Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “STILBAMIDINE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 919 records · Page 51Linked to original sources
PubMed1999

Oestrogen receptors in the brainstem of the female sheep: relationship to noradrenergic cells and cells projecting to the medial preoptic area.

Oestrogen regulates the secretion of gonadotropin releasing hormone (GnRH) and this could be mediated by noradrenergic systems originating in the brainstem. Whilst it is known that noradrenergic cells possess oestrogen receptors (ER), it is not known whether ER-immunoreactive (-ir) cells in the brainstem project to the regions of the hypothalamus in which GnRH neurons are found. We have used dual-label immunocytochemistry to determine the extent to which ER-alpha is found in noradrenergic cells in the brainstem of the ovariectomized (OVX) ewe. Noradrenergic/adrenergic cells were identified by immunostaining for dopamine beta-hydroxylase (DBH). Cells that stained for both DBH and ER were found in both the A1 and A2 cell groups, with the highest levels found in the most caudal regions. In the A1 group, at the most caudal extent, 73% of ER-ir cells were DBH-positive and 19% of DBH-ir cells were ER-positive. The degree of co-localization decreased in a linear manner towards the rostral brainstem. In the caudal half of A2, 9-14% of ER-ir cells were DBH-positive and 20-25% of DBH cells were ER-positive. Less than 2% of DBH-ir cells in the A5 group were dual-labelled and none of the cells in the A6 and A7 groups were ER-positive. The retrograde tracer FluoroGold was injected into the preoptic area of nine OVX ewes and labelled cells were examined in the brainstem to determine the extent of co-localization of ER. Only injections in the rostroventral part of the medial preoptic area near to the organum vasculosum of the lamina terminalis resulted in the labelling of cells in the brainstem. One ewe with very strong labelling of the brainstem was selected for detailed mapping. In the ventrolateral medulla, half the ER-ir cells in the most caudal regions were retrogradely labelled. Almost all the ER-ir cells in the mid-region of the ventrolateral medulla were retrogradely labelled but no co-localization of retrograde tracer and ER was observed rostral to obex. There were many ER-ir cells and retrogradely-labelled cells in the nucleus of the solitary tract but only a few double-labelled cells. Similarly, numerous ER-ir cells and retrogradely labelled cells were observed around the lateral edges of the caudal fourth ventricle and across to the lateral parabrachial nucleus but there were few double-labelled cells. These results suggest differential regulation of noradrenergic cells by oestrogen, with a direct action of the hormone confined to the cells in the most caudal region of the A1 and A2 cell groups. The cells of the caudal ventrolateral medulla which contain ER-ir cells that project to the preoptic area may be important in the mediation by noradrenaline of the actions of oestrogen on GnRH secretion in the ewe.

Animals↗
PubMed2001

Noradrenergic projections from the A1 field to the preoptic area in the brain of the ewe and Fos responses to oestrogen in the A1 cells.

Previous studies have shown that there is a population of noradrenergic cells in the caudal A1 field of the brainstem of the ewe that contain oestrogen receptors and project to the preoptic area, where gonadotrophin releasing hormone (GnRH) neurones are located. There are some discrepancies in the literature regarding the extent of this projection and the location of the cells in the A1 region. The issue has been a focus of attention because the positive feedback response to oestrogen that causes the ovulatory GnRH/luteinizing hormone surge may originate from this brainstem region. The aim of the present study was to determine the extent of the projections to the preoptic area and to determine whether the caudal A1 cells are activated by oestrogen. Eleven ovariectomized ewes received an injection of the retrograde tracer FluoroGold into the preoptic hypothalamus and four of these also received an i.m. injection of oestrogen 2 h before tissue collection. A further three sheep received i.m. oil injections to act as controls for those receiving oestrogen. Dopamine-beta-hydroxylase (DBH)-positive, retrogradely labelled cells were found within the A1 field in sheep that received preoptic FluoroGold injections. Cells in the vicinity of the A2 and A6 fields, that were retrogradely labelled with FluoroGold, were not DBH-positive. Thus, cells in the A1 field provide a direct noradrenergic projection to the preoptic area and may be involved in the control of the secretion of GnRH in this species. Cells that project to the preoptic hypothalamus from more rostrally located areas of the brainstem are not noradrenergic. In the animals that received oestrogen, double-labelling immunohistochemistry was performed throughout the A1 field for FluoroGold, DBH and Fos. DBH cells of the A1 field expressed Fos only in the oestrogen-treated animals and not in the oil-treated animals. There was a decline in the number of DBH cells that were retrogradely labelled from the caudal region of A1 towards obex. There was a similar gradient in the number of cells that were double-labelled for Fos and FluoroGold. We conclude that there is a population of noradrenergic cells in the caudal A1 field that project to the preoptic area; this is a larger group of cells than previously reported. Oestrogen elicits an acute Fos response in these cells, which may be involved in the time-delayed positive feedback response on GnRH cells. The caudal-to-rostral gradient in the labelling with FluoroGold and Fos in DBH-positive cells is similar to that seen previously for oestrogen receptor in DBH-positive cells in the A1 field.

Animals↗
PubMed2001

Insulin and glucose administration stimulates Fos expression in neurones of the paraventricular nucleus that project to autonomic preganglionic structures.

Insulin and glucose play a key role in the control of body energy homeostasis. However, the anatomical organization of the network of central insulin and glucose sensitive areas is still unclear. In the present study, we used a multiple-labelling technique combining retrograde tracing and Fos-like immunohistochemistry, to analyse the anatomical projections from hypothalamic neurones activated by the combined stimulus of insulin and glucose. After intraperitoneal injections of a bolus of insulin plus glucose, Fos-like immunoreactive neurones were observed in the paraventricular nucleus (PVN), ventromedial and arcuate nuclei, as well as the lateral hypothalamic area. In addition, neurones projecting to the autonomic preganglionic levels in the brainstem and spinal cord potentially involved in the control of glucose metabolism were identified by injections of fluorochrome tracers. Thus, Fluorogold was injected into the intermediolateral cell column of the lower spinal cord and Fast Blue was injected into the dorsal motor nucleus of the vagus. Perikarya of descending neurones were detected chiefly in the dorsal, medial and lateral parvocellular subnuclei and also in the posterior magnocellular subnucleus of the PVN. In contrast, insulin-glucose activated neurones in the PVN were observed mainly in the medial parvocellular and posterior magnocellular subnuclei. Fluorogold/Fos double-labelled neurones were only observed in the ventral zone of the medial parvocellular subnucleus. These data indicate that, within the PVN, there could be neurones responding to insulin-glucose administration, which are involved in the sympathetic control of the classical regulatory structures of body energy homeostasis, such as the liver and pancreas, and which could play a role in the output of the neuronal circuitry controlling food intake.

Amidines↗
PubMed2001

Evidence that orexin-containing neurones provide direct input to gonadotropin-releasing hormone neurones in the ovine hypothalamus.

Orexins A and B (ORX) have been added recently to the growing list of neuropeptides implicated in feeding and drinking behaviour as well as neuroendocrine function. In the present study, we have used single and dual labelling immunohistochemistry and a rabbit polyclonal anti-orexin-A antibody, which recognizes both ORX A and B, to examine ORX pathways in the sheep hypothalamus. ORX immunoreactive cells were distributed in the dorsomedial hypothalamic nucleus, lateral hypothalamic area, zona incerta and perifornical area; a few cells were also observed in the anterior hypothalamic area. In contrast to distribution in the rat brain, most of the ORX immunoreactive cells are localized to the dorsomedial hypothalamic nucleus and perifornical area; scattered cells are found in lateral hypothalamic area. ORX immunoreactive fibres were widely distributed throughout the hypothalamus and preoptic area with dense innervation of the medial preoptic area and bed nucleus of stria terminalis. Dual labelling demonstrated widespread expression of the long form of the leptin receptor within all ORX cells that were examined. Thirty percent of the gonadotropin releasing hormone (GnRH) cells that were examined had ORX immunoreactive terminals in close contact with no regional or sex differences. FluoroGold injections into the preoptic area retrogradely labelled a subpopulation of ORX cells in the lateral hypothalamic/perifornical area, showing ORX cells of this region project to the preoptic and could potentially provide input to GnRH cells. These findings suggest an integral role for ORX in the regulation of GnRH cells in the sheep and thus provide evidence of a novel mechanism whereby leptin can influence reproductive neuroendocrine function.

Afferent Pathways↗
PubMed2003

Central administration of neuropeptide FF causes activation of oxytocin paraventricular hypothalamic neurones that project to the brainstem.

Neuropeptide FF (NPFF), a morphine modulatory peptide, is emerging as an important neuromodulator in the context of central autonomic and neuroendocrine regulation. NPFF immunoreactivity and receptors have been identified in discrete autonomic regions within the brain and spinal cord, including the hypothalamic paraventricular nucleus (PVN). In this study, we examined the effects of intracerebroventricular (i.c.v.) administration of NPFF on activation of chemically identified PVN neurones that project to the brainstem nucleus of the solitary tract (NTS). In conscious rats, i.c.v. NPFF at a dose of 10 micro g, but not 8 micro g, caused an increase in arterial blood pressure. Immunohistochemical analysis revealed a dose-dependent increase in activated (Fos positive) PVN neurones following i.c.v. NPFF administration compared to controls receiving i.c.v. saline. Activated PVN neurones were located predominantly in the parvocellular compartment of the nucleus with relatively few Fos positive cells in the magnocellular subdivision. Chemical identification of activated neurones revealed significant number of activated cells to be oxytocin positive, whereas only few vasopressin, tyrosine hydroxylase (TH) or corticotrophin-releasing factor (CRF) neurones were double-labelled. Injection of the retrograde tracer fluorogold into the NTS resulted in labelling of significant numbers of parvocellular oxytocin, but not vasopressin, TH or CRF, PVN neurones. We conclude that centrally administered NPFF stimulates brainstem-projecting oxytocin PVN neurones. Oxytocin released from terminals within the NTS oxytocin thus modulate the activity of ascending visceral autonomic pathways that synapse initially within the NTS.

Animals↗
PubMed1999

Differential projection patterns of superior and inferior collicular neurons onto posterior paralaminar nuclei of the thalamus surrounding the medial geniculate body in the rat.

The thalamic nuclei at the medial border of the medial geniculate body (i.e. the suprageniculate nucleus, the medial division of the medial geniculate nucleus, the posterior intralaminar nucleus and the peripeduncular nucleus) which relay sensory information to the amygdala are thought to receive convergent input from multiple sites. In order to delineate the organization of these multimodal thalamic nuclei, the locations of superior and inferior collicular neurons projecting to these nuclei were studied by means of retrograde transport methods. Small injections of the tracer Miniruby were made into single paralaminar thalamic nuclei. Injections of Miniruby into the suprageniculate nucleus labelled predominantly neurons in the stratum opticum of the superior colliculus, whereas injections into the medial division of the medial geniculate body, the posterior intralaminar nucleus and the peripeduncular nucleus labelled predominantly neurons in the deep layers of the superior colliculus. These injections also labelled neurons in the inferior colliculus. The majority of retrogradely labelled neurons were found in the external nucleus of the inferior colliculus and here predominantly in layer 2. Injections focused onto the medial division of the medial geniculate body additionally labelled magnocellular neurons in layer 3 of the external nucleus and a few neurons in the central nucleus. More ventrally located injections, focused onto the posterior intralaminar and peripeduncular nucleus, almost exclusively labelled neurons in layer 1 of the external nucleus and the dorsal part of the dorsal nucleus. After injections into the suprageniculate nucleus, only neurons in layer 2 were found. Neurons in the central nucleus of the inferior colliculus were only found after injections that involved the medial division of the medial geniculate body. The present results suggest that, despite a considerable degree of convergence in this thalamic region, each of these thalamic nuclei receives a unique pattern of projections from the superior and inferior colliculi. It appears that the thalamic nuclei may be concerned mainly, but not exclusively, with a single sensory modality, and give rise to parallel multimodal and unimodal pathways to the amygdala.

Animals↗
PubMed1999

Intrastriatal grafting of a GDNF-producing cell line protects striatonigral neurons from quinolinic acid excitotoxicity in vivo.

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor with a therapeutic potential in neurodegenerative disorders. GDNF is expressed in the adult striatum, but its signalling tyrosine kinase receptor, c-ret, has not been detected in this structure by in situ hybridization. In the present work, we first examined c-ret and GDNF receptor alpha 1 (GFR-alpha 1) expression using an RNAse protection assay, and found that both receptors are expressed in the adult rat striatum. We then examined whether GDNF was able to regulate the phenotype and/or prevent the degeneration of striatal projection neurons in a well-characterized model of excitotoxic damage. A fibroblast cell line, engineered to overexpress GDNF, was grafted in adult rats striatum 24 h before quinolinic acid (QUIN) injection. QUIN injection alone or in combination with the control cell line induced a loss of glutamic acid decarboxylase 67 (GAD)-, preprotachykinin A (PPTA)-, prodynorphin (DYN)- and preproenkephalin (PPE)-positive neurons. GDNF selectively prevented: (i) the loss of a subpopulation of striatonigral neurons expressing GAD and PPTA; (ii) the atrophy of PPTA-positive neurons; and (iii) the decrease in GAD, PPTA and DYN mRNA expression, after QUIN injection. Moreover, in unlesioned animals, GDNF increased the size of PPTA-positive neurons and up-regulated their mRNA levels. In contrast, GDNF showed no effect in intact or lesioned striatopallidal PPE-positive neurons. Thus, our findings show that GDNF selectively regulates the phenotype and protects striatonigral neurons from QUIN-induced excitotoxicity, suggesting that GDNF may be used for the treatment of striatonigral degenerative disorders, e.g. Huntington's disease and multiple system atrophy.

Animals↗
PubMed2000

The distribution and origin of the calretinin-containing innervation of the nucleus accumbens of the rat.

The nucleus accumbens of the rat consists of several subregions that can be distinguished on the basis of histochemical markers. For example, the calcium-binding protein calbindin D28k is a useful marker of the core compartment of the nucleus accumbens. Calretinin, another calcium-binding protein, is found in a dense fibre plexus in the accumbal shell and septal pole regions. The source of the accumbal calretinin innervation is not known. We examined the distribution of calretinin in the nucleus accumbens and used tract-tracing and lesion methods to determine the source of this calretinin innervation. Intense calretinin immunoreactivity was present in the medial shell, but the density of calretinin axons diminished sharply in the ventrolateral shell. Regions of dense calretinin immunostaining and those areas with calbindin-like immunoreactive cell bodies were generally segregated in the nucleus accumbens, although some overlap in the transition region between the core and shell was seen. Small clusters of calretinin-immunoreactive fibres were seen in the core, where they were restricted to calbindin-negative patches. Injections of the anterograde tracer biotinylated dextran amine into the paraventricular thalamic nucleus labelled fibres in calretinin-rich regions of the accumbens. Conversely, injections of Fluoro-gold into the accumbal shell retrogradely labelled numerous cells in the paraventricular thalamic nucleus that were calretinin-immunoreactive. Electrolytic lesions of the paraventricular thalamic nucleus reduced calretinin levels in the shell by approximately 80%. These data indicate that the calretinin innervation of the nucleus accumbens is derived primarily from the thalamic paraventricular nucleus, and marks accumbal territories that are largely complementary to those defined by calbindin.

Afferent Pathways↗
PubMed2002

Expression of BCL-2 via adeno-associated virus vectors rescues thalamic neurons after visual cortex lesion in the adult rat.

Lesions of the mammalian visual cortex cause the retrograde degeneration of the thalamic neurons projecting to the damaged cortex. The proto-oncogene bcl-2 is known to inhibit neuronal apoptosis induced by a variety of noxious stimuli and preserve the functional integrity of the injured cells. Here we have tested whether the overexpression of bcl-2 via adeno-associated virus (AAV) vectors is able to protect the neurons in the lateral geniculate nucleus after visual cortex ablation in adult rats. Recombinant AAV vectors encoding Bcl-2 (AAV-Bcl-2) or green fluorescent protein (AAV-GFP) as a control were stereotaxically injected into the geniculate. Three weeks after vector injection, the ipsilateral visual cortex was removed by aspiration, and cell survival was assessed 2 weeks later. We found that 20% of the geniculate neurons were transduced by the Bcl-2 vector. These cells were completely protected from death following cortical ablation. Delivery of AAV-GFP transduced an identical number of geniculate neurons but had no effect on cell survival after lesion. The total number of surviving geniculate neurons was found to be significantly higher in animals injected with AAV-Bcl-2 than in rats injected with AAV-GFP or in control lesioned rats. These data indicate that Bcl-2 gene therapy with AAV vectors represents an effective treatment to promote neuronal survival after central nervous system insults.

Animals↗
PubMed2003

Activation of the amygdalo-entorhinal pathway in fear-conditioning in rat.

Several studies implicate a role for the amygdala in processing of emotional memories that might partially occur in the connections between the amygdala and the hippocampal-parahippocampal areas. The present study was designed to determine if the pathway from the amygdala to the entorhinal cortex becomes activated during acquisition of fear-conditioning. First, the retrograde tracer Fluoro-Gold (FG) was iontophoresed into the entorhinal cortex in rats. Following habituation, animals were divided into five groups: (i) controls that received another habituation session; (ii) animals given a tone only; (iii) animals given a footshock only; (iv) animals given an unpaired presentation of a shock and a tone; and (v) conditioned animals that received a single tone-footshock pairing. Then double-immunohistochemistry against c-Fos and FG or glutamate decarboxylase (GAD67) was performed. The numbers and densities of labelled neurons were calculated in the lateral and basal nuclei of the amygdala. In conditioned animals the number and density of c-Fos-positive nuclei increased in dorsolateral and medial divisions of the lateral nucleus compared with the control group (P < 0.05). Additionally, in the medial division of the lateral nucleus, the percentage of c-Fos/FG double-labelled neurons was higher in the conditioned animals compared with the other groups (P < 0.05). Only a very few GAD67-positive interneurons expressed c-Fos. These data indicate that a part of the amygdalo-entorhinal pathway is activated during acquisition of fear-conditioning. These data support the idea that emotionally relevant sensory information in the lateral nucleus can influence information processing in the hippocampal and parahippocampal areas via the amygdalo-entorhinal pathway.

Amygdala↗
PubMed1997

Number, distribution and neuropeptide content of rat knee joint afferents.

Retrograde tracing with Fluoro-Gold was used to identify the complete population of knee joint afferents in the lumbar dorsal root ganglia of adult female Wistar rats. There was an average of 581 +/- 31 (mean +/- S.D.) afferents supplying each joint. These were found distributed from L1 to L5 with the great majority localised in the L3 and L4 ganglia. Electron microscopy of the posterior articular nerve of the knee revealed an average of 103 +/- 15 (mean +/- S.D.) myelinated and 513 +/- 39 unmyelinated axonal profiles. Since about 50-60% of the unmyelinated profiles would be expected to be sympathetic efferents, these numbers are consistent with the numbers of afferents found by Fluoro-Gold retrograde tracing and suggest that the posterior articular nerve contains about 50% of the total number of knee joint afferents in the rat. Immunohistochemistry revealed that an average of 10% of identified joint afferents expressed substance P-like immunoreactivity and that 33% expressed calcitonin gene-related peptide-like immunoreactivity.

Animals↗
PubMed1998

Increase of extracellular glutamate and expression of Fos-like immunoreactivity in the ventral tegmental area in response to electrical stimulation of the prefrontal cortex.

Electrical stimulation of the medial prefrontal cortex caused glutamate release in the ventral tegmental area (VTA) of freely moving animals. Cathodal stimulation was given through monopolar electrodes in 0.1-ms pulses at an intensity of 300 microA and frequencies of 4-120 Hz. Glutamate was measured in 10-min perfusate samples by HPLC coupled with fluorescence detection following precolumn derivatization with o-phthaldialdehyde/beta-mercaptoethanol. The stimulation-induced glutamate release was frequency dependent and was blocked by the infusion of the sodium channel blocker tetrodotoxin (10 microM) through the dialysis probe. The stimulation also induced bilateral Fos-like immunoreactivity in ventral tegmental neurons, with a significantly greater number of Fos-positive cells on the stimulated side. These findings add to a growing body of evidence suggesting that the medial prefrontal cortex regulates dopamine release in the nucleus accumbens via its projection to dopamine cell bodies in the VTA.

Animals↗
PubMed2000

Pretreatment with calpain inhibitor CEP-4143 inhibits calpain I activation and cytoskeletal degradation, improves neurological function, and enhances axonal survival after traumatic spinal cord injury.

The pathophysiology of traumatic spinal cord injury (SCI) involves abnormal activation of the neutral cysteine protease calpain I (EC 3.4.22.17). In the present study we examined the effect of the calpain inhibitor CEP-4143 on cytoskeletal protection and neurological recovery after SCI in adult rats. Microinjection of 50 mM CEP-4143 into the T7 vertebral segment 10 min before a 35-g clip compression injury resulted in inhibition of calpain activation at 2 and 4 h postinjury, as determined by western blotting for calpain I-mediated spectrin degradation, and significantly attenuated the degradation of dephosphorylated NF200 neurofilament protein at 4 and 8 h postinjury. To examine the in vivo chronic neuroprotective effects of CEP-4143, animals underwent microinjection with saline or 50 mM CEP-4143 10 min before injury, followed by weekly blinded behavioral assessments for 6 weeks. Animals receiving CEP-4143 treatment showed significant improvement over saline-treated controls on the Basso Beattie Bresnahan locomotor rating scale (p < 0.02) and inclined plane test (p < 0.05). Counts of neurons in the red nucleus retrogradely labeled by fluoro-gold after introduction distal to the injury site were significantly higher in CEP-4143-treated animals. Finally, morphometric assessment of the injury site by computer-assisted image analysis revealed significant tissue preservation in CEP-4143-treated animals. We conclude that the calpain antagonist CEP-4143 exhibits biochemical, behavioral, and anatomical neuroprotection following traumatic SCI.

Animals↗
PubMed2001

Contribution of cranial nerve ganglia to innervation of the walls of the rat external acoustic meatus.

The retrograde neuronal tracer, fluorogold, was used to determine the relative contributions of neurons in selected cranial nerve ganglia to the somatosensory innervation of the external acoustic meatus in the rat. Frozen sections from the trigeminal (semilunar), facial (geniculate), glossopharyngeal (superior petrosal) and vagal (jugular) nerve ganglia were examined by epifluoresence microscopy 10 to 14 days after application of the tracer dye fluorogold to the superior, inferior, anterior and posterior walls of the external acoustic meatus. The anterior wall of the canal makes a large contribution to the trigeminal ganglion and a lesser contribution to the other 3 ganglia. The trigeminal ganglion is also a major recipient from the posterior wall with smaller contributions from that wall to the geniculate and vagal ganglia. The superior wall projects a relatively constant supply to all 4 ganglia while the inferior wall primarily relays to the trigeminal and geniculate ganglia sending smaller contributions to the vagal and glossopharyngeal ganglia. In conclusion, neurons in these 4 cranial nerve ganglia contribute an overlapping supply to the 4 walls of the external ear meatus, and there is no evidence of a preferential distribution of nerve supply from one particular ganglion or nerve to specific walls of the external acoustic meatus.

Animals↗
PubMed2003

Antibodies to myelin-associated glycoprotein accelerate preferential motor reinnervation.

Predegeneration of nerve enhances its ability to support axon regeneration. Trophic factors are upregulated by reactive Schwann cells while potentially inhibitory molecules are removed. These experiments isolate the effects of one such inhibitory molecule, the myelin-associated glycoprotein (MAG), to determine its role in modifying regeneration after nerve repair. Suture of the mouse femoral nerve was followed by daily intraperitoneal injection of antibodies to MAG, antibodies to HNK-1, a specific muscle pathway marker, or no further treatment. Regeneration was assayed by double-labeling the femoral cutaneous and muscle branches with horseradish peroxidase and fluoro-gold after 4 weeks or 6 weeks of regeneration. Four weeks after nerve repair, selective reinnervation of the muscle branch by motoneurons, or preferential motor reinnervation (PMR), was not seen in either controls or L2-antibody-treated animals. In contrast, treatment with MAG antibodies resulted in dramatic PMR. By 6 weeks, the controls had achieved borderline specificity, substantial PMR developed in the L2 antibody group and the MAG group changed little. Blocking access to MAG in the distal nerve stump thus accelerated and enhanced PMR. Sensory regeneration was depressed by both antibody treatments at 4 weeks but recovered by 6 weeks. Antibody administration has a generalized effect on sensory regeneration that is unrelated to the behavior of motoneurons in the same nerve.

Animals↗
PubMedDate not supplied

Innervation of the rat pineal gland by nerve fibres originating in the sphenopalatine, otic and trigeminal ganglia. A retrograde in vivo neuronal tracing study.

The innervation of the rat pineal gland from the sphenopalatine, otic, superior cervical and trigeminal ganglia was investigated in animals by use of in vivo retrograde tracings. A solution of 2% Fluorogold was iontophoretically injected into the superficial pineal gland in a series of Wistar rats. After a survival time of 4-10 days, the animals were fixed by perfusion and the brains, sphenopalatine, otic, superior cervical and trigeminal ganglia were investigated with a fluorescence microscope. Many retrogradely labelled perikarya were found in the superior cervical ganglia, but a smaller number of neurones were also labelled in the sphenopalatine, otic and trigeminal ganglia. Injections of the tracer into the subarachnoidal space were used as the control for unspecific uptake and transport of the tracer. The input to the pineal gland from the parasympathetic sphenopalatine and otic ganglia might be involved in the regulation of the annual rhythms of the pineal gland. The projections from the sensory trigeminal ganglion could be involved in the control of the blood flow of the gland.

Afferent Pathways↗
PubMed1997

Calcitonin gene-related peptide is increased in hindlimb motoneurons after exercise.

Calcitonin gene-related peptide (CGRP) is a neuroactive peptide present in some spinal cord motoneurons and at their motor endplates in skeletal muscle. Although detectable levels of CGRP change after surgical and pharmacological interruptions of neuromuscular connectivity, a clear understanding of its physiological role in the motor system is lacking. The purpose of this study was to investigate whether downhill running exercise, which elicits muscle damage and repair, also elicits changes in CGRP levels in hindlimb motoneurons. Twenty female Wistar rats were divided into five groups: control (c), 48 hours post-exercise (48 hr), 72 hours (72 hr), two weeks (2 wks) and four weeks (4 wks). Exercise groups ran downhill for one 30 minute period. Histological examination of muscle from ankle extensors (triceps surae, TS) and flexors (anterior crural, AC) indicated the characteristic presence of histiocytes by 48 hr post-exercise in TS but not in AC. Paraformaldehyde-fixed, 30 microm sections of lumbar spinal cord (L2-L4) from the same animals were incubated with polyclonal antisera to CGRP. The number of CGRP-positive TS motor nuclei increased significantly by 48 hr after exercise (p = 0.001) vs control and returned to baseline values by 4 wks (p > 0.05). In contrast, no significant changes were observed in the AC motoneuron pool at any post-exercise interval (p > 0.05). The temporal changes in CGRP levels in TS motoneurons suggest that expression of this neuropeptide may be differentially regulated by exercise-induced changes in neuromuscular function, possibly as related to muscle tissue damage/repair mechanisms and thus to remodeling at the neuromuscular junction.

Animals↗