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Relevant bibliographies by topics / Rat cholinergic neurones

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Academic literature on the topic 'Rat cholinergic neurones'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Rat cholinergic neurones"

1

Ekelund, K. M., and E. Ekblad. "Structural, neuronal, and functional adaptive changes in atrophic rat ileum." Gut 45, no. 2 (August 1, 1999): 236–45. http://dx.doi.org/10.1136/gut.45.2.236.

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BACKGROUNDInactivity of the gut leads to atrophic changes of which little is known.AIMSTo investigate structural, neuronal, and functional changes occurring in bypassed rat ileum.METHODSMorphometry was used to characterise the atrophic changes. The numbers of enteric neurones, their expression of neurotransmitters, and the presence of interstitial cells of Cajal were studied using immunocytochemistry and in situ hybridisation. Motor activity was studied in vitro.RESULTSAdaptive changes in bypassed ileum include atrophy and remodelling of the gut wall. The total numbers of submucous and myenteric neurones per unit length increased one and four weeks after bypass but were identical to sham operated intestine 10 weeks after bypass. Neurones expressing vasoactive intestinal peptide, neuropeptide Y, or pituitary adenylate cyclase activating peptide decreased gradually in number in bypassed ileum. Nitric oxide synthase expressing neurones were increased, particularly in the myenteric ganglia. No change in the frequency and distribution of interstitial cells of Cajal was noted. The contractile response elicited by electrical stimulation of sham operated ileum consisted of a fast cholinergic twitch followed by a slower non-adrenergic, non-cholinergic contraction. In the bypassed ileum an identical biphasic contraction was elicited; however, the entire response was non-adrenergic, non-cholinergic. The relaxatory response to electrical stimulation in sham operated ileum was nitric oxide mediated; after bypass it was non-nitrergic.CONCLUSIONSNotable atrophic changes were seen in the rat ileum after bypass. The enteric nervous system reacted with neuronal cell death and plasticity in terms of release and expression of neurotransmitters.

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Atterwill, Christopher K. "Brain Reaggregate Cultures in Neurotoxicological Investigations: Studies with Cholinergic Neurotoxins." Alternatives to Laboratory Animals 16, no. 3 (March 1989): 221–30. http://dx.doi.org/10.1177/026119298901600304.

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The number of neurotoxicants which produce ‘lesions’ in organotypic brain reaggregate cultures in vitro, which correlate with known in vivo actions, is growing. With respect to cholinergic neurones, this includes kainic acid, organophosphorus compounds and, in our hands, ethylcholine mustard aziridinium (ECMA) and aluminium. We have demonstrated that in vitro exposure to low concentrations of ECMA (12.5μM) produces a two-stage lesion in rat whole-brain reaggregate cultures, corresponding to initial direct inhibition of choline acetyltransferase (ChAT), followed by a later loss of cholinergic neurones. Higher concentrations of ECMA (25–50μM) are more generally cytotoxic and also cause lesions in non-cholinergic cerebellar granule neurones in monolayer culture. Aluminium (0.1–0.01mM) similarly reduces ChAT activity in rat whole-brain reaggregate cultures. Both agents may be useful in providing brain cholinergic lesions in vitro analagous to those occurring in types of dementia in vivo. The use of brain reaggregates in a ‘stepwise’ procedure for testing potential neurotoxicants is also described.

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Kumamoto, Eiichi, and Yuzo Murata. "GABAA-receptor channels on rat cholinergic septal neurones in culture." Neuroscience Research Supplements 19 (January 1994): S51. http://dx.doi.org/10.1016/0921-8696(94)92404-x.

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Atterwill, Christopher K., Wendy J. Davies, and Michael A. Kyriakides. "An Investigation of Aluminium Neurotoxicity using some In Vitro Systems." Alternatives to Laboratory Animals 18, no. 1_part_1 (November 1990): 181–90. http://dx.doi.org/10.1177/026119299001800119.1.

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It has been shown that acute exposure in vitro to high concentrations of aluminium chloride does not appear to perturb neural function in terms of the electrophysiological properties of lower vertebrate leech neurones. Longer term exposure in vitro, however, both non-specifically inhibits cellular differentiation and also produces neural cytotoxicity in the rat midbrain micromass, mixed cell culture model. Furthermore, previous studies from this laboratory have demonstrated a reduction of cholinergic neuronal function in brain organotypic reaggregate cultures following long-term, but not short-term, exposure. More-immature neural cells appear to be most sensitive to the effects of aluminium. Relating these data to the tiered in vitro test system for neurotoxicants previously proposed by Atterwill (13), it is apparent that the neurotoxic effects of aluminium are detectable in a first-stage procedure using the micromass culture model, but not following acute exposure in freshly isolated, ex vivo leech neurones. Functional cholinergic toxicity was also detected in the organotypic reaggregate cultures proposed as a second level screen.

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BINNS, K. E., and T. E. SALT. "The functional influence of nicotinic cholinergic receptors on the visual responses of neurones in the superficial superior colliculus." Visual Neuroscience 17, no. 2 (March 2000): 283–89. http://dx.doi.org/10.1017/s0952523800172116.

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In the rat, the superficial gray layer (SGS) of the superior colliculus receives glutamatergic projections from the contralateral retina and from the visual cortex. A few fibers from the ipsilateral retina also directly innervate the SGS, but most of the ipsilateral visual input is provided by cholinergic afferents from the opposing parabigeminal nucleus (PBG). Thus, visual input carried by cholinergic afferents may have a functional influence on the responses of SGS neurones. When single neuronal extracellular recording and iontophoretic drug application were employed to examine this possibility, cholinergic agonists were found to depress responses to visual stimulation. Lobeline and 1-acetyl-4-methylpiperazine both depressed visually evoked activity and had a tendency to reduce the background firing rate of the neurones. Carbachol depressed the visual responses without any significant effect on the ongoing activity, while the muscarinic receptor selective agonist methacholine increased the background activity of the neurones and reduced their visual responses. Lobeline was chosen for further studies on the role of nicotinic receptors in SGS. Given that nicotinic receptors are associated with retinal terminals in SGS, and that the activation of presynaptic nicotinic receptors normally facilitates transmitter release (in this case glutamate release), the depressant effects of nicotinic agonists are intriguing. However, many retinal afferents contact inhibitory neurones in SGS; thus it is possible that the increase in glutamate release in turn facilitates the liberation of GABA which goes on to inhibit the visual responses. We therefore attempted to reverse the effects of lobeline with GABA receptor antagonists. The depressant effects of lobeline on the visual response could not be reversed by the GABAA antagonist bicuculline, but the GABAB antagonist CGP 35348 reduced the effects of lobeline. We hypothesize that cholinergic drive from the parabigeminal nucleus may activate presynaptic nicotinic receptors on retinal terminals, thereby facilitating the release of glutamate onto inhibitory neurones. Consequently GABA is released, activating GABAB receptors, and thus the ultimate effect of nicotinic receptor activation is to depress visual responses.

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Yang, Qiner, Anders Hamberger, Nastaran Khatibi, Torgny Stigbrand, and Kenneth G. Haglid. "Presence of S-100β in cholinergic neurones of the rat hindbrain." NeuroReport 7, no. 18 (November 1996): 3093–100. http://dx.doi.org/10.1097/00001756-199611250-00060.

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Cross, A. J., and J. F. W. Deakin. "Cortical serotonin receptor subtypes after lesion of ascending cholinergic neurones in rat." Neuroscience Letters 60, no. 3 (October 1985): 261–65. http://dx.doi.org/10.1016/0304-3940(85)90587-7.

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8

Pearson, R. C. A., M. V. Sofroniew, and T. P. S. Powell. "Hypertrophy of cholinergic neurones of the rat basal nucleus following section of the corpus callosum." Brain Research 338, no. 2 (July 1985): 337–40. http://dx.doi.org/10.1016/0006-8993(85)90164-7.

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9

Vidal, S., B. Raynaud, D. Clarous, and M. J. Weber. "Neurotransmitter plasticity of cultured sympathetic neurones. Are the effects of muscle-conditioned medium reversible?" Development 101, no. 3 (November 1, 1987): 617–25. http://dx.doi.org/10.1242/dev.101.3.617.

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Muscle-conditioned medium (CM) induces choline acetyltransferase (CAT) activity in primary cultures of new-born rat sympathetic neurones and depresses the development of tyrosine hydroxylase (TOH). By following these two enzymes, we have determined whether (1) the effects of CM are reversible and (2) the neurones progressively lose their sensitivity to CM with time in culture. When neurones were cultured in the presence of 50% CM (CM+ medium), TOH activity developed slowly but CAT activity developed at a high rate. When the cultures were then switched to unconditioned medium (CM- medium), CAT activity remained elevated and continued to develop at higher rate than in cultures that were never exposed to CM. On the other hand, the switch to CM- medium was accompanied by a transition from a low to a high rate of TOH development. CAT induction by CM was thus essentially irreversible, whereas the impairment of TOH development was fully reversible. Conversely, we studied the effects of altering CM- to CM+ medium at progressively later culture days. CAT remained fully inducible for at least 2 to 3 weeks. On the other hand, TOH activity, which initially developed rapidly in CM- medium, first decreased to low levels after a switch to CM+ medium and then increased again, but at a slower rate. Neuronal depolarization by elevated K+ and exposure to CM have mirror-image, and antagonistic, effects on both CAT and TOH developments (Raynaud et al. 1987a). Walicke, Campenot & Patterson (1977) showed that a previous depolarization reduced the induction of cholinergic traits by a subsequent exposure to CM. We found that (1) such a depolarization only delayed the induction of CAT by several days and did not prevent the transition to a state of low TOH expression caused by CM and (2) an exposure of the cultures to elevated K+ after exposure to CM did not cause a decline in CAT activity. These data thus suggest that a state of high TOH expression can superimpose on a previously induced state of elevated CAT expression, but that the induction of CAT caused by a delayed exposure to CM is accompanied by a transition from a high to a lower state of TOH expression. In addition, neuronal depolarization does not stabilize the noradrenergic phenotype in a permanent manner and can not reverse cholinergic expression of sympathetic neurones to a purely noradrenergic phenotype.

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Momiyama, Toshihiko. "A patch-clamp analysis of GABAergic synaptic inputs to large cholinergic neurones in the rat striatum." Japanese Journal of Pharmacology 76 (1998): 89. http://dx.doi.org/10.1016/s0021-5198(19)40474-5.

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Dissertations / Theses on the topic "Rat cholinergic neurones"

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Duguid, Gail Louise. "The involvement of the cholinergic and glutamatergic neurotransmitter systems in neuronal processes underlying recognition memory in the rat." Thesis, University of Bristol, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368392.

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Jourdain, Anne. "Studies on the collateralization of some basal forebrain and mesopontine tegmental projection systems in the rat." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27969.

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Many basal forebrain and mesopontine tegmental cholinergic projection systems tend to overlap in their origins. This raises the possibility that these projection systems are collateralized to innervate divergent areas. In experiment one, the degree to which basal forebrain and mesopontine tegmental neurons that innervate the reticular thalamic nucleus have axons that collateralize to innervate the cortex as well was examined with a retrograde fluorescence labeling method combined with immunohistochemistry. A significant portion of the labeled neurons in the region of the nucleus basalis magnocellularis and pedunculopontine tegmental nucleus projecting to the reticular thalamic nucleus were observed to be also labeled (double-labeled) following intracortical tracer injections. Many of these double-labeled neurons displayed choline acetyltransferase choline acetyltransferase immunoreactivity. It was also shown that numerous basal forebrain neurons that innervated the reticular thalamic nucleus contained the calcium-binding protein, parvalbumin. These neurons tended to be located more rostrally than the ChAT immunoreactive neurons; primarily in the region of the ventral pallidum. There was some indication that parvalbumin-containing neurons in the basal forebrain that innervate the reticular thalamic nucleus also have axons that branch to innervate the cortex. Finally, none of the basal forebrain neurons innervating the reticular thalamic nucleus was found to contain somatostatin. In experiment two, the degree to which basal forebrain neurons have axons that collateralize to innervate the interpeduncular nucleus and hippocampus was examined with retrograde fluorescence labeling methods. Labeled neurons projecting to both of these limbic structures were observed only occasionally. Comparison of the distribution of single labeled neurons innervating each of these structures revealed that within the region of origin, in the horizontal limb of the diagonal band, neurons innervating the interpeduncular nucleus tended to be located dorsally to those innervating the hippocampus. The results of these experiments are discussed in relation to their anatomical and functional implications toward a greater understanding of the basal forebrain and mesopontine cholinergic and non-cholinergic projection systems.
Medicine, Faculty of
Graduate

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Reece, Laura J. "Cholinergic effects on developing hippocampal neurons in vitro /." Thesis, Connect to this title online; UW restricted, 1990. http://hdl.handle.net/1773/10558.

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Nair, Sunila. "Effects of 3,4-methylenedioxymethamphetamine (MDMA) on Cholinergic neurons in the rat brain." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1123857787.

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5

Perry, Theresa Fried. "Functional relationship between forebrain cholinergic projections and somatostatin neurons in the rat." Thesis, Virginia Tech, 1990. http://hdl.handle.net/10919/41603.

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The two neuron types that initially degenerate with Alzheimer's Disease are the cholinergic projections from the septum to the hippocampus and from the substantia innominata to the cortex, and the somatostatinergic neurons in the hippocampus and cortex. The functional relationship between these two types of neurons was investigated using folic acid, a neuro-excitant, and cysteamine, a somatostatin depleter. Folic acid causes a neuron to fire at a much higher rate than normal (Spector, 1971). Folic acid was injected into either the septum or the substantia innominata, and the long-term effect of the resulting acute hyperactivity of the cholinergic neurons on somatostatin neurons was measured as somatostatin-like immunoreactivity in the hippocampus and cortex. Glutamic acid decarboxylase activity, a marker for gamma-amino butyric acid (GABA) neurons, was also measured because it has been shown to decrease in the cortex after injection of folic acid into the substantia innominata. The administration of folic acid to the cholinergic neurons did not have a significant long-term effect on somatostatin-like immunoreactivity nor glutamic acid decarboxylase activity; therefore, a hyperactivity of the cholinergic neurons did not result in degeneration of GABAergic nor somatostatinergic neurons. Cysteamine causes a short-term depletion of somatostatin. Cysteamine was injected subcutaneously and the effect of an acute decrease of brain somatostatin on the cholinergic neurons was studied by measuring high affinity choline uptake, an indicator of cholinergic activity. Administration of cysteamine had no measured effect on high affinity choline uptake in the hippocampus or frontal cortex; therefore, a depletion of somatostatin did not effect cholinergic activity. The assay for high affinity choline uptake was tested by injection of pentobarbital, a drug known to decrease high affinity choline uptake. We detected a decrease in high affinity choline uptake after pentobarbital administration, indicating that if cysteamine were decreasing high affinity choline uptake, the assay would have detected it.
Master of Science

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6

Carnes, Benjamin J. Carnes. "Compensatory Cortical Sprouting Across the Lifespan of the Rat." Ohio University Honors Tutorial College / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ouhonors1461167224.

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Dutar, Patrick. "Les systèmes cholinergiques centraux chez le rat adulte et le rat âgé : étude des caractéristiques électrophysiologies et pharmacologiques." Paris 6, 1986. http://www.theses.fr/1986PA066464.

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Etude in vivo chez le rat adulte et âgé à l'aide d'approches multidisciplinaires des caractéristiques des neurons cholinergiques des voies septo-hippocampique et basalo-corticale. Les caractéristiques physiologiques ont été décrites par enregistrements extra et intracellulaires, les propriétés pharmacologiques par applications iontophorétiques, les modifications de ces propriétés ont été étudiées au cours du vieillissement. Enfin une étude anatomique par marquage histologique à la peroxydase a été menée pour définir la voie basalo-corticole.

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8

Zhang, Zi Wei ZW. "Plasticity of neuroanatomical relationships between cholinergic and dopaminergic axon varicosities and pyramidal cells in the rat medial prefrontal cortex." Thèse, 2011. http://hdl.handle.net/1866/6281.

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Les systèmes cholinergique et dopaminergique jouent un rôle prépondérant dans les fonctions cognitives. Ce rôle est exercé principalement grâce à leur action modulatrice de l’activité des neurones pyramidaux du cortex préfrontal. L’interaction pharmacologique entre ces systèmes est bien documentée mais les études de leurs interactions neuroanatomiques sont rares, étant donné qu’ils sont impliqués dans une transmission diffuse plutôt que synaptique. Ce travail de thèse visait à développer une expertise pour analyser ce type de transmission diffuse en microscopie confocale. Nous avons étudié les relations de microproximité entre ces différents systèmes dans le cortex préfrontal médian (mPFC) de rats et souris. En particulier, la densité des varicosités axonales en passant a été quantifiée dans les segments des fibres cholinergiques et dopaminergiques à une distance mutuelle de moins de 3 µm ou à moins de 3 µm des somas de cellules pyramidales. Cette microproximité était considérée comme une zone d’interaction probable entre les éléments neuronaux. La quantification était effectuée après triple-marquage par immunofluorescence et acquisition des images de 1 µm par microscopie confocale. Afin d’étudier la plasticité de ces relations de microproximité, cette analyse a été effectuée dans des conditions témoins, après une activation du mPFC et dans un modèle de schizophrénie par déplétion des neurones cholinergiques du noyau accumbens. Les résultats démontrent que 1. Les fibres cholinergiques interagissent avec des fibres dopaminergiques et ce sur les mêmes neurones pyramidaux de la couche V du mPFC. Ce résultat suggère différents apports des systèmes cholinergique et dopaminergique dans l’intégration effectuée par une même cellule pyramidale. 2. La densité des varicosités en passant cholinergiques et dopaminergiques sur des segments de fibre en microproximité réciproque est plus élevée comparé aux segments plus distants les uns des autres. Ce résultat suggère un enrichissement du nombre de varicosités axonales dans les zones d’interaction. 3. La densité des varicosités en passant sur des segments de fibre cholinergique en microproximité de cellules pyramidales, immunoúactives pour c-Fos après une stimulation visuelle et une stimulation électrique des noyaux cholinergiques projetant au mPFC est plus élevée que la densité des varicosités de segments en microproximité de cellules pyramidales non-activées. Ce résultat suggère un enrichissement des varicosités axonales dépendant de l’activité neuronale locale au niveau de la zone d'interaction avec d'autres éléments neuronaux. 4. La densité des varicosités en passant des fibres dopaminergiques a été significativement diminuée dans le mPFC de rats ayant subi une déplétion cholinergique dans le noyau accumbens, comparée aux témoins. Ces résultats supportent des interrelations entre la plasticité structurelle des varicosités dopaminergiques et le fonctionnement cortical. L’ensemble des donneès démontre une plasticité de la densité locale des varicosités axonales en fonction de l’activité neuronale locale. Cet enrichissement activité-dépendant contribue vraisemblablement au maintien d’une interaction neurochimique entre deux éléments neuronaux.
The cognitive functions of the rat medial prefrontal cortex (mPFC) are modulated by ascending modulatory systems such as the cholinergic and dopaminergic afferent systems. However, despite the well-documented pharmacological interactions between the cholinergic and dopaminergic afferents and pyramidal cells in the PFC, there is only scarce neuroanatomical data on the reciprocal interrelationships between these neuronal elements in the mPFC. This might be due to the diffuse rather than synaptic transmission mode of intercellular communication of the cholinergic system in the mPFC. For these reasons, the neuroanatomical relationships between the cholinergic and dopaminergic systems and pyramidal cells in the mPFC are examined, with an emphasis on the local density of the cholinergic and dopaminergic axon varicosities. To analyze the plasticity of these interrelationships, the two systems were examined in condition of increased neuronal activity in the mPFC, or of decrease dopaminergic activity in a model of schizophrenia. The microproximity relationships between cholinergic and dopaminergic fibers as well as with pyramidal cells were studied in the mPFC of rats and mice. In particular, the number of axon varicosities in cholinergic and dopaminergic fiber segments within 3 µm from each other or from pyramidal cells were quantified. This microproximity was considered as a possible interaction zone between two neuronal elements. Quantification was performed using triple immunofluorescence labeling and acquisition of 1 µm optic sections using confocal microscopy. To assess the plasticity of these relationships, the analysis has been performed in control condition as well as after a cortical activation or a decreased dopaminergic input in a schizophrenia model. Our results demonstrate a neuroanatomical convergence of cholinergic and dopaminergic fibers on the same pyramidal cell from layer V (output) of mPFC, suggestinggests the integration of different types of inputs by the same pyramidal cell, which may be transmitted to subcortical areas to execute prefrontal cognitive control. Close apposition between cholinergic and dopaminergic fibers could also be seen in the mPFC. There was an increase of the density of cholinergic and dopaminergic en passant varicosities on those fiber segments within microproximity of each other, compared to those outside the reciprocal microproximity, supporting functional importance of the close apposition between those two ascending neuromodulatory systems into the mPFC. There was enrichment of cholinergic en passant varicosities on the fiber segments within microproximity of c-Fos activated pyramidal cells in the mPFC of visually and HDB electrically stimulated rats, indicating association between axonal varicosity density and the local neuronal activity. There was decrease of dopaminergic en passant varicosities in the mPFC of rats with ChAT depletion in the N.Acc., compared to controls. This evidence supports the association between dopaminergic axonal varicosities and relevant neuronal activity in a complex neuronal network. This thesis shows that the density of cholinergic and dopaminergic axonal varicosity density in the mPFC is influenced by and contributes to the relevant local neuronal activity from the interactions of different transmitter systems. Such interactions of different systems in a complex and intricate prefrontal neuronal network endeavour to maintain the delicate balance for cognitive processes.

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Yu-ting, Wang, and 王昱婷. "Cholinergic Effects on the Neurons of the Rat Suprachiasmatic Nucleus." Thesis, 2005. http://ndltd.ncl.edu.tw/handle/05452627226220672171.

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碩士
長庚大學
基礎醫學研究所
93
The suprachiasmatic nucleus (SCN) is the master pacemaker in mammals, with two anatomically and functionally distinct divisions of dorsal (dSCN) and ventral SCN (vSCN). In the SCN, both muscarinc and nictonic cholinergic receptors have been shown to be present and acetylcholine acts directly on SCN neurons. In this study, I used the cell-attached recording technique to investigate the effects of cholinergic agents on the SCN neurons, focusing on the time-dependent responses of both dSCN and vSCN neurons. I found that cholinergic agents altered the spontaneous firing rate (SFR) and the effects exhibited a circadian rhythm. Comparing the response profiles of muscarine (Musc) and nicotine (Nict) to that of carbachol (CCh) indicated that the carbachol responses were most likely mediated by the mAChR such as M1-mAChR on the dSCN neurons. The cholinergic responses of dSCN and vSCN neurons were in a similar way. However, the muscarinic responses of dSCN and vSCN neurons differed during the early night and during the low and high concentration. These data suggested that cholinergic effects on the neurons of the SCN might play an important role.

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Li, Meng-Jiyuan, and 李孟娟. "Cholinergic Modulation in A7 Noradrenergic Neurons in Rats." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/03942421735677930894.

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碩士
臺灣大學
動物學研究所
98
Acetylcholine (ACh) is one of principal neurotransmitters involved in pain modulation. Many behavioral studies have shown that central or peripheral ACh administrations can evoke analgesia, and have proved that cholinergic agonists can serve as a synergistic role of α2 adrenergic receptors-mediated antinociception in the spinal cord. Moreover, recent behavioral researches also indicate that there might be supraspinal interactions between muscarinic cholinergic system and noradrenergic (NAergic) pain descending pathway. Nevertheless, there is currently no direct evidence to support this argument. In this study, we investigated the effect of carbachol (CCh), a cholinergic agonist, on NAergic neurons of A7 catecholamine cell group, which projects NAergic fibers to the dorsal horn of the spinal cord to modulate nociceptive signaling. Whole-cell recordings were made from A7 neurons in voltage-clamp mode with membrane voltage clamped at -70 mV in brainstem slices taken from rat pups. Bath application of 25 μM CCh evoked inward currents, which were blocked by 1.5 μM atropine, a muscarinic acetylcholine receptor (mAChR) antagonist, suggesting that carbachol-induced currents (ICCh) were mediated through mAChR. Furthermore, ICCh were significantly attenuated with the existence of high concentration of himbacine, a dose-selective antagonist of mAChRs, showing that mAChRs on NAergic A7 neurons activated by CCh were M1-like mAChRs. Surprisingly, the ICCh were not blocked with internal administration of GDP-β-S, a non-catalytic analogue of GDP, suggesting that the ICCh were G-protein-independent. Bath application of U73122, a phospholipase C inhibitor, slightly but significantly blocked the ICCh, showing that phospholipase C was not the major participant in ICCh. The ICCh were reversed at about -12.6 mV and blocked by extracellular application of NMDG substituted for Na+, showing that ICCh were caused through opening a nonselective cation channel, presumably by transient receptor potential (TRP) channels. Indeed, ICCh were significantly attenuated by several antagonists of TRP channels, including 2APB, SKF96365 and ruthenium red. Besides, high frequency stimulation at pedunculopontine tegmental nucleus (PPTg) evoked an inward current partially blocked by atropine, suggesting PPTg projected their axons to NAergic A7 neurons. There was an auto-inhibition in PPTg-A7 synaptic transmission. These results indicate that mAChR modulate the NAergic A7 neurons via activating TRP channels without the requirement of G-protein and phospholipase C, and there is endogenous ACh released from PPTg onto NAergic A7 neurons. The above results provide an evidence of supraspinal interaction between muscarinic cholinergic system and NAergic descending pain pathway.

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Book chapters on the topic "Rat cholinergic neurones"

1

Sakamoto, Takashi, Masahiro Kurisaka, and Koreaki Mori. "Changes of Muscarinic Cholinergic Receptors and Cholinergic Neurons in Experimental Acute Hydrocephalic Rat Brains." In Annual Review of Hydrocephalus, 13–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-662-11155-0_9.

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Itakura, Toru, Hideyoshi Yokote, Norihiko Komai, and Mamoru Umemoto. "Autotransplantation of Parasympathetic Cholinergic Neurons into Alzheimer Model Rat Brain." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 765–68. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_156.

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Hefti, F., J. Hartikka, and B. Will. "Effects of Nerve Growth Factor on Cholinergic Neurons of the Rat Forebrain." In Brain Plasticity, Learning, and Memory, 495–504. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4684-5003-3_49.

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4

Varon, Silvio, Theo Hagg, H. Lee Vahlsing, and Marston Manthorpe. "Nerve Growth Factor in Vivo Actions on Cholinergic Neurons in the Adult Rat CNS." In Cell Function and Disease, 235–48. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0813-3_21.

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McRae, Amanda, Annelie Wigander, Kerstin Lundmark, Kaj Blennow, Carl-Gustav Gottfries, Ronald J. Polinski, and Annica Dahlström. "CSF of Patients with Alzheimer’s Disease Contain Antibodies Recognizing Cholinergic Cells in the Rat CNS, and can Protect Cholinergic Neuronal Cultures." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 31–36. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5847-3_8.

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Arimatsu, Yasuyoshi, and Mami Miyamoto. "Co-Localization of Cholinergic and GABAergic Traits in in Vitro Septohippocampal Neurons from Developing Rats." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 627–30. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_127.

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Hama, Tokiko, Mami Miyamoto, Kaori Noguchi, Nobuyuki Takei, Hiroko Tsukui, Chika Nishio, Yoichi Kushima, and Hiroshi Hatanaka. "Interleukin-6 as a Neurotrophic Factor for Promoting Survival of Septal Cholinergic Neurons and Mesencephalic Catecholaminergic Neurons from Postnatal Rats." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases, 637–40. Boston, MA: Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_129.

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Chang, Howard T., and Hui Kuo. "Calcium-Binding Protein (Calbindin D-28k) Immunoreactive Neurons in the Basal Forebrain of the Monkey and the Rat: Relationship with the Cholinergic Neurons." In Advances in Experimental Medicine and Biology, 119–26. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4757-0145-6_4.

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Hatanaka, Hiroshi, Nobuyuki Takei, and Hiroko Tsukui. "Nerve Growth Factor-Mediated Induction of Choline Acetyltransferase in Fetal and Neonatal Rat Septal Cholinergic Neurons in Organotypic Culture." In Neural Development and Regeneration, 651–52. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73148-8_61.

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Hefti, F., and B. H. Gähwiler. "Cholinergic Neurons of the Rat Forebrain in Slice Cultures; Interactions with Target Tissue and Effects of Nerve Growth Factor." In Neural Development and Regeneration, 81–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73148-8_8.

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