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At least 19 recordsLinked to original sources
PubMed1999

Modulatory effect of imetit, a histamine H3 receptor agonist, on C-fibers, cholinergic fibers and mast cells in rabbit lungs in vitro.

The pharmacological mechanisms involved in the interactions between C-fibers, cholinergic fibers and mast cells were investigated in tracheally perfused rabbit lungs by measuring the simultaneous release of substance P and histamine in lung effluents. The amounts of substance P and histamine released in lung superfusates were measured by radioimmunoassay (RIA) after administration of capsaicin and carbachol. Capsaicin (10(-4) M) induced a simultaneous increase in substance P (273 +/- 56% of baseline) and histamine (460 +/- 138%) release. Similarly, carbachol (10(-4) M) caused an increase in the release of both substance P (367 +/- 111%) and histamine (1379 +/- 351%). The effect of capsaicin was prevented by pretreating the lungs with the tachykinin NK1 receptor antagonist SR 140333 (10(-7) M), and atropine (10(-6) M). SR 140333 prevented the carbachol-induced release of substance P but not of histamine. Exogenous substance P induced an increase in histamine release (136 +/- 7%) which was significantly greater in lungs perfused with the neutral endopeptidase inhibitor, thiorphan (10(-5) M) (272 +/- 35%). This effect was prevented by atropine (10(-6) M). Pretreatment of lungs with imetit (5 x 10(-8) M), a selective H3 receptor agonist, prevented the capsaicin-induced release of both mediators. Imetit also blocked the carbachol-induced release of substance P but not of histamine. Exogenous substance P-evoked histamine release was inhibited by imetit. Therefore, it can be concluded that substance P released through the action of capsaicin can activate cholinergic fibers, leading to cholinoceptor stimulation with subsequent activation of C-fibers and mast cells. While the presence of presynaptic H3 receptors modulating substance P-induced acetylcholine release was only surmised, the existence of modulating histamine H3 receptors on C-fibers was confirmed.

Animals↗
PubMedDate not supplied

Systematic regional variations in the loss of cortical cholinergic fibers in Alzheimer's disease.

The loss of cortical cholinergic fibers in Alzheimer's disease was investigated using choline acetyltransferase immunohistochemistry and acetylcholinesterase histochemistry. Within both the normal and Alzheimer's cerebral cortex, the two methods revealed an identical pattern of fiber staining. In the normal brain, cholinergic fiber density was highest in limbic and paralimbic cortical zones, intermediate in most sensory-motor and association zones, and lowest within the primary visual and visual association areas of the occipital lobe. In general, supragranular cortical layers contained a higher density of cholinergic fibers, and most of these were oriented vertically. In Alzheimer's disease, an overall 55% loss of cortical cholinergic fibers was detected. There was, however, marked regional variations in the extent of this loss in different cortical areas. Cortical areas within the temporal lobe, particularly the temporal association areas, displayed a dramatic loss of cholinergic fibers. By contrast, the anterior cingulate cortex, primary visual, primary somatosensory, and primary motor cortex displayed a relative preservation of cholinergic fibers. As a whole, greater loss of cholinergic fibers was detected in supragranular layers and in fibers oriented vertical to the cortical surface. These results indicate that cholinomimetic therapies are likely to have different effects on cholinergic transmission in various cortical areas. The precise mechanisms that lead to the regional variations in cortical cholinergic denervation in Alzheimer's disease remain to be elucidated.

Aged↗
PubMed1992

Nerve growth factor promotes collateral sprouting of cholinergic fibers in the septohippocampal cholinergic system of aged rats with fimbria transection.

Nerve growth factor (NGF) was injected intraventricularly into aged (24 months) rats with unilateral fimbria transection. Controls received intraventricular injections of cytochrome c. A quantitative analysis of acetylcholinesterase (AChE)-positive fibers was used to evaluate whether the NGF treatment can stimulate regeneration and reinnervation of the cholinergic axons in the septohippocampal system of aged rats with fimbria transection. A marked increase in the density of AChE-positive fibers was observed in the lateral septum, the dorsal fornix and the dorsal hippocampus of the NGF-treated animals, as compared to the controls. In the lateral septum, the increase was observed in the 2-month NGF-treated animals but not in the 15-day NGF-treated animals. In the dorsal fornix at the level of the dorsal hippocampus, the increase was observed on both the lesioned and unlesioned sides of both the 15-day and 2-month NGF-treated animals. In the denervated (lesioned side) hippocampus, the increase took place in the dorsal hippocampus but not in the ventral hippocampus of both the 15-day and 2-month NGF-treated animals. There was no recovery of AChE-positive fibers on the lesioned side of the fimbria distal to the lesion site even in the 2-month NGF-treated animals. These results demonstrate that intraventricular injections of NGF can stimulate collateral sprouting of intact cholinergic axons in the septohippocampal system and promote cholinergic reinnervation of the denervated hippocampus of aged rats with fimbria transection.

Acetylcholinesterase↗
PubMed1991

Cholinergic fiber growth in co-cultures of CNS tissue.

In co-cultures prepared from the septum and the hippocampus, cholinergic fibers originating in the septal slices grew into the neighboring hippocampal tissue and established functional cholinergic connections with pyramidal cells. To get further insight into the mechanisms governing cholinergic fiber growth, we have added TTX to the growth medium (2 x 10(-7) M) to block propagated electrical activity. Under these conditions, considerably fewer cholinergic cells appeared to survive. A few cholinergic fibers still invaded hippocampal target tissue, but their number was markedly reduced compared with control cultures. Simultaneous application of NGF together with TTX, however, not only increased enzyme levels and enhanced survival of cholinergic neurons, but also led to hippocampal ingrowth in virtually all septo-hippocampal co-cultures. These data, therefore, suggest, that in the absence of spiking activity, cholinergic fibers are capable of growing into a co-cultured target tissue. To test the specificity of growth of septal cholinergic fibers, we have co-cultured septal slices with slices of various brain areas which in situ lack a major cholinergic innervation, in particular the cerebellum. In the vast majority of such co-cultures, cholinergic fibers remained restricted within the septal slices, without innervating cerebellar tissue. This failure might in part be related to the lack of trophic factors released by the target tissue. We have, therefore, grown septo-cerebellar cultures in the presence and absence of NGF. Following application of 100 ng/ml NGF during the entire growth of the cultures, numerous AChE-positive fibers originating in the septal slices invaded the co-cultured cerebellar slices.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

[Guiding effect of embryonic fimbria graft on cholinergic fiber growth in hippocampus of adult rats].

In view of the fact that in embryonic and neonatal central nervous system (CNS), the pathway of developing fiber tracts is capable of guiding the axonal growth, it would be interesting to know whether a similar effect exists on the axonal growth in adult CNS. Embryonic fimbria was grafted into the hippocampus of the adult rat. Two weeks later, the grafts were examined for cholinergic fibers with AChE histochemical method. It was found that a lot of cholinergic fibers appeared in the embryonic graft, but none of them in the adult fimbria graft as control. If the fimbria-fornix was transected at the time of grafting, no cholinergic fibers could subsequently be detected in both the embryonic graft and the host hippocampus. If a suspension of embryonic fimbria was used as a graft, only a few of long cholinergic fibers could be found in the grafted area. However, if tissue fragments of embryonic fimbria adhered to a strip of nitrocellulose filter were grafted as previously, numerous cholinergic fibers from the host hippocampus were found to be attracted around the strip and grow along the surface of the filter. The results seem to indicate that grafted embryonic fimbria or its tissue fragments are able to guide cholinergic fiber growth in adult hippocampus. It is possible that embryonic fimbria and other pathways of developing CNS fiber tracts provide a natural substrate for guiding axonal growth in adult CNS.

Acetylcholine↗
PubMed2004

Effects of two years of estrogen loss or replacement on nucleus basalis cholinergic neurons and cholinergic fibers to the dorsolateral prefrontal and inferior parietal cortex of monkeys.

The present study examined the long-term (2 years) effects of estrogen loss or estrogen replacement therapy (ERT) on cholinergic neurons in the nucleus basalis of Meynert and on cholinergic fibers in the prefrontal and parietal cortex of adult female cynomolgus monkeys. Cholinergic fiber density in layer II of the prefrontal cortex was decreased in monkeys who were ovariectomized and treated with placebo for 2 years. In contrast, ovariectomized monkeys receiving ERT for 2 years had fiber densities that were comparable to those of intact controls. No differences in parietal cholinergic fiber density or nucleus basalis cholinergic neuron number or volume were found among intact, ovariectomized, or ERT monkeys. Our results suggest that ERT is effective in preventing region-specific changes in cortical cholinergic fibers that result from the loss of circulating ovarian hormones. These modest but appreciable effects on cholinergic neurobiology following long-term estrogen loss and ERT may contribute to changes in visuospatial attention function that is mediated by the prefrontal cortex.

Acetylcholine↗
PubMed1998

Relationship between plaques, tangles, and loss of cortical cholinergic fibers in Alzheimer disease.

Recent observations in our laboratory have indicated substantial and systematic regional variations in the loss of cortical cholinergic fibers in Alzheimer disease (AD). Previous attempts to study the relationship between cortical cholinergic loss and the density of cortical pathological lesions have resulted in conflicting findings. Furthermore, most reports have correlated density of plaques and tangles with the residual level of cholinergic innervation rather than its loss. The purpose of the present study was to determine the relationship between loss of cholinergic axons and density of tangles and beta-amyloid (Abeta) deposits in various cortical areas of AD brains. Abeta deposits and tangles were observed throughout the cerebral cortex. Quantitative analysis revealed almost no correlation between loss of cholinergic fibers and the density of Abeta deposits. Qualitative observations revealed similar results when cored and neuritic plaques were considered separately. By contrast, cholinergic fiber loss displayed a significant correlation with the density of tangles (r = 0.52-0.79). However, in a few areas, such as the cingulate cortex, tangle density appeared to be unrelated to the loss of cholinergic fibers. These results indicate that cortical cholinergic denervation in AD is related to cytoskeletal pathology. However, the lack of a perfect relationship with cytoskeletal pathology implicates additional factors in the cholinergic pathology of AD.

Aged↗
PubMedDate not supplied

Cholinergic fiber aberrations in nucleus basalis lesioned rat and Alzheimer's disease.

Innervation density and morphological aberrations of cholinergic fibers were studied with choline acetyltransferase (ChAT) immunocytochemistry and acetylcholinesterase (AChE) histochemistry in 30-35 month-old aged rats and rats with long-term bilateral lesions of the magnocellular basal nucleus (MBN). In addition, AChE histochemistry was performed on human cortical sections derived from autopsy brains of normal aged and Alzheimer's disease (AD) patients. A limited but variable number of morphological alterations were observed in ChAT-immunoreactive fibers in the cortex and the hippocampus of the aged control rats. The aged MBN-lesioned rats displayed a severely reduced number of cholinergic fibers in the denervated areas of the neocortex, whereas the surviving fibers showed a strongly increased number of aberrations. Fiber anomalies were also observed in the cortex of the aged human subjects and Alzheimer patients, the latter showing a higher incidence of such aberrations. Only a part of these distended profiles were seen in close association with senile plaques as detected in the AChE-stained material. These findings suggest that experimental MBN lesions combined with aging share with AD the induction of large quantities of fiber malformations. Implications of possible mechanisms in both conditions are discussed.

Acetylcholinesterase↗
PubMed2001

Regulation of regional cerebral blood flow by cholinergic fibers originating in the basal forebrain.

The intracranial neural vasodilative system of cholinergic fibers projecting from the basal forebrain to the cortex was discovered by Biesold, Inanami, Sato and Sato (Biesold, D., Inanami, O., Sato, A., Sato, Y., 1989. Stimulation of the nucleus basalis of Meynert increases cerebral cortical blood flow in rats. Neurosci. Lett. 98, 39-44) using laser Doppler flowmetry in anesthetized rats. This cholinergic vasodilative system, which operates by increasing extracellular ACh release, relies upon activation of both muscarinic and nicotinic cholinergic receptors in the parenchyma of the cortex. Further, the involvement of nitric oxide in this cholinergic vasodilation, indicates the necessity to this system of neurons, which contain nitric oxide synthase. The increase in cortical blood flow elicited by this cholinergic vasodilative system is independent of systemic blood pressure and is not coupled to cortical metabolic rates. This cholinergic vasodilative system may be activated by somatic afferent stimulation. Most of the data presented here were obtained in anesthetized animals.

Animals↗
PubMed1988

Cholinergic neurons in the rat hippocampus do not compensate for the loss of septohippocampal cholinergic fibers.

In recent studies a small number of choline acetyltransferase (ChAT)-immunoreactive, supposedly cholinergic, neurons intrinsic to the rat hippocampus have been described. Here we report that these neurons are not capable of sprouting in response to removal of the cholinergic input to the hippocampus from the medial septum/diagonal band complex. One month after unilateral transection of the fimbria-fornix an almost complete lack of cholinergic fibers persists in all layers of the dorsal hippocampus and fascia dentata ipsilateral to the lesion when compared to the contralateral hippocampus or to unlesioned control rats. These results indicate that the well-known phenomenon of collateral sprouting in response to partial deafferentation is a specific process that spares a distinct group of cholinergic cells in the rat hippocampus.

Animals↗
PubMed1991

Role of cholinergic fibers in a center essential to animal hypnosis.

We previously found that the center from which animal hypnosis is controlled in the rabbit is located in the area that includes the brachium conjunctivum and locus coeruleus (LC-BC) of the brainstem. Microinjection was used to investigate functions of cholinergic fibers in this area in relation to animal hypnosis. The duration of animal hypnosis (DAH) induced by inversion was diminished to about 60% of the controls by microinjecting atropine into the LC-BC, whereas microinjection of carbachol prolonged the DAH to 3.5 times that of the controls. Flexor muscle contraction of the upper extremities, induced by electrical stimulation of the motor cortex (CFM), was enhanced by atropine and suppressed by carbachol. In normal rabbits; hard pressing on the ear base or the lumbar paravertebral area reduced CFM (pressing effect), and this effect was partially antagonized by atropine microinjected into the LC-BC. The results suggest that cholinergic fibers in the LC-BC modulate functions involved in animal hypnosis.

Animals↗
PubMed1999

GM1 and piracetam do not revert the alcohol-induced depletion of cholinergic fibers in the hippocampal formation of the rat.

Chronic alcohol consumption causes a depletion of the cholinergic fiber network in the rat hippocampal formation, which is not ameliorated by alcohol withdrawal. Following withdrawal from alcohol, there is a further loss of intrinsic hippocampal cholinergic neurons. In this study, we investigated whether treatment with putative neuroprotective agents during the entire withdrawal period would have beneficial effects upon the hippocampal cholinergic innervation. Adult male rats were alcohol-fed for 6 months and subsequently withdrawn from alcohol for 6 months. Some animals were treated with either ganglioside GM1 (35 mg/kg body weight s.c.), vehicle (saline s.c.), or piracetam (800 mg/kg body weight p.o.) for the entire withdrawal period. Choline acetyltransferase (ChAT) immunoreactive (IR) fibers and neurons were analyzed quantitatively in all four animal groups. There were no significant differences in the density of the ChAT-IR hippocampal fiber network when the pure withdrawal and withdrawal + vehicle groups were compared to the withdrawal + GM1 or withdrawal + piracetam groups. In contrast, the number of ChAT-IR interneurons in the hippocampal formation was higher in the withdrawal + GM1 or withdrawal + piracetam groups than in the pure withdrawal and withdrawal + vehicle groups. These results indicate that, in the doses used, neither neuroprotective agent had an effect upon the extrinsic cholinergic innervation, but they had a beneficial effect upon the hippocampal intrinsic cholinergic system.

Animals↗
PubMed2005

A part of cholinergic fibers in mouse superior cervical ganglia contain GABA or glutamate.

The localizations and functions of glutamate and GABA, the major amino acid neurotransmitters in the central nervous system, are still unclear in the peripheral nervous system. We immunohistochemically double-stained mouse superior cervical ganglia with antibodies for the vesicular acetylcholine transporter (VAchT), GAD65, the vesicular glutamate transporters 1-3 (VGluTs1-3), the marker of the sympathetic preganglionic neuron (SPN), GABAergic, and glutamatergic terminals, respectively. All GAD65-positive terminals showed VAchT immunoreactivity, indicating that GABAergic fibers originate from SPNs. VGluT2-immunoreactive terminals showing colocalization with VAchT were observed, but VGluT1 and 3 immunoreactive terminals were not. Colocalization of GAD65 and VGluT2 was rarely found. All VGluT2-immunopositive terminals were also immunopositive for neuronal nitric oxide synthase (nNOS), a marker for the subpopulation of the SPNs, while about half of the GABA-immunopositive fibers were immunopositive for nNOS. The origin of these fibers was discussed.

Acetylcholine↗
PubMed1999

Effects of age and sex on the water maze performance and hippocampal cholinergic fibers in rats.

We have examined if age-related deterioration of spatial memory and cholinergic innervation of the dentate gyrus is gender-specific. Aging progressively affected the performance of male and female rats in place discrimination version of the water maze task. On repeated acquisition task, only old males, but not old females, were significantly impaired relative to young and adult animals of both sexes. In parallel, we found that the age-associated reduction of the density of cholinergic fibers in the dentate gyrus was significantly more profound in old males than in age-matched females. These results suggest that, although male and female rats have an identical pattern of reference memory decline, impairment of the working memory and deterioration of the hippocampal cholinergic system are slower to develop in females than in males.

Age Factors↗
PubMed1980

Effects of field stimulation on cholinergic fibers of the pelvic region in the isolated guinea pig ureter.

Electrical activities have been recorded in a preparation consisting of the pelvic region and the upper ureter of the guinea pig. Train field stimulation of the pelvic region evoked a train of nerve action potentials followed by a multiphasic smooth muscle action potential after a latency of about 2.5--8.0 sec. This smooth muscle response was abolished by tetrodotoxin and dibucaine, and also by cholinergic blocking agents. The response was furthermore, inhibited by decreasing Ca/4 concentration and increasing Mg/+ concentration in Tyrode solution. This is therefore considered to be the response synaptically evoked by cholinergic fibers in the pelvic region. Mechanical activities have been investigated on the same preparations by the Magnus method. Acetylcholine (10(-7)--10(-4) g/ml) produced a group of twitch responses which were antagonized by cholinergic blocking agents. The responsiveness of the preparations to acetylcholine was markedly decreased by removal of the pelvic region. Cholinesterase activities in the calyx-pelvis and upper ureter have been estimated by the biochemical method. A preparation consisting of calyx-pelvis exhibited twice the enzyme activity as compared with the upper ureter. These results suggesteds that there is a cholinergic innervation in the pelvic region of the guinea pig ureter which also takes part in control of the ureteric activity.

Acetylcholine↗
PubMed1977

Evidence for a cholinergic fiber tract connecting the thalamus with the head of the striatum of the rat.

Placement of electrolytic lesions in the zona incerta or parafascicular nucleus of the rat forebrain resulted in a marked reduction of choline acetyltransferase (ChAc) activity in the head of the striatum 2-4 weeks later. Lesions of the habenula did not cause this effect implying that concomitant destruction of the fasciculus retroflexus with the parafascicular nucleus was not responsible for the effects observed. The data suggest that there is a cholinergic fiber tract connection between the parafascicular nucleus of the thalamus and the head of the striatum in the rat forebrain.

Animals↗
PubMed1998

Brain-derived neurotrophic factor stimulates hindlimb stepping and sprouting of cholinergic fibers after spinal cord injury.

Neurotrophic factors have been proposed as a therapeutic treatment for traumatic brain and spinal cord injury. The present study determined whether exogenous administration of one such factor, brain-derived neurotrophic factor (BDNF), could effect behavioral recovery and/or histopathological changes after spinal cord injury. Adult rats received a mild or moderate contusion injury or complete transection of the mid-thoracic spinal cord. Immediately thereafter, they were infused intrathecally with vehicle or BDNF for 28 days. Behavioral recovery was evaluated for 6 weeks after injury, at which time the rats were sacrificed and the spinal cord tissue was examined histologically. The infusion of BDNF resulted in acute stimulation of hindlimb activity. These effects included activation of alternating airstepping in injured rats when the hindlimbs were unloaded as well as slight improvements in the rate of recovery in open field locomotion score. BDNF infusion was also associated with enhanced growth of cholinergic fibers at the injury epicenter, but did not affect white matter sparing or density of serotonergic axons at or below the injury site. Based on immunohistochemical detection of BDNF protein distribution, these described effects are likely to be mediated by the activation of cells and axons within the central injury region and the along the peripheral rim of the spinal cord. Together, these findings demonstrate that the exogenous infusion of BDNF after spinal trauma can influence postinjury outcome through mechanisms that include acute stimulation of hindlimb activity and neuritogenesis at the injury site.

Animals↗