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PubMed1994

Neuronal nitric oxide synthase is induced in spinal neurons by traumatic injury.

Nitric oxide appears to mediate the immune functions of macrophages, the influence of endothelial cells on blood vessel relaxation, and also to serve as a neurotransmitter in the central and peripheral nervous system. Macrophage nitric oxide synthase is inducible with massive increases in new nitric oxide synthase protein synthesis following immune stimulation of macrophages. By contrast, endothelial nitric oxide synthase and neuronal nitric oxide synthase are thought to be constitutive with activation induced by calcium entry into cells in the absence of new protein synthesis. Developmental studies showing the transient expression of neuronal nitric oxide synthase in embryonic and early postnatal life in rodent spinal motoneurons and cerebral cortical plate neurons (Bredt and Snyder, unpublished observations) implies inducibility of neuronal nitric oxide synthase. Moreover, neuronal nitric oxide synthase expression is greatly enhanced in sensory ganglia following peripheral axotomy. Staining for NADPH diaphorase in spinal motoneurons is greatly increased following ventral root avulsion. In many parts of the Central Nervous System NADPH diaphorase staining reflects nitric oxide synthase. In the present study, we have combined in situ hybridization for neuronal nitric oxide synthase, immunohistochemical staining of neuronal nitric oxide synthase, and NADPH diaphorase staining to establish that neuronal nitric oxide synthase expression is markedly augmented in spinal motoneurons following avulsion. The generality of this effect is evident from augmented staining in nucleus dorsalis following spinal cord transection.

Amino Acid Oxidoreductases↗
PubMed1995

Immunolocalization of putative neurotransmitters innervating autonomic regulating neurons (correction of neurones) of cat ventral medulla.

This study investigated possible sites of contact of nerve fibers containing a range of putative neurotransmitter substances onto neurons in the cat ventral medulla oblongata concerned with autonomic, particularly cardiovascular, regulation. The parasympathetic preganglionic neurons of the nucleus ambiguous (correction of ambiguus) were identified by retrograde horseradish peroxidase tracing from the vagus nerve, and the groups of neurons in the A1 and C1 cell areas and the raphe nucleus by catecholamine enzyme or 5-hydroxytryptamine (5-HT) immunohistochemistry, respectively. Immunoreactive (-ir)nerve fibers and terminals in the vicinity if these neurons were visualized by subjecting the sections to a dual-staining technique using a brown peroxidase-diaminobenzidine reaction product and a blue alkaline phosphatase-Fast blue reaction product. By employing monochrome photography with combinations of blue and orange-red filters, it was possible to discriminate neural elements displaying one or the other reaction product, or colocalization of reaction products. The results revealed the presence of calcitonin gene-related peptide (CGRP) and galanin (GAL)-ir in some motoneurons of the nucleus ambiguus, but not in those innervating the heart via the cardiac vagus nerve. The latter group of parasympathetic efferent neurons were found to be densely innervated by fibers immunoreactive for dopamine beta-hydroxylase (DBH, indicating noradrenaline), glycine (GLY), gamma-aminobutyric acid (GABA), 5-HT, enkephalin (ENK), neuropeptide Y (NPY), substance P (SP), and thyrotropin-releasing hormone (TRH), and, to a lesser extent, by other neuropeptide-ir fibers. The catecholamine cells of the rostral C1 and caudal A1 groups showed a broadly similar pattern of innervation, most noticeably by fibers immunoreactive for DBH, GABA, 5-HT, cholecystokinin (CCK), CGRP, ENK, GAL, NPY, and SP. The 5-HT-ir neurons of the raphe nucleus, some also containing SP, TRH, ENK, or corticotropin-releasing factor (CRF)-ir, were most prominently innervated by terminals containing DBH, GABA, CCK, ENK, NPY, TRH, somatostatin (SRIF), and vasoactive intestinal polypeptide (VIP)-ir. Although the proof that these groups of neurons receive functional synaptic contacts from the immunoreactive fibers awaits further ultrastructural studies, the results do suggest that a wide range of putative transmitters may influence the activity of efferent neurons in the cat medulla controlling autonomic functions.

Animals↗
PubMed2005

Injuring neurons induces neuronal differentiation in a population of hippocampal precursor cells in culture.

A novel population of hippocampal precursor cells (HPCs) that can be induced to differentiate into astrocytes and oligodendrocytes can be derived from hippocampal cultures grown in serum-free media. The HPCs are PDGF-responsive, do not proliferate with bFGF, and grow as sheets of cells rather than gathering into neurospheres. The HPCs share many markers (A2B5, GD3, poly-sialylated neuronal common adhesion molecule (PSA-NCAM), and NG2) with oligodendrocyte precursor cells (OPCs). The HPCs do not express markers for mature neurons, astrocytes, or oligodendrocytes. Like OPCs, the HPCs differentiate into glial fibrillary acidic protein (GFAP)+ astrocytes and GalC+ oligodendrocytes with the addition of bone morphogenetic protein-4 (BMP-4) and triiodothyronine (T3), respectively. They do not differentiate into neurons with the addition or withdrawal of basic fibroblast growth factor (bFGF), brain-derived neurotrophic factor (BDNF), or retinoic acid (RA). These HPCs can be stimulated to differentiate into neuron-like cells by the induction of neuronal injury or cell death in nearby cultured neurons or by conditioned medium from injured neuronal cultures. Under these conditions, HPCs grow larger, develop more extensive dendritic processes, become microtubule-associated protein-2-immunoreactive, express large voltage-dependent sodium currents, and form synaptic connections. The conversion of endogenous pluripotent precursor cells into neurons in response to local brain injury may be an important component of central nervous system homeostasis.

Animals↗
PubMed1998

Neuronal nuclear antigen (NeuN): a marker of neuronal maturation in early human fetal nervous system.

Neuronal nuclear antigen (NeuN) immunocytochemistry was studied in 15 normal human fetal nervous systems of 8-24 weeks gestation and in four term neonates. Material was derived from products of conception or from autopsy. Antigen retrieval was enhanced for immunocytochemistry by microwave heating of formalin-fixed paraffin sections. NeuN appears highly specific as a marker of neuronal nuclei in human fetal brain. Only rare nuclei are recognized in the germinal matrix. Cerebellar external granule cells are more strongly immunoreactive than postmigratory internal granule cells until 24 weeks gestation; by term most internal and only a few external granule cells are recognized by NeuN antibody. In the cerebrum, some reactive nuclei are demonstrated along radial glial fibers, particularly near the cortical plate. Within the cortical plate, only deep neurons (future layers 4-6) are marked at 19-22 weeks, but by 24 weeks most neurons in the cortical plate exhibit immunoreactivity, though at term some in layer 2 are still non-reactive. Some neurons fail to be recognized by NeuN at all ages: Cajal-Retzius cells, Purkinje cells, inferior olivary and dentate nucleus neurons, and sympathetic ganglion cells are examples. Despite their common origin in the cerebellar tubercle, basal pontine neurons are strongly reactive even before midgestation, hence NeuN does not predict embryonic origin. Neurons of dorsal root and cranial nerve ganglia are reactive even at 8 weeks. This study of normal fetal central nervous system provides a basis for neuropathological evaluation and as a prelude to applications in cerebral dysgeneses.

Antigens, Nuclear↗
PubMedDate not supplied

Mathematical models of cochlear nucleus onset neurons: I. Point neuron with many weak synaptic inputs.

The cochlear nucleus (CN) presents a unique opportunity for quantitatively studying input-output transformations by neurons because it gives rise to a variety of different response types from a relatively homogeneous input source, the auditory nerve (AN). Particularly interesting among CN neurons are Onset (On) neurons, which have a prominent response to the onset of sustained sounds followed by little or no response in the steady-state. On neurons contrast sharply with their AN inputs, which respond vigorously throughout stimuli. On neurons can entrain to stimuli (firing once per cycle of a periodic stimulus) at up to 1000 Hz, unlike their AN inputs. To understand the mechanisms underlying these response patterns, we tested whether an integrate-to-threshold point-neuron model with a fixed refractory period can account for On discharge patterns for tones, systematically examining the effect of membrane time constant and the number and strength of the exclusively excitatory AN synaptic inputs. To produce both onset responses to high-frequency tone bursts and entrainment to a broad range of low-frequency tones, the model must have a short time constant ( approximately 0.125 ms) and a large number (>100) of weak synaptic inputs, properties that are consistent with the electrical properties and anatomy of On-responding cells. With these parameters, the model acts like a coincidence detector with a threshold-like relationship between the instantaneous discharge rates of the output and the inputs. Onset responses to high-frequency tone bursts result because the threshold effect enhances the initial response of the AN inputs and suppresses their relatively lower sustained response. However, when the model entrains across a broad range of frequencies, it also produces short interspike intervals at the onset of high-frequency tone bursts, a response pattern not found in all types of On neurons. These results show a tradeoff, that may be a general property of many neurons, between following rapid stimulus fluctuations and responding without short interspike intervals at the onset of sustained stimuli.

Acoustic Stimulation↗
PubMed1998

Retrograde axonal transport of neurotrophins: differences between neuronal populations and implications for motor neuron disease.

During development, neurons die if they do not receive neurotrophin support from the target cells they are innervating. Neurotrophins are delivered from the target to the cell bodies of the innervating neurons by interacting with specific receptors located on the nerve terminals and then together are retrogradely transported to the cell body. This process consists of a number of distinct events including endocytosis of neurotrophin and its receptor into coated vesicles; vesicle sorting followed by retrograde axonal transport to the cell body, where interaction of the activated receptor initiates a signalling cascade at the cell body that causes the survival response. It has recently been shown that the signalling molecules associated with retrograde transport differ between neuronal populations. In sympathetic but not sensory neurons, a wortmannin-sensitive molecule (phosphatidylinositol kinase) is essential for the retrograde transport of neurotrophins. In sensory but not sympathetic neurons, a rapamycin-sensitive molecule (pp70S6K) is associated with retrograde transport of neurotrophins. This is strong evidence that sympathetic and sensory neurons utilize different signalling pathways to perform the same cellular function; retrograde transport. These findings may provide clues to understanding neurological diseases, such as motor neuron disease, in which axonal transport is impaired specifically in motor neurons.

Animals↗
PubMed2006

Novel role of neuronal Ca2+ sensor-1 as a survival factor up-regulated in injured neurons.

A molecular basis of survival from neuronal injury is essential for the development of therapeutic strategy to remedy neurodegenerative disorders. In this study, we demonstrate that an EF-hand Ca2+-binding protein neuronal Ca2+ sensor-1 (NCS-1), one of the key proteins for various neuronal functions, also acts as an important survival factor. Overexpression of NCS-1 rendered cultured neurons more tolerant to cell death caused by several kinds of stressors, whereas the dominant-negative mutant (E120Q) accelerated it. In addition, NCS-1 proteins increased upon treatment with glial cell line-derived neurotrophic factor (GDNF) and mediated GDNF survival signal in an Akt (but not MAPK)-dependent manner. Furthermore, NCS-1 is significantly up-regulated in response to axotomy-induced injury in the dorsal motor nucleus of the vagus neurons of adult rats in vivo, and adenoviral overexpression of E120Q resulted in a significant loss of surviving neurons, suggesting that NCS-1 is involved in an antiapoptotic mechanism in adult motor neurons. We propose that NCS-1 is a novel survival-promoting factor up-regulated in injured neurons that mediates the GDNF survival signal via the phosphatidylinositol 3-kinase-Akt pathway.

Animals↗
PubMed1997

Comparison of the expression of c-fos, nur77 and egr1 mRNAs in rat hypothalamic magnocellular neurons and their putative afferent projection neurons: cell- and stimulus-specific induction.

Hypothalamic magnocellular neurons and their afferent inputs provide a model system in which to study the regulation of inducible transcription factors in the brain in vivo. Osmotic stimulation of rats produced by graded infusions of saline at different tonicities was found to lead to the induction of c-fos, nur77 and egr1 mRNAs in magnocellular neurons, as well as in putative afferent neurons, including those in structures of the forebrain (subfornical organ, median preoptic nucleus and organum vasculosum of the lamina terminalis). The results presented suggest that stronger levels of osmotic stimulation recruit additional afferents from the forebrain and brainstem that can act on magnocellular neurons via alternative receptors. A single systemic injection of the peptide cholecystokinin produced robust induction of c-fos and nur77 mRNAs in afferent neurons of the brainstem nucleus tractus solitarii and in magnocellular neurons. Despite the fact that these two neuronal populations are clearly electrically active, egr1 was not induced by this stimulus, providing examples of cell- and stimulus-specificity of its expression. This study re-emphasizes that the induction of transcription factors is largely dependent on the nature of the afferent input and does not correlate necessarily to the electrical activity of the neuron.

Animals↗
PubMed1976

[Development of neuronal structure in the hippocampus during pre- and post-natal ontogenesis in the albino rat. II. Neurohistological demonstration of the development of interneurons and of the relationship between long- and short-axonal neurons].

In this paper qualitative results are presented from GOLGI preparations by light microscopic evaluation about the appearance and the ontogenetic changes on GOLGI-II-type neurons of the rat hippocampus from 15 stages of age between the 20th embryonic and the 20th postnatal day. Interneurons are already detectable in all the hippocampal regions in the prenatal period. Their postnatal growth expresses above all in lengthening rather than in multiplication of the amount of dendrites. Cells predetermined for developing spines show already early in the postnatal period a rather large amount of spines. The further multiplication of the spine density remains minimal that never values of adult pyramids will be reached. The form of the dendritic and axonic fields of neurons with short axons is very variable. Nevertheless three main categories of GOLGI-II-type neurons can be distinguished: 1. neurons, the axonic and dendritic ramifications of which strongly remain within the layer (do not exist within the stratum pyramidale), 2. neurons, which are able to contact afferent fibres in other layers by means of ascending and/or descending dendrites, 3. basket cells, the axons of which have direct influence on the perikarya of pyramidal neurons. Within the region CA4b interneurons of the 2nd group could be found, dendrites of which penetrate into layers of the fascia dentata. Such a fact does not exist at the multipolare, efferent neurons of the same region and could never be seen at any axonic ramification. In the presented paper aspects of influencing the maturation of pyramides by interneurons are discussed. Also has been tried to summarize the results about the neuronal structure of the rat hippocampus by schemes of frontal sections from four selected stages of age.

Age Factors↗
PubMed2001

Progressive neuronal and motor dysfunction in mice overexpressing the serine protease inhibitor protease nexin-1 in postmitotic neurons.

Perturbation of the homeostasis between proteases and their inhibitors has been associated with lesion-induced or degenerative neuronal changes. Protease nexin-1 (PN-1), a secreted serine protease inhibitor, is constitutively expressed in distinct neuronal cell populations of the adult CNS. In an earlier study we showed that transgenic mice with ectopic or increased expression of PN-1 in postnatal neurons have altered synaptic transmission. Here these mice are used to examine the impact of an extracellular proteolytic imbalance on long-term neuronal function. These mice develop disturbances in motor behavior from 12 weeks on, with some of the histopathological changes described in early stages of human motor neuron disease, and neurogenic muscle atrophy in old age. In addition, sensorimotor integration, measured by epicranial multichannel recording of sensory evoked potentials, is impaired. Our results suggest that axonal dysfunction rather than cell death underlies these phenotypes. In particular, long projecting neurons, namely cortical layer V pyramidal and spinal motor neurons, show an age-dependent vulnerability to PN-1 overexpression. These mice can serve to study early stages of in vivo neuronal dysfunction not yet associated with cell loss.

Amyloid beta-Protein Precursor↗
PubMed1999

Alternatively spliced isoforms of FE65 serve as neuron-specific and non-neuronal markers.

FE65 is predominantly expressed in brain and is especially rich in the regions with the highest densities of neurons. The FE65 protein binds to an intracellular domain of the beta-amyloid precursor protein (betaPP) and may modulate the production of beta-amyloid peptide (AP). One of FE65 exons, a mini-exon (exon 9, 6 bp), is alternatively spliced, giving rise to two isoforms varying only in 6 base pairs. We quantitated the two isoforms by a sensitive reverse transcription-competitive polymerase chain reaction technique, and characterized their expressions in various tissues and cell cultures, and the kinetics of expression of the two isoforms in P19 embryonal carcinoma cell lines during neuronal differentiation. Our results show that the exon 9-inclusive (E9) form, the more abundant form in brain, was exclusively expressed in neurons, while the exon 9-exclusive (DeltaE9) form was widely expressed in all non-neuronal cells, but was not expressed in differentiated neurons. When P19 cells were differentiated to neurons, expression of FE65 was significantly up regulated ( approximately 30-fold) and the splicing pattern of the FE65 pre-mRNA was switched from the DeltaE9 pattern to the E9 form. Based upon their distinctive expression patterns, these two isoforms may serve as neuronal and non-neuronal markers, and determination of their ratios may have applications in neuropathological diagnosis.

Aged↗
PubMed2000

Segmental and laminar organization of the spinal neurons projecting to the periaqueductal gray (PAG) in the cat suggests the existence of at least five separate clusters of spino-PAG neurons.

The present retrograde tracing study in the cat describes the spinal cord projections to the periaqueductal gray (PAG), taking into account different regions of the PAG and all spinal segments. Results show that injecting different parts of the PAG leads to different laminar and segmental distributions of labeled spinal neurons. The impression was gained that at least five separate clusters of spinal neurons exist. Cluster I neurons are found in laminae I and V throughout the length of the cord and are probably involved in relaying nociceptive information to the PAG. Cluster II neurons lie in the ventrolateral part of laminae VI-VII of the C1-C4 spinal cord and were labeled by injecting the ventrolateral or lateral part of the rostrocaudal PAG or the deep tectum. Cluster III neurons are located in lamina X of the thoracic and upper lumbar cord and seem to target the PAG and the deep tectum. Cluster IV neurons are located in the medial part of laminae VI-VII of the lumbosacral cord and seem to project predominantly to the lateral and ventrolateral caudal PAG. These neurons may play a role in conveying tactile stimuli to the PAG during mating behavior. Neurons of cluster V are located in the lateral part of lamina I of L6-S2 and in laminae V-VII and X of S1-S3. They are labeled only after injections into the central portion of the lateral and ventrolateral caudal PAG and probably relay information concerning micturition and mating behavior.

Animals↗
PubMed2004

Scrapie-specific neuronal lesions are independent of neuronal PrP expression.

In the transmissible spongiform encephalopathies (TSE), accumulation of the abnormal disease-specific prion protein is associated with neurodegeneration. Previous data suggested that abnormal prion protein (PrP) could induce neuronal pathology only when neurons expressed the normal form of PrP, but conflicting evidence also has been reported. Understanding whether neuronal PrP expression is required for TSE neuropathological damage in vivo is essential for determining the mechanism of TSE pathogenesis. Therefore, these experiments were designed to study scrapie pathogenesis in vivo in the absence of neuronal PrP expression. Hamster scrapie (strain 263K) was used to infect transgenic mice expressing hamster PrP in the brain only in astrocytes. These mice previously were shown to develop clinical scrapie, but it was unclear whether the brain pathology was caused by damage to astrocytes, neurons, or other cell types. In this electron microscopic study, neurons demonstrated TSE-specific pathology despite lacking PrP expression. Abnormal PrP was identified around astrocytes, primarily in the extracellular spaces of the neuropil, but astrocytes showed only reactive changes and no damage. Therefore, in this model the pathogenesis of the disease appeared to involve neuronal damage associated with extracellular astrocytic accumulation of abnormal PrP acting upon nearby PrP-negative neurons or triggering the release of non-PrP neurotoxic factors from astrocytes.

Animals↗
PubMed2003

Neuronal assemblies: single cortical neurons are obedient members of a huge orchestra.

Spontaneous cortical activity of single neurons is often either dismissed as noise, or is regarded as carrying no functional significance and hence is ignored. Our findings suggest that such concepts should be revised. We explored the coherent population activity of neuronal assemblies in primary sensory area in the absence of a sensory input. Recent advances in real-time optical imaging based on voltage-sensitive dyes (VSDI) have facilitated exploration of population activity and its intimate relationship to the activity of individual cortical neurons. It has been shown by in vivo intracellular recordings that the dye signal measures the sum of the membrane potential changes in all the neuronal elements in the imaged area, emphasizing subthreshold synaptic potentials and dendritic action potentials in neuronal arborizations originating from neurons in all cortical layers whose dendrites reach the superficial cortical layers. Thus, the VSDI has allowed us to image the rather illusive activity in neuronal dendrites that cannot be readily explored by single unit recordings. Surprisingly, we found that the amplitude of this type of ongoing subthreshold activity is of the same order of magnitude as evoked activity. We also found that this ongoing activity exhibited high synchronization over many millimeters of cortex. We then investigated the influence of ongoing activity on the evoked response, and showed that the two interact strongly. Furthermore, we found that cortical states that were previously associated only with evoked activity can actually be observed also in the absence of stimulation, for example, the cortical representation of a given orientation may appear without any visual input. This demonstration suggests that ongoing activity may also play a major role in other cortical function by providing a neuronal substrate for the dependence of sensory information processing on context, behavior, memory and other aspects of cognitive function.

Action Potentials↗
PubMed2005

Constitutive neuronal expression of CCR2 chemokine receptor and its colocalization with neurotransmitters in normal rat brain: functional effect of MCP-1/CCL2 on calcium mobilization in primary cultured neurons.

Chemokines and their receptors are well described in the immune system, where they promote cell migration and activation. In the central nervous system, chemokine has been implicated in neuroinflammatory processes. However, an increasing number of evidence suggests that they have regulatory functions in the normal nervous system, where they could participate in cell communication. In this work, using a semiquantitative immunohistochemistry approach, we provide the first neuroanatomical mapping of constitutive neuronal CCR2 localization. Neuronal expression of CCR2 was observed in the anterior olfactory nucleus, cerebral cortex, hippocampal formation, caudate putamen, globus pallidus, supraoptic and paraventricular hypothalamic nuclei, amygdala, substantia nigra, ventral tegmental area, and in the brainstem and cerebellum. These data are largely in accordance with results obtained using quantitative autoradiography with [(125)I]MCP-1/CCL2 and RT-PCR CCR2 mRNA analysis. Furthermore, using dual fluorescent immunohistochemistry we studied the chemical phenotype of labeled neurons and demonstrated the coexistence of CCR2 with classical neurotransmitters. Indeed, localization of CCR2 immunostaining is observed in dopaminergic neurons in the substantia nigra pars compacta and in the ventral tegmental area as well as in cholinergic neurons in the substantia innominata and caudate putamen. Finally, we show that the preferential CCR2 ligand, MCP-1/CCL2, elicits Ca(2+) transients in primary cultured neurons from various rat brain regions including the cortex, hippocampus, hypothalamus, and mesencephalon. In conclusion, the constitutive neuronal CCR2 expression in selective brain structures suggests that this receptor could be involved in neuronal communication and possibly associated with cholinergic and dopaminergic neurotransmission and related disorders.

Animals↗
PubMed2006

Localization of the neurons active during paradoxical (REM) sleep and projecting to the locus coeruleus noradrenergic neurons in the rat.

Locus coeruleus (LC) noradrenergic neurons are active during wakefulness, slow their discharge rate during slow wave sleep, and stop firing during paradoxical sleep (PS). A large body of data indicates that their inactivation during PS is due to a tonic GABAergic inhibition. To localize the neurons responsible for such inhibition, we first examined the distribution of retrogradely and Fos double-immunostained neurons following cholera toxin b subunit (CTb) injection in the LC of control rats, rats selectively deprived of PS for 3 days, and rats allowed to recover for 3 hours from such deprivation. We found a significant number of CTb/Fos double-labeled cells only in the recovery group. The largest number of CTb/Fos double-labeled cells was found in the dorsal paragigantocellular reticular nucleus (DPGi). It indeed contained 19% of the CTb/Fos double-labeled neurons, whereas the ventrolateral periaqueductal gray (vlPAG) contained 18.3% of these neurons, the lateral paragigantocellular reticular nucleus (LPGi) 15%, the lateral hypothalamic area 9%, the lateral PAG 6.7%, and the rostral PAG 6%. In addition, CTb/Fos double-labeled cells constituted 43% of all the singly CTb-labeled cells counted in the DPGi compared with 29% for the LPGi, 18% for the rostral PAG, and 10% or less for the other structures. Although all these populations of CTb/Fos double-labeled neurons could be GABAergic and tonically inhibit LC neurons during PS, our results indicate that neurons from the DPGi constitute the best candidate for this role.

Animals↗
PubMed1990

An intracellular study of respiratory neurons in the rostral ventrolateral medulla of the rat and their relationship to catecholamine-containing neurons.

Intracellular recording and labelling with Lucifer yellow of respiratory neurons in the rostral ventrolateral medulla were carried out in urethane-anaesthetised rats. A combined immunofluorescence and immunoperoxidase technique enabled an assessment of the tyrosine hydroxylase immunoreactivity, as well as an examination of the morphology of inspiratory and expiratory neurons in this part of the medulla oblongata. The results demonstrate: a) that respiratory neurons in the rostral ventrolateral medulla of the rat are intermingled with catecholamine-containing neurons of the C1 cell group, but are not themselves catecholamine-containing; b) that many non-spinally projecting respiratory neurons have axonal arborisations within the ventrolateral medulla in the same region as the C1 cell group, other respiratory neurons, and neurons reported to have a cardiovascular function; and c) that the dendrites of respiratory neurons in this region radiate throughout the ventrolateral medulla and frequently approach the ventral surface.

Animals↗
PubMed1991

Local circuit neurons of macaque monkey striate cortex: III. Neurons of laminae 4B, 4A, and 3B.

We continue an investigation of the organization of local circuit neurons (largely inhibitory, GABAergic neurons, with smooth or sparsely spined dendrites) in the primary visual cortex of macaque monkey (Lund, '87: J. Comp. Neurol. 257:60-92; Lund et al., '88: J. Comp. Neurol. 276:1-29). This account covers local circuit neurons of layers 4B, 4A, and 3B; these three layers each receive different intrinsic second-order relays of principal thalamic inputs as well as receiving primary thalamic inputs in the case of two of the three laminae (4A and 3B). The study shows the existence of a number of different local circuit neurons making interlaminar projections between 4B, 4A, and 3B; each provides specific cross links between different combinations of the three laminae. It is known that the functional properties recorded physiologically from layers 4B, 4A, and 3B differ from one another and so these anatomical cross links may allow for correlation between different attributes of visual stimuli, e.g., color or motion, while still enabling separate processing of these different attributes to proceed in each of the three layers and be passed on to extrastriate areas. Whereas no spine-bearing neurons of layers 4B, 4A, or 3B provide "feedback" circuits to layer 4C (the source of their major intrinsic excitatory afferents), some of the local circuit neurons provide precisely structured axon feedback projections to divisions of 4C. The local circuit neurons also project to either lamina 5 or lamina 6, but not both and to superficial layers 3A, 2, and 1. Some local circuit neuron axon projections are of a dimension that would be confined to single functional clusters, e.g., cytochrome-rich "blobs," others reach out far enough to contact nearest neighbor "unlike" functional clusters, and yet others spread far enough to link repeating clusters of single function.

Aging↗