizes trkA, trkB, and trkC) and low‐affinity p75 neurotrophin receptor (p75NTR) was examined in the human brain from embryonic weeks 10 to 34 of gestation. In the embryonic week 10 specimen in which only brainstem regions were available for evaluation, trk immunoreactivity (trk‐ir) was observed in the ventral cochlear, solitary, raphe, spinal trigeminal, and hypoglossal nuclei, as well as the vestibular complex and medullary reticular formation. At this time point of gestation, p75NTR‐immunoreactive (p75NTR‐ir) staining was observed within these same regions plus the inferior olivary and ambiguus nuclei. At embryonic week 14, trk‐ir neurons were seen within the subplate zone of the entorhinal cortex, basal forebrain, caudate nucleus, putamen, external segment of the globus pallidus, specific thalamic nuclei, lateral mammillary nucleus, habenula nucleus, select brainstem nuclei, and the dentate nucleus of cerebellum. At this gestational time point, p75NTR‐ir neurons were observed in each of these structures, with the exception of the caudate nucleus, specific thalamic nuclei, lateral mammillary nucleus, and habenula nucleus. Additionally, p75NTR‐ir neurons were observed within the corpus callosum. The staining pattern for both trk and p75NTR remained unchanged at embryonic weeks 15 to 16 except for the addition of trk‐ir and p75NTR‐ir within the cortical subplate zone, hippocampus, and subthalamic nucleus. By embryonic week 18, trk‐ir neurons were widely expressed within mostly all thalamic nuclei. In contrast, trk‐ir was no longer seen within the hypoglossal, cuneate, and gracile nuclei at this time point. This staining pattern for trk and p75NTR remained virtually unchanged from embryonic weeks 19 to 20 and embryonic weeks 16 to 20, respectively. From embryonic weeks 22 to 34, the distribution of both trk‐ir and p75NTR‐ir neurons changed gradually. During this period, neurons in most thalamic and some brainstem nuclei became progressively immunonegative for trk, whereas neurons in the neocortical subplate zone, corpus callosum, and hilar region of dentate gyrus gradually lost immunoreactivity for p75NTR. These data demonstrate an important and complex role for both the high‐ (trk) and low‐(p75) affinity neurotrophin receptors during the development of multiple neuronal systems in the human brain. © 1996 Wiley‐Liss, Inc.
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