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PubMed1996

Distribution of immunoreactivity for the NK1 receptor on different subpopulations of sympathetic preganglionic neurons in the rat.

The distribution of immunoreactivity to the receptor for substance P, the neurokinin 1 (NK1) receptor, was examined in preganglionic sympathetic neurons of the rat by using immunohistochemistry and retrograde neuronal tracing. About one-third of all sympathetic preganglionic neurons were NK1 receptor immunoreactive, and most of the NK1 receptor-immunoreactive neurons were also nitric oxide synthase immunoreactive. The proportions of sympathetic preganglionic neurons projecting to the superior and inferior mesenteric ganglia, adrenal gland, and lumbar sympathetic chain which were NK1 receptor-immunoreactive were determined. Most (89%) of the preganglionic neurons projecting to the adrenal glands were NK1 receptor immunoreactive. Few (17%) of the preganglionic neurons projecting to the L5 sympathetic chain ganglion were immunoreactive for the receptor, while preganglionic neurons projecting to the prevertebral ganglia were NK1 receptor immunoreactive at intermediate frequencies (61-64%). Thus, substance P acting on NK1 receptors is likely to be important in the preganglionic pathways to the adrenal medulla and viscera via the prevertebral ganglia, but is unlikely to be important in pathways to the lumbar sympathetic chain. The co-localisation of the NK1 receptor with the enzyme nitric oxide synthase was also examined. The majority of NK1 receptor-immunoreactive neurons were also nitric oxide synthase immunoreactive. Thus NK1 receptors occur on preganglionic neurons over many spinal segments and in a range of preganglionic pathways, as well as in a range of combinations with nitric oxide synthase. The heterogeneity of preganglionic neurons showing NK1 receptor immunoreactivity may reflect the involvement of NK1-mediated transmission in a variety of functional pathways, most notably the preganglionic projections to the adrenal medulla and to the viscera.

Adrenal Glands↗
PubMed2005

Astrocytes in the arcuate nucleus and median eminence that take up a fluorescent dye from the circulation express leptin receptors and neuropeptide Y Y1 receptors.

Following systemic injection, several different dyes and markers are found to accumulate rapidly in cells in the arcuate nucleus and median eminence, and the capillaries in this region appear specialised for exchange of molecules. The present study used hydroxystilbamidine (FluoroGold equivalent) to identify cells that take up molecules from the circulation in these regions; 2-6 h following injection, uptake was seen in the external and intermediate zones of the median eminence and the adjacent ventral part of the arcuate nucleus, but not in other regions of the hypothalamus. The labelled cells were small; double-labelling experiments revealed that they expressed glial fibrillary acid protein (GFAP), but not NeuN, Agouti-related protein (AgRP) or beta-endorphin. They had the morphology of astrocytes and were readily distinguished from tanycytes by staining for vimentin. Many of these labelled astrocytes also expressed leptin receptors and neuropeptide Y Y1 receptors. The surrounding neurons that expressed these receptors did not take up this dye. This demonstrates that astrocytes take up molecules from the circulation in the median eminence and adjacent arcuate nucleus, and may have a significant signalling role in regulation of food intake.

Animals↗
PubMed2006

Protection of corticospinal tract neurons after dorsal spinal cord transection and engraftment of olfactory ensheathing cells.

Transplantation of olfactory ensheathing cells (OECs) into the damaged rat spinal cord leads to directed elongative axonal regeneration and improved functional outcome. OECs are known to produce a number of neurotrophic molecules. To explore the possibility that OECs are neuroprotective for injured corticospinal tract (CST) neurons, we transplanted OECs into the dorsal transected spinal cord (T9) and examined primary motor cortex (M1) to assess apoptosis and neuronal loss at 1 and 4 weeks post-transplantation. The number of apoptotic cortical neurons was reduced at 1 week, and the extent of neuronal loss was reduced at 4 weeks. Biochemical analysis indicated an increase in BDNF levels in the spinal cord injury zone after OEC transplantation at 1 week. The transplanted OECs associated longitudinally with axons at 4 weeks. Thus, OEC transplantation into the injured spinal cord has distant neuroprotective effects on descending cortical projection neurons.

Animals↗
PubMed1995

Phagocytic microglia during delayed neuronal loss in the facial nucleus of the rat: time course of the neuronofugal migration of brain macrophages.

The injection of Fluoro-Gold (FG) into the whisker pad of rats yields a stable fluorescent labeling of the motoneurons in the lateral facial subnucleus. Following resection of 8-10 mm of the facial nerve, the microglia phagocytose the FG-preloaded neurons and assume the label. Employing this vital labeling of microglia in situ we studied the fate of same after completion of phagocytic activity. Starting at 56 days post resection (DPR) the FG-labeled microglia spread out from the lateral facial subdivision and invaded the entire facial nucleus. The quantitative analysis of this redistribution of the fluorescent marker revealed a prolonged increase in the number of labeled microglia strictly proportional to the delayed loss of neurons. The differentiation between microglia and shrunken neurons was performed with the new method of immunoquenching: the staining of vibratome sections with anti-rat neuron-specific enolase (NSE) combined with an ABC-HRP kit and DAB as detector totally extinguished (quenched) all fluorescence from the pre-labeled facial motoneurons. The fluorescent microglia were additionally stained with GSA I-B4 and OX-42, which should completely quench all fluorescence in the section. However, a few small round cells, always closely opposed to neuronal perikarya, still fluoresced. These NSE-negative, GSA I-B4 and OX-42 negative, but fluorescent cells may represent a new, immunologically uncharacterized microglial cell type, that participates in neuronophagia.

Animals↗
PubMed1992

Evidence for commissurally projecting parvalbumin-immunoreactive basket cells in the dentate gyrus of the rat.

The fluorescent retrograde tracer, fluorogold, was used to identify commissurally projecting neurons in the hippocampus and dentate gyrus. After injection of fluorogold into the hippocampus, the contralateral hippocampus was evaluated for fluorogold-immunoreactive or fluorescent neurons. In addition to observing labeled hilar neurons and CA3 pyramidal cells that previously have been reported to send commissurally projecting axons to the contralateral hippocampus, the authors unexpectedly found a population of fluorogold-labeled cells in the granule cell layer with the morphology and location of GABA-immunoreactive basket cells. Immunocytochemical staining revealed that all fluorogold-labeled cells of the granule cell layer were immunoreactive for parvalbumin. However, not all parvalbumin cells, shown previously to be a subset of GABA neurons, were fluorogold-labeled. The association between fluorogold transport and parvalbumin immunoreactivity was unique for these cells of the granule cell layer. In the adjacent hilus, relatively few of the many fluorogold-labeled cells were parvalbumin- or GABA-immunoreactive. These results (1) identify a population of presumed inhibitory neurons that apparently form commissural projections; (2) document that all of these cells contain the calcium-binding protein parvalbumin; and (3) indicate that the vast majority of commissurally projecting hilar neurons are neither parvalbumin- nor GABA-immunoreactive.

Animals↗
PubMed2001

Immunohistochemical distribution of enkephalin, substance P, and somatostatin in the brainstem of the leopard frog, Rana pipiens.

The brainstems of frogs contain many of the neurochemicals that are found in mammals. However, the clustering of nuclei near the ventricles makes it difficult to distinguish individual cell groups. We addressed this problem by combining immunohistochemistry with tract tracing and an analysis of cell morphology to localize neuropeptides within the brainstem of Rana pipiens. We injected a retrograde tracer, Fluoro-Gold, into the spinal cord, and, in the same frog, processed adjacent sections for immunohistochemical location of antibodies to the neuropeptides enkephalin (ENK), substance P (SP), and somatostatin (SOM). SOM+ cells were more widespread than cells containing immunoreactivity (ir) to the other substances. Most reticular nuclei in frog brainstem contained ir to at least one of these chemicals. Cells with SOM ir were found in nucleus (n.) reticularis pontis oralis, n. reticularis magnocellularis, n. reticularis paragigantocellularis, n. reticularis dorsalis, the optic tectum, n. interpeduncularis, and n. solitarius. ENK-containing cell bodies were found in n. reticularis pontis oralis, n. reticularis dorsalis, the nucleus of the solitary tract, and the tectum. The midbrain contained most of the SP+ cells. Six nonreticular nuclei (griseum centrale rhombencephali, n. isthmi, n. profundus mesencephali, n. interpeduncularis, torus semicircularis laminaris, and the tectum) contained ir to one or more of the substances but did not project to the spinal cord. The descending tract of V, and the rubrospinal, reticulospinal, and solitary tracts contained all three peptides as did the n. profundus mesencephali, n. isthmi, and specific tectal layers. Because the distribution of neurochemicals within the frog brainstem is similar to that of amniotes, our results emphasize the large amount of conservation of structure, biochemistry, and possibly function that has occurred in the brainstem, and especially in the phylogenetically old reticular formation.

Animals↗
PubMed2002

Primary motor neurons fail to up-regulate voltage-gated sodium channel Na(v)1.3/brain type III following axotomy resulting from spinal cord injury.

Epilepsy occurs in a small proportion of patients with spinal cord injury (SCI), but whether it is due to concomitant traumatic head injury or to changes in cortical motor neurons secondary to axotomy within the spinal cord is not known. Na(v)1.3/brain type III sodium channel expression is up-regulated following peripheral axotomy of dorsal root ganglion (DRG) and facial motor neurons, but, to date, Na(v)1.3 expression has not been examined in upper (cortical) motor neurons following axotomy associated with SCI. In the present study, we examine Na(v)1.3 expression in upper motor neurons within rat primary motor cortex following midthoracic (T9) dorsal column transection, which severs the axons of those cells. Axotomized pyramidal cells were identified by retrograde transport of fluorogold. Immunolabeled cells were confined to layer V of the primary motor cortex and exhibited low levels of Na(v)1.3 staining. After axotomy, no significant changes were detected in Na(v)1.3 density or distribution in injured or uninjured cells, compared with control brains, in contrast to up-regulation of Na(v)1.3 in ipsilateral DRG neurons after sciatic nerve transection. These results do not preclude a role for voltage-gated sodium channels in post-SCI epilepsy but suggest that up-regulated expression of Na(v)1.3 channel is not involved.

Animals↗
PubMed2003

Motor cortical control of cardiovascular bulbar neurones projecting to spinal autonomic areas.

There is evidence that the motor cortex is involved in cardiovascular adjustments associated with somatic motor activity, as it has functional connections with the ventrolateral medulla, a brainstem region critically involved in the control of blood pressure and the regulation of plasma catecholamine levels. The ventrolateral medulla sends projections to the spinal intermediolateral nucleus, where preganglionic neurones controlling heart and blood vessels (T2 segment) and adrenal medulla (T8 segment) are found. The aim of the present study was to determine whether electrical stimulation of the rat motor cortex induces cardiovascular responses and Fos expression in ventrolateral medulla neurones projecting to the T2 and T8 segments. After a set of experiments designed to record cardiovascular parameters (blood pressure and plasma catecholamine levels), injections of retrograde tracer (Fluorogold) were performed in the intermediolateral nucleus of two groups of rats, at the T2 or at the T8 segmental levels. Five days later, the motor cortex was stimulated in order to induce Fos expression in the ventrolateral medulla. Stimulation of the motor cortex induced: (1). hypotension and a significant decrease in plasma noradrenaline levels, and (2). a significant increase in the number of the double-labelled neurones in the rostral ventrolateral medulla projecting to T2. These data demonstrate that cardiovascular adjustments, preparatory to, or concomitant with, motor activity may be initiated in the motor cortex and transmitted to cardiac and vasomotor spinal preganglionic neurones, via the ventrolateral medulla.

Animals↗
PubMed2004

Projections from the trigeminal nuclear complex to the cochlear nuclei: a retrograde and anterograde tracing study in the guinea pig.

In addition to input from auditory centers, the cochlear nucleus (CN) receives inputs from nonauditory centers, including the trigeminal sensory complex. The detailed anatomy, however, and the functional implications of the nonauditory innervation of the auditory system are not fully understood. We demonstrated previously that the trigeminal ganglion projects to CN, with terminal labeling most dense in the marginal cell area and secondarily in the magnocellular area of the ventral cochlear nucleus (VCN). We continue this line of study by investigating the projection from the spinal trigeminal nucleus to CN in guinea pig. After injections of the retrograde tracers FluoroGold or biotinylated dextran amine (BDA) in VCN, labeled cells were found in the spinal trigeminal nuclei, most densely in the pars interpolaris and pars caudalis with ipsilateral dominance. The anterograde tracers Fluoro-Ruby or BDA were stereotaxically injected into the spinal trigeminal nucleus. Most labeled puncta were found in the marginal area of VCN and the fusiform cell layer of dorsal cochlear nucleus (DCN). A smaller number of labeled puncta was located in the molecular and deep layers of DCN and the magnocellular area of VCN. The trigeminal projection to CN may provide somatosensory information necessary for pursuing a sound source or for vocal production. These projections may have a role in the generation and modulation of tinnitus.

Afferent Pathways↗
PubMed2005

Activation and circuitry of uterine-cervix-related neurons in the lumbosacral dorsal root ganglia and spinal cord at parturition.

Stimulation of the uterine cervix at parturition activates neural circuits involving primary sensory nerves and supraspinally projecting neurons of the lumbosacral spinal cord, resulting in output of hypothalamic neurohormones. Dorsal root ganglia (DRG) and spinal neurons of these circuits are not well-characterized. The objectives of this study were to detail the activation of DRG and spinal neurons of the L6/S1 levels that are stimulated at late pregnancy, verify hypothalamic projections of activated spinal neurons, and determine whether activated neurons express estrogen receptor-alpha (ERalpha). Expression of phosphorylated cyclic-AMP response element-binding protein (PCREB) and Fos immunohistochemistry were used to "mark" activated DRG and spinal neurons, respectively. Retrograde tracing identified uterine-cervix-related and spinohypothalamic neurons. Baseline PCREB expression in the DRG increased during pregnancy and peaked during the last trimester. Some PCREB-expressing neurons contained retrograde tracer identifying them as cervix-related neurons. Fos-expressing neurons were few in spinal cords of nonpregnant and day 22 pregnant rats but were numerous in parturient animals. Some Fos-expressing neurons located in the dorsal half of the spinal cord contained retrograde tracer identifying them as spinohypothalamic neurons. Some DRG neurons expressing PCREB also expressed ERalpha, and some spinal neurons activated at parturition projected axons to the hypothalamus and expressed ERalpha. These results indicate that DRG and spinal cord neurons are activated at parturition; that those in the spinal cord are present in areas involved in autonomic and sensory processing; that some spinal neurons project axons to the hypothalamus, ostensibly part of a neuroendocrine reflex; and that sensory and spinal neurons can respond to estrogens. Moreover, some activated sensory neurons may be involved in the animal's perception of labor pain.

Analysis of Variance↗
PubMed2006

Degeneration of neuronal cell bodies following axonal injury in Wld(S) mice.

The phenotype of Wld(S) ("slow Wallerian degeneration") mice demonstrates prolonged survival of injured axons. However, whether the Wld(S) mutation delays degeneration of the neuronal cell body following axonal injury is unclear. We used a retrograde model of axonal transport failure in Wld(S) mice to test whether the mutant Wld(S) protein has any beneficial effect on the neuronal cell body. Retrograde axonal transport was physically blocked by optic nerve crush and confirmed by the absence of Fluoro-Gold labeling in wild-type and in Wld(S) mice. After this axonal injury, there was marked protection of axonal degeneration in the Wld(S) phenotype, as confirmed by immunohistochemistry and electron microscopy. However, the Wld(S) protein, localized in the nucleus of retinal ganglion cells, did not prevent or delay degeneration of the retinal ganglion cell body, confirmed by TUNEL staining and Fluoro-Gold labeling. These results imply that, after axonal injury, Wallerian degeneration of axons and degeneration of the neuronal cell body have different mechanisms, which are autonomous and independent of each other. Although the Wld(S) phenotype can be used to demonstrate stable enucleate axons, the mutation is unlikely to protect neurons in neurodegenerative diseases in which there is failure of retrograde transport.

Analysis of Variance↗
PubMed2007

Oral administration of metal chelator ameliorates motor dysfunction after a small hemorrhage near the internal capsule in rat.

Cerebral hemorrhage leads to local production of free iron, radicals, cytokines, etc. To investigate whether a decrease of iron-mediated radical production influences functional recovery after intracerebral hemorrhage (ICH), a modified ICH rat model with a small hemorrhage near the internal capsule (IC) accompanied with relatively severe motor dysfunction was first developed. Then clioquinol (CQ), an iron chelator that reduces hydroxyl radical production, was orally administrated. Injection of different doses of Type IV collagenase (1.4 mul 1-200 U/ml) into the left striatum near the IC in Wistar rats showed that injection of 7.5 U/ml collagenase resulted in a small hemorrhoidal lesion near the IC with relatively severe motor dysfunction (IC model). Retrograde labeling of neurons in the sensory-motor cortex and axons in the corticospinal tract using Fluoro-gold (FG) injection into the spinal cord (C3-C4) showed that few labeled neurons in the sensory-motor cortex were detected in the IC model, FG-labeled axons disappeared, and FG-including ED-1-positive cells appeared within 24 hr in the IC. Assessments of behavior and histologic analysis after oral administration of CQ in the IC model indicated that oral administration of CQ prevented a decrease of FG-labeled neurons, and resulted in better motor-function recovery. CQ inhibited hydrogen peroxide-induced cell toxicity in oligodendrocytes in vitro, but not in neurons. Our data suggests that CQ ameliorated motor dysfunction after a small hemorrhage near the IC by a mechanism that is related to reduction of chain-reactive hydroxyl radical production in oligodendrocytes.

Administration, Oral↗
PubMed1990

Dual-label retrograde transport: CNS innervation of the mouse thymus distinct from other mediastinum viscera.

Two different retrogradely transported tracers were identified and used to distinguish between the innervation of the thymus gland and the innervation of adjacent tissues residing within the mouse mediastinum. To determine the best procedure for peripheral dual-labeled retrograde transport, several different tracers, vehicles, and injection protocols were developed and/or tested. In the periphery, it proved ineffective to use Rhodamine latex microspheres (Luma-Fluor) as a retrograde transport agent. Horseradish peroxidase (HRP) suspended in the water-soluble carrier KY Jelly and Fluoro-Gold (FG) in an aqueous solution was the most effective combination of retrograde transport tracers. Equivalent doses of each of these tracers were determined, and injections of HRP or FG into the thymus and the esophagus produced distinct and separate patterns of labeled neurons in the spinal cord or brain stem. Throughout these CNS areas, some neurons contained both tracers suggesting that 1) these areas are innervated by neurons that give rise to collaterals to these tissues, 2) that the retrograde tracers are transported by nerves that innervate the lymphatics of the mediastinum, and/or 3) that some diffusion of the tracers occurs from the test organs and tissues to other organs and tissues of the mediastinum.

Animals↗
PubMed1993

Age-related loss of knee joint afferents in mice.

Previous work in our laboratory revealed markedly different rates of age-related death of four monoaminergic neuronal populations in the C57BL/6 mouse. Although dorsal root ganglion neurons (DRGns) have been reported not to suffer similar age-related death in rodents, we determined if there is age-related death of the subpopulation of DRGns innervating the knee joints of C57BL/6 mice, which are known to develop degenerative arthritis with aging. The somata of dorsal root ganglion neurons innervating the mouse knee joint (KJ-DRGns) were identified by retrograde tracing with Fluoro-Gold (FG). Lumbar ganglia were serially sectioned and the numbers of FG-labelled KJ-DRGns counted at five ages encompassing the animal's life span. Changes in size of the total population of lumbar DRGns (L-DRGns) were estimated by counting nucleated somata from every fifth toluidine blue-stained serial section from the L3 and L4 lumbar ganglia at three different ages. Using a computer-assisted video morphometric technique somal areas were measured from random sections to determine the distribution of sizes of neurons in the KJ-DRGn and general lumbar DRGn populations at different ages. Counts of FG-labelled joint afferents were 238.5 +/- 80.3 (mean +/- SD) KJ-DRGns per knee at 2 months of age, declining to 103.2 +/- 20.1 by 24 months, representing a 57% loss over the average life span of the C57 mice. The loss occurred in two phases, with a rapid rate over the first 8 months of life and a more moderate rate of loss over the remaining months. L-DRGn numbers revealed a slower overall rate of loss in comparison to the KJ-DRGn population with an average 33.7% loss over the life span of this mouse. Somal size measurements revealed that the larger sizes of KJ-DRGns were lost over the first 8 months of life, with little change in the distribution of somal sizes thereafter. The distributions of sizes of the L-DRGn population did not change significantly over the life spans of the mice. The data provides evidence that the age-related loss of KJ-DRGns is significantly greater than DRGns in general, and may be particularly apparent in the population of larger sized presumed mechanoreceptor neurons. The loss of the KJ-DRGns is approximately reciprocal to the incidence rate of knee joint osteoarthritis reported for the C57BL/6 mice.

Aging↗
PubMed1997

Selective ablation of rat knee joint innervation with injected immunotoxin: a potential new model for the study of neuropathic arthritis.

Neuropathic arthropathy is a severe chronic degenerative condition associated with decreased or absent sensory innervation of the involved joint. Existing animal models of neuropathic arthritis are limited by the technical difficulties of obtaining either highly selective or complete joint denervation in a minimally invasive fashion. We undertook experiments to determine the feasibility of using the newly described method of selective neuronal lesioning with injected immunotoxin as a means of creating a more tractable model of neuropathic arthritis. Retrograde tracing with fluorochrome revealed that the knee joint of the female Wistar rat is supplied by 581 +/- 31 (mean +/- SD) joint afferents. Immunohistochemistry confirmed that virtually all sensory neurons in the rat express the cell surface receptor Thy 1. Injection of rat knee joints with an immunotoxin targeted toward Thy 1 resulted in the selective ablation of an average of 88% of the joint afferents identified with fluorochrome that are normally found in the ipsilateral L3 and L4 ganglia.

Afferent Pathways↗
PubMed2001

Unique neuronal tracers show migration and differentiation of SVZ progenitors in organotypic slices.

Continual neurogenesis in the subventricular zone (SVZ) of postnatal and adult mammalian forebrain has been well documented, but the mechanisms underlying cell migration and differentiation in this region are poorly understood. We have developed novel in vivo and in vitro methods to investigate these processes. Using stereotaxic injections of a variety of tracers/tracker [Cholera Toxin beta subunit (CTb-), Fluorogold (FG), and Cell Tracker Green (CTG)], we could efficiently label SVZ cells. Over several days, labeled cells migrate along the rostral migratory stream (RMS) to their final differentiation site in the olfactory bulb (OB). The compatibility of these tracers/trackers with immunohistochemistry allows for cell labeling with multiple dyes (e.g., CTb and CTG) and/or specific cell antigens. To investigate the dynamics of migration we labeled SVZ progenitor cells with small injections of CTG and monitored the movements of individual cells in fresh parasagittal brain slices over several hours using time-lapse confocal microscopy. Our observations suggest that tangential cell migration along the RMS occurs more rapidly than radial cell migration into the OB granule cell layer. To investigate migration over longer time periods, we developed an in vitro organotypic slice in which labeled SVZ progenitors migrate along the RMS and differentiate within the OB. The phenotypic characteristics of these cells in vitro were equivalent to those observed in vivo. Taken together, these methods provide useful tools investigating cell migration and differentiation in a preparation that maintains the anatomical organization of the RMS.

Animals↗
PubMed2002

Distributions of estrogen receptors alpha and beta in sympathetic neurons of female rats: enriched expression by uterine innervation.

Estrogen modulates many features of the sympathetic nervous system, including cell numbers and ganglion synapses, and can induce uterine sympathetic nerve degeneration. However, distributions of estrogen receptors alpha and beta within sympathetic neurons have not been described, and their regulation by target tissue or estrogen levels has not been explored. We used immunofluorescence and retrograde tracing to define estrogen receptor expression in sympathetic neurons at large in pre- and paravertebral ganglia and in those projecting to the uterine horns. Estrogen receptor alpha immunoreactivity was present in 29 +/- 1%, while estrogen receptor beta was expressed by 92 +/- 1% of sympathetic neurons at large. The proportions of neurons expressing these receptors were comparable in the superior cervical and thoraco-lumbar paravertebral ganglia from T11 through L5, and in the suprarenal, celiac, and superior mesenteric prevertebral ganglia. Injections of FluoroGold into the uterine horns resulted in labeled neurons, with peak occurrences in T13, L1, and the suprarenal ganglion. Uterine-projecting neurons showed small but significantly greater incidence of estrogen receptor beta expression relative to the neuronal population at large, whereas the proportion of uterine-projecting neurons with estrogen receptor alpha-immunoreactivity was nearly threefold greater. Numbers of estrogen receptor-expressing neurons were not altered by acute estrogen administration. We conclude that the vast majority of sympathetic neurons express estrogen receptor beta immunoreactive protein, whereas a smaller, presumably overlapping subset expresses the estrogen receptor alpha. Expression of the latter apparently can be enhanced by target-mediated mechanisms.

Animals↗
PubMed2001

Transneuronal tracing from sympathectomized lumbar epaxial muscle in female rats.

Pseudorabies virus (PRV) has been used as a transneuronal tracer to study central neural networks, including the central control of the lordosis-producing, lumbar epaxial muscles. Within muscles, however, the sympathetic innervation of blood vessels poses a confounding source of tracer labeling in the CNS. The present study destroyed sympathetic nerves before injection of PRV, thereby allowing for a more selective uptake by somatic motoneurons. Specifically, a focal sympathectomy was created by the injection of dopamine-beta-hydroxylase immunotoxin (DHIT). When PRV was injected into control rats, both somatic motoneurons within the ventral horn of the spinal cord and sympathetic preganglionic neurons within the intermediolateral column (IML) of the spinal cord became labeled. Additionally, labeled neurons were observed in many brain regions, including those previously implicated in the control of the lordosis reflex (e.g., the medullary reticular formation; MRF) and those previously implicated in the control of vasomotor tone (e.g., the rostral ventrolateral medulla; RVLM). When injected into DHIT-pretreated animals, PRV labeling in ventral horn neurons persisted in many animals; however, labeling in IML was eliminated in almost every case. In these animals, PRV labeling was absent in brain areas traditionally associated with vasomotor tone, such as RVLM, whereas labeling persisted in brain areas previously implicated in the control of the lordosis response, such as MRF. The results support the connectivity of spinal and medullary structures with the somatic control of the lordosis-producing muscles and provide a more detailed description of these portions of the putative lordosis-relevant neurocircuitry.

Animals↗