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Journal articles on the topic 'Rat cholinergic neurones'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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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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2

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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3

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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4

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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5

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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6

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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7

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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10

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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11

Yamaguchi, K., Y. Nakajima, S. Nakajima, and P. R. Stanfield. "Modulation of inwardly rectifying channels by substance P in cholinergic neurones from rat brain in culture." Journal of Physiology 426, no. 1 (July 1, 1990): 499–520. http://dx.doi.org/10.1113/jphysiol.1990.sp018151.

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12

Allen, T. G., J. A. Sim, and D. A. Brown. "The whole-cell calcium current in acutely dissociated magnocellular cholinergic basal forebrain neurones of the rat." Journal of Physiology 460, no. 1 (January 1, 1993): 91–116. http://dx.doi.org/10.1113/jphysiol.1993.sp019461.

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13

Pearson, R. C. A., J. W. Neal, and T. P. S. Powell. "Hypertrophy of cholinergic neurones of the basal nucleus in the rat following damage of the contralateral nucleus." Brain Research 382, no. 1 (September 1986): 149–52. http://dx.doi.org/10.1016/0006-8993(86)90123-x.

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14

Bolton, Renee F., James Cornwall, and Oliver T. Phillipson. "Collateral axons of cholinergic pontine neurones projecting to midline, mediodorsal and parafascicular thalamic nuclei in the rat." Journal of Chemical Neuroanatomy 6, no. 2 (March 1993): 101–14. http://dx.doi.org/10.1016/0891-0618(93)90031-x.

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15

Song, S. Y., K. Saito, K. Noguchi, and S. Konishi. "Adrenergic and cholinergic inhibition of Ca2+ channels mediated by different GTP-binding proteins in rat sympathetic neurones." Pfl�gers Archiv European Journal of Physiology 418, no. 6 (July 1991): 592–600. http://dx.doi.org/10.1007/bf00370576.

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16

Gronier, B., and K. Rasmussen. "Activation of midbrain presumed dopaminergic neurones by muscarinic cholinergic receptors: an in vivo electrophysiological study in the rat." British Journal of Pharmacology 124, no. 3 (June 1998): 455–64. http://dx.doi.org/10.1038/sj.bjp.0701850.

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17

Martínez‐Serrano, Alberto, Martin Olsson, Monte A. Gates, and Anders Björklund. "In utero gene transfer reveals survival effects of nerve growth factor on rat brain cholinergic neurones during development." European Journal of Neuroscience 10, no. 1 (January 1998): 263–71. http://dx.doi.org/10.1046/j.1460-9568.1998.00046.x.

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18

Bassil, Anna K., Narinder B. Dass, and Gareth J. Sanger. "The prokinetic-like activity of ghrelin in rat isolated stomach is mediated via cholinergic and tachykininergic motor neurones." European Journal of Pharmacology 544, no. 1-3 (August 2006): 146–52. http://dx.doi.org/10.1016/j.ejphar.2006.06.039.

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19

Lovick, T. A. "Tonic GABAergic and cholinergic influences on pain control and cardiovascular control neurones in nucleus paragigantocellularis lateralis in the rat." Pain 31, no. 3 (December 1987): 401–9. http://dx.doi.org/10.1016/0304-3959(87)90168-0.

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20

Krantis, A., and R. K. Harding. "Peptide YY induces nerve-mediated responses in the guinea pig intestine." Canadian Journal of Physiology and Pharmacology 69, no. 11 (November 1, 1991): 1713–18. http://dx.doi.org/10.1139/y91-254.

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The actions of peptide YY (PYY) were studied in longitudinal organ-bath preparations of the guinea pig intestine. PYY induced concentration-dependent (10−9 – 5 × 10−8 M) relaxations of tissue from the duodenum, jejunum, ileum, and colon. These responses were unaffected by adrenergic blockade and atropine treatment but could be prevented by tetrodotoxin. The pharmacology of PYY actions in segments of the small and large intestine indicated the involvement of intrinsic nonadrenergic, noncholinergic inhibitory neurones in the relaxation response to this peptide. All tissues could be made tachyphylactic to PYY without affecting their ability to respond to the direct acting muscle relaxants ATP or papaverine. Moreover, nicotinic ganglion stimulated relaxations and cholinergic nerve-mediated contractions were also unaffected. These results show applied PYY to have potent neurogenic actions in the guinea pig intestine with some similarities to PYY actions in the rat intestine.Key words: intestine, guinea pig, peptide YY, relaxations.

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21

Hösli, Elisabeth, and L. Hösli. "Cellular localization of estrogen receptors on neurones in various regions of cultured rat CNS: coexistence with cholinergic and galanin receptors." International Journal of Developmental Neuroscience 17, no. 4 (July 1999): 317–30. http://dx.doi.org/10.1016/s0736-5748(99)00038-6.

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22

Augood, S. J., G. W. Arbuthnott, and P. C. Emson. "Identified cholinergic neurones in the adult rat brain are enriched in GAP-43 mRNA: a double in situ hybridisation study." Journal of Chemical Neuroanatomy 9, no. 1 (July 1995): 17–26. http://dx.doi.org/10.1016/0891-0618(95)00059-g.

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23

Manier, Monique, Patrick Mouchet, and Claude Feuerstein. "Immunohistochemical evidence for the coexistence of cholinergic and catecholaminergic phenotypes in neurones of the vagal motor nucleus in the adult rat." Neuroscience Letters 80, no. 2 (September 1987): 141–46. http://dx.doi.org/10.1016/0304-3940(87)90643-4.

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24

Prud'homme, Marie-Jeanne, Eric Houdeau, Rachid Serghini, Yves Tillet, Michael Schemann, and Jean-Paul Rousseau. "Small intensely fluorescent cells of the rat paracervical ganglion synthesize adrenaline, receive afferent innervation from postganglionic cholinergic neurones, and contain muscarinic receptors." Brain Research 821, no. 1 (March 1999): 141–49. http://dx.doi.org/10.1016/s0006-8993(99)01094-x.

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25

Scheibler, Peter, Mihail Pesic, Heike Franke, Robert Reinhardt, Kerstin Wirkner, Peter Illes, and Wolfgang Nörenberg. "P2X2 and P2Y1 immunofluorescence in rat neostriatal medium-spiny projection neurones and cholinergic interneurones is not linked to respective purinergic receptor function." British Journal of Pharmacology 143, no. 1 (September 2004): 119–31. http://dx.doi.org/10.1038/sj.bjp.0705916.

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26

Moragues, N., P. Ciofi, G. Tramu, and M. Garret. "Localisation of GABAA receptor ϵ-subunit in cholinergic and aminergic neurones and evidence for co-distribution with the θ-subunit in rat brain." Neuroscience 111, no. 3 (May 2002): 657–69. http://dx.doi.org/10.1016/s0306-4522(02)00033-7.

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27

Atterwill, C. K., P. Collins, J. Meakin, A. M. Pillar, and A. K. Prince. "Effect of nerve growth factor and thyrotropin releasing hormone on cholinergic neurones in developing rat brain reaggregate cultures lesioned with ethylcholine mustard aziridinium." Biochemical Pharmacology 38, no. 10 (May 1989): 1631–38. http://dx.doi.org/10.1016/0006-2952(89)90311-0.

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28

Belai, A., and G. Burnstock. "Evidence for coexistence of ATP and nitric oxide in non-adrenergic, non-cholinergic (NANC) inhibitory neurones in the rat ileum, colon and anococcygeus muscle." Cell and Tissue Research 278, no. 1 (October 1994): 197–200. http://dx.doi.org/10.1007/bf00305792.

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29

Belai, A., and G. Burnstock. "Evidence for coexistence of ATP and nitric oxide in non-adrenergic, non-cholinergic (NANC) inhibitory neurones in the rat ileum, colon and anococcygeus muscle." Cell and Tissue Research 278, no. 1 (September 1, 1994): 197–200. http://dx.doi.org/10.1007/s004410050207.

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30

Liu, Xinhuai, Ion R. Popescu, Janna V. Denisova, Rachael L. Neve, Roderick A. Corriveau, and Andrei B. Belousov. "Regulation of Cholinergic Phenotype in Developing Neurons." Journal of Neurophysiology 99, no. 5 (May 2008): 2443–55. http://dx.doi.org/10.1152/jn.00762.2007.

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Specification of neurotransmitter phenotype is critical for neural circuit development and is influenced by intrinsic and extrinsic factors. Recent findings in rat hypothalamus in vitro suggest the role of neurotransmitter glutamate in the regulation of cholinergic phenotype. Here we extended our previous studies on the mechanisms of glutamate-dependent regulation of cholinergic phenotypic properties in hypothalamic neurons. Using immunocytochemistry, electrophysiology, and calcium imaging, we demonstrate that hypothalamic expression of choline acetyltransferase (the cholinergic marker) and responsiveness of neurons to acetylcholine (ACh) receptor agonists increase during chronic administration of an N-methyl-d-aspartate receptor (NMDAR) blocker, MK-801, in developing rats in vivo and genetic and pharmacological inactivation of NMDARs in mouse and rat developing neuronal cultures. In hypothalamic cultures, an inactivation of NMDA receptors also induces ACh-dependent synaptic activity, as do inactivations of PKA, ERK/MAPK, CREB, and NF-κB, which are known to be regulated by NMDA receptors. Interestingly, the increase in cholinergic properties in developing neurons that is induced by NMDAR blockade is prevented by the blockade of ACh receptors, suggesting that function of ACh receptor is required for the cholinergic up-regulation. Using dual recording of monosynaptic excitatory postsynaptic currents, we further demonstrate that chronic inactivation of ionotropic glutamate receptors induces the cholinergic phenotype in a subset of glutamatergic neurons. The phenotypic switch is partial as ACh and glutamate are coreleased. The results suggest that developing neurons may not only coexpress multiple transmitter phenotypes, but can also change the phenotypes following changes in signaling in neuronal circuits.

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31

Murchison, David, Angelika N. McDermott, Candi L. LaSarge, Kathryn A. Peebles, Jennifer L. Bizon, and William H. Griffith. "Enhanced Calcium Buffering in F344 Rat Cholinergic Basal Forebrain Neurons Is Associated With Age-Related Cognitive Impairment." Journal of Neurophysiology 102, no. 4 (October 2009): 2194–207. http://dx.doi.org/10.1152/jn.00301.2009.

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Alterations in neuronal Ca2+ homeostasis are important determinants of age-related cognitive impairment. We examined the Ca2+ influx, buffering, and electrophysiology of basal forebrain neurons in adult, middle-aged, and aged male F344 behaviorally assessed rats. Middle-aged and aged rats were characterized as cognitively impaired or unimpaired by water maze performance relative to young cohorts. Patch-clamp experiments were conducted on neurons acutely dissociated from medial septum/nucleus of the diagonal band with post hoc identification of phenotypic marker mRNA using single-cell RT-PCR. We measured whole cell calcium and barium currents and dissected these currents using pharmacological agents. We combined Ca2+ current recording with Ca2+-sensitive ratiometric microfluorimetry to measure Ca2+ buffering. Additionally, we sought changes in neuronal firing properties using current-clamp recording. There were no age- or cognition-related changes in the amplitudes or fractional compositions of the whole cell Ca2+ channel currents. However, Ca2+ buffering was significantly enhanced in cholinergic neurons from aged cognitively impaired rats. Moreover, increased Ca2+ buffering was present in middle-aged rats that were not cognitively impaired. Firing properties were largely unchanged with age or cognitive status, except for an increase in the slow afterhyperpolarization in aged cholinergic neurons, independent of cognitive status. Furthermore, acutely dissociated basal forebrain neurons in which choline acetyltransferase mRNA was detected had the electrophysiological profiles of identified cholinergic neurons. We conclude that enhanced Ca2+ buffering by cholinergic basal forebrain neurons may be important during aging.

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32

Corsetti, Veronica, Carla Perrone-Capano, Michael Sebastian Salazar Intriago, Elisabetta Botticelli, Giancarlo Poiana, Gabriella Augusti-Tocco, Stefano Biagioni, and Ada Maria Tata. "Expression of Cholinergic Markers and Characterization of Splice Variants during Ontogenesis of Rat Dorsal Root Ganglia Neurons." International Journal of Molecular Sciences 22, no. 11 (May 23, 2021): 5499. http://dx.doi.org/10.3390/ijms22115499.

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Dorsal root ganglia (DRG) neurons synthesize acetylcholine (ACh), in addition to their peptidergic nature. They also release ACh and are cholinoceptive, as they express cholinergic receptors. During gangliogenesis, ACh plays an important role in neuronal differentiation, modulating neuritic outgrowth and neurospecific gene expression. Starting from these data, we studied the expression of choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) expression in rat DRG neurons. ChAT and VAChT genes are arranged in a “cholinergic locus”, and several splice variants have been described. Using selective primers, we characterized splice variants of these cholinergic markers, demonstrating that rat DRGs express R1, R2, M, and N variants for ChAT and V1, V2, R1, and R2 splice variants for VAChT. Moreover, by RT-PCR analysis, we observed a progressive decrease in ChAT and VAChT transcripts from the late embryonic developmental stage (E18) to postnatal P2 and P15 and in the adult DRG. Interestingly, Western blot analyses and activity assays demonstrated that ChAT levels significantly increased during DRG ontogenesis. The modulated expression of different ChAT and VAChT splice variants during development suggests a possible differential regulation of cholinergic marker expression in sensory neurons and confirms multiple roles for ACh in DRG neurons, both in the embryo stage and postnatally.

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33

Rohrer, H. "Cholinergic neuronal differentiation factors: evidence for the presence of both CNTF-like and non-CNTF-like factors in developing rat footpad." Development 114, no. 3 (March 1, 1992): 689–98. http://dx.doi.org/10.1242/dev.114.3.689.

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Catecholaminergic sympathetic neurons are able to change their transmitter phenotype during development and to acquire cholinergic properties. Cholinergic sympathetic differentiation is only observed in fibers innervating specific targets like the sweat glands in the rat footpad. A function for ciliary neurotrophic factor (CNTF) in this process has been implied as it is able to induce cholinergic properties (ChAT, VIP) in cultured chick and rat neurons. We show here that a CNTF-like, VIP-inducing activity is present in rat footpads and that its increases 6-fold during the period of cholinergic sympathetic differentiation. Immunohistochemical analysis of P21 rat footpads demonstrated CNTF-like immunoreactivity in Schwann cells but not in sweat glands, the target tissue of cholinergic sympathetic neurons. The expression of this factor in footpads seems to be dependent on the presence of intact nerve axons, as nerve transection results in a loss of CNTF-like cholinergic activity and immunoreactivity. Immunoprecipitation experiments with rat footpad extracts provided evidence for the presence of ChAT-inducing factors other than CNTF, which may independently or together with CNTF be involved in the determination of sympathetic neuron phenotype.

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34

Yan, Jing, Wenhui Zhao, Meixia Guo, Xuefei Han, and Zhiwei Feng. "CXCL12 Regulates the Cholinergic Locus and CHT1 Through Akt Signaling Pathway." Cellular Physiology and Biochemistry 40, no. 5 (2016): 982–92. http://dx.doi.org/10.1159/000453155.

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Background: CXCL12 is pivotal for cholinergic neurons, and it induces the expressions of several genes that are essential for synthesis and storage of acetylcholine(ACh), specifically choline acetyltransferase, vesicular ACh transporter (VAChT), and choline transporter. The present study explored the impact of pharmacological Akt inhibition upon cholinergic gene expression. Methods: Western blotting was employed to determine the level of p-AKT, RT-PCR to check the mRNA levels of and CHT1(choline transporter1),VAChT and ChAT, ELISA to decipher the secretion of ACh and the activity of choline acetyltransferase. Results: Here we demonstrated, in the rat pheochromocytoma cell line PC12 and in primary rat neuronal cultures, that CXCL12-evoked up-regulation of CHT1, VAChT and ChAT was mediated by Akt. Inhibition of Akt by the pharmacological inhibitor GSK690693 eliminated CXCL12-stimulated increases in cholinergic gene expression. Moreover, treatment with GSK690693 reversed CXCL12-evoked increases in choline acetyltransferase activity and ACh production. Conclusion: Our results suggest that CXCL12 contributes to cholinergic gene expression via Akt signaling pathway.

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35

Feldstein, J. B., R. A. Gonzales, S. P. Baker, C. Sumners, F. T. Crews, and M. K. Raizada. "Decreased alpha 1-adrenergic receptor-mediated inositide hydrolysis in neurons from hypertensive rat brain." American Journal of Physiology-Cell Physiology 251, no. 2 (August 1, 1986): C230—C237. http://dx.doi.org/10.1152/ajpcell.1986.251.2.c230.

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The expression of alpha 1-adrenergic receptors and norepinephrine (NE)-stimulated hydrolysis of inositol phospholipid has been studied in neuronal cultures from the brains of normotensive (Wistar-Kyoto, WKY) and spontaneously hypertensive (SH) rats. Binding of 125I-2-[beta-(4-hydroxyphenyl)-ethyl-aminomethyl] tetralone (HEAT) to neuronal membranes was 68-85% specific and was rapid. Competition-inhibition experiments with various agonists and antagonists suggested that 125I-HEAT bound selectively to alpha 1-adrenergic receptors. Specific binding of 125I-HEAT to neuronal membranes from SH rat brain cultures was 30-45% higher compared with binding in WKY normotensive controls. This increase was attributed to an increase in the number of alpha 1-adrenergic receptors on SH rat brain neurons. Incubation of neuronal cultures of rat brain from both strains with NE resulted in a concentration-dependent stimulation of release of inositol phosphates, although neurons from SH rat brains were 40% less responsive compared with WKY controls. The decrease in responsiveness of SH rat brain neurons to NE, even though the alpha 1-adrenergic receptors are increased, does not appear to be due to a general defect in membrane receptors and postreceptor signal transduction mechanisms. This is because neither the number of muscarinic-cholinergic receptors nor the carbachol-stimulated release of inositol phosphates is different in neuronal cultures from the brains of SH rats compared with neuronal cultures from the brains of WKY rats. These observations suggest that the increased expression of alpha 1-adrenergic receptors does not parallel the receptor-mediated inositol phosphate hydrolysis in neuronal cultures from SH rat brain.

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36

Schirmer, S. U., I. Eckhardt, H. Lau, J. Klein, Y. C. DeGraaf, K. S. Lips, C. Pineau, et al. "The cholinergic system in rat testis is of non-neuronal origin." REPRODUCTION 142, no. 1 (July 2011): 157–66. http://dx.doi.org/10.1530/rep-10-0302.

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The cholinergic system consists of acetylcholine (ACh), its synthesising enzyme, choline acetyltransferase (CHAT), transporters such as the high-affinity choline transporter (SLC5A7; also known as ChT1), vesicular ACh transporter (SLC18A3; also known as VAChT), organic cation transporters (SLC22s; also known as OCTs), the nicotinic ACh receptors (CHRN; also known as nAChR) and muscarinic ACh receptors. The cholinergic system is not restricted to neurons but plays an important role in the structure and function of non-neuronal tissues such as epithelia and the immune system. Using molecular and immunohistochemical techniques, we show in this study that non-neuronal cells in the parenchyma of rat testis express mRNAs forChat,Slc18a3,Slc5a7andSlc22a2as well as for the CHRN subunits in locations completely lacking any form of innervation, as demonstrated by the absence of protein gene product 9.5 labelling. We found differentially expressed mRNAs for eight α and three β subunits of CHRN in testis. Expression of the α7-subunit of CHRN was widespread in spermatogonia, spermatocytes within seminiferous tubules as well as within Sertoli cells. Spermatogonia and spermatocytes also expressed the α4-subunit of CHRN. The presence of ACh in testicular parenchyma (TP), capsule and isolated germ cells could be demonstrated by HPLC. Taken together, our results reveal the presence of a non-neuronal cholinergic system in rat TP suggesting a potentially important role for non-neuronal ACh and its receptors in germ cell differentiation.

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Kamondi, A., J. A. Williams, B. Hutcheon, and P. B. Reiner. "Membrane properties of mesopontine cholinergic neurons studied with the whole-cell patch-clamp technique: implications for behavioral state control." Journal of Neurophysiology 68, no. 4 (October 1, 1992): 1359–72. http://dx.doi.org/10.1152/jn.1992.68.4.1359.

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1. The whole-cell patch-clamp technique was used to study the membrane properties of identified cholinergic and noncholinergic laterodorsal tegmental neurons in slices of rat brain maintained in vitro. 2. On the basis of their expression of the transient outward potassium current IA and the transient inward calcium current IT, three classes of neurons were observed: type I neurons exhibited a large IT; type II neurons exhibited a prominent IA; and type III neurons exhibited both IA and IT. 3. Combining intracellular deposition of biocytin with NADPH diaphorase histochemistry revealed that the vast majority of type III neurons were cholinergic, whereas only a minority of type I and type II neurons were cholinergic. Thus mesopontine cholinergic neurons possess intrinsic ionic currents capable of inducing burst firing. 4. Delineation of the intrinsic membrane properties of identified mesopontine cholinergic neurons, in concert with recent results regarding the responses of these neurons to neurotransmitter agents, has led us to present a unifying and mechanistic hypothesis of brain stem cholinergic function in the control of behavioral states.

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Dorn, Roland, Bernhard Loy, Georg Dechant, and Galina Apostolova. "Neurogenomics of the Sympathetic Neurotransmitter Switch Indicates That Different Mechanisms Steer Cholinergic Differentiation in Rat and Chicken Models." Dataset Papers in Neuroscience 2013 (September 26, 2013): 1–9. http://dx.doi.org/10.7167/2013/520930.

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Vertebrate sympathetic neurons have the remarkable potential to switch their neurotransmitter phenotype from noradrenergic to cholinergic—a phenomenon that has been intensively studied in rat and chicken models. In both species, loss of noradrenergic markers and concomitant upregulation of cholinergic markers occurs in response to neuropoietic cytokines such as ciliary neurotrophic factor (CNTF). However, other aspects of the neurotransmitter switch including developmental timing, target tissues of cholinergic neurons, and dependence on neurotrophic factors differ between the two species. Here we compare CNTF-triggered transcriptome changes in both species by using DNA microarrays. CNTF induced changes in 1130 out of 16084 analyzed genomic loci in rat sympathetic neurons. When this set of genes was compared to CNTF-induced changes in the chicken transcriptome, a surprisingly small overlap was found—only 94 genes were regulated in the same direction in chicken and rat. The differential responses of the transcriptome to neuropoietic cytokines provide additional evidence that the cholinergic switch, although conserved during vertebrate evolution, is a heterogeneous phenomenon and may result from differential cellular mechanisms.

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Grider, J. R., and G. M. Makhlouf. "Colonic peristaltic reflex: identification of vasoactive intestinal peptide as mediator of descending relaxation." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 1 (July 1, 1986): G40—G45. http://dx.doi.org/10.1152/ajpgi.1986.251.1.g40.

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Isolated segments of rat and guinea pig midcolon were used to examine the neurotransmitters responsible for ascending contraction and descending relaxation components of the peristaltic reflex. Graded radial stretch of the extreme orad end caused only descending relaxation accompanied by significant release of vasoactive intestinal peptide (VIP) in rat (82%, P less than 0.005) and guinea pig (47%, P less than 0.05). Radial stretch of the caudad end caused only ascending contraction without VIP release. VIP antiserum (1:480 to 1:60) inhibited descending relaxation in a concentration-dependent manner at all grades of stretch (40 +/- 12% to 74 +/- 15%) but augmented ascending contraction (25 +/- 7% to 108 +/- 21%). Axonal blockade with tetrodotoxin and ganglionic blockade with hexamethonium abolished both components, indicating the participation of cholinergic neurons. Atropine and the tachykinin antagonist [D-Pro2,D-Trp7,9]substance P inhibited ascending contraction but not descending relaxation; their combination abolished ascending contraction at all grades of stretch. We conclude that cholinergic neurons coupled to VIP motor neurons regulate descending relaxation and that cholinergic neurons coupled to tachykinin and cholinergic motor neurons regulate ascending contraction.

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Rao, M. S., P. H. Patterson, and S. C. Landis. "Multiple cholinergic differentiation factors are present in footpad extracts: comparison with known cholinergic factors." Development 116, no. 3 (November 1, 1992): 731–44. http://dx.doi.org/10.1242/dev.116.3.731.

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Sweat glands in rat footpads contain a neuronal differentiation activity that switches the phenotype of sympathetic neurons from noradrenergic to cholinergic during normal development in vivo. Extracts of developing and adult sweat glands induce changes in neurotransmitter properties in cultured sympathetic neurons that mimic those observed in vivo. We have characterized further the factors present in the extract and compared their properties to those of known cholinergic factors. When assayed on cultured rat sympathetic neurons, the major activities in footpad extracts from postnatal day 21 rat pups that induce choline acetyltransferase (ChAT) and vasoactive intestinal peptide (VIP) and reduce catecholamines and neuropeptide Y (NPY) are associated with a soluble protein of 22–26 × 10(3) M(r) and a pI of 5.0. These properties are similar to those of ciliary neurotrophic factor (CNTF). Moreover, the purified fraction from footpads has ciliary neurotrophic activity. Antibodies to CNTF that immunoprecipitate all differentiation activity from sciatic nerve extracts, a rich source of CNTF, immunoprecipitate 80% of the cholinergic activity in the footpad extracts, 50% of the VIP and 20% of the NPY activities. Neither CNTF protein nor CNTF mRNA, however, can be detected in immunoblot and northern analysis of footpads even though both CNTF protein and mRNA are evident in sciatic nerve. CNTF-immunoreactivity is associated with a sparse plexus of sensory fibers in the footpad but not with sweat glands or the Schwann cells associated with them. In addition, in situ hybridization studies with oligonucleotide probes failed to reveal CNTF mRNA in sweat glands. Comparison of the sweat gland differentiation activity with the cholinergic differentiation factor from heart cells (CDF; also known as leukemia inhibitory factor or LIF) suggests that most of the cholinergic activity in foot pads is biochemically distinct from CDF/LIF. Further, antibodies that block the activity of CDF/LIF purified from heart-cell-conditioned medium do not block the ChAT-inducing activity present in footpad extracts of postnatal day 8 animals. A differentiation factor isolated from skeletal muscle did not induce cholinergic properties in sympathetic neuron cultures and therefore is unlikely to be the cholinergic differentiation factor produced by sweat glands. Taken together, our data suggest that there are at least two differentiation molecules present in the extracts and that the major cholinergic activity obtained from footpads is related to, but distinct from, CNTF. The second factor remains to be characterized. In addition, CNTF associated with sensory fibers may make a minor contribution to the cholinergic inducing activity present in the extract.

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Jhamandas, Jack H., Caroline Cho, Balvinder Jassar, Kim Harris, David MacTavish, and Jacob Easaw. "Cellular Mechanisms for Amyloid β-Protein Activation of Rat Cholinergic Basal Forebrain Neurons." Journal of Neurophysiology 86, no. 3 (September 1, 2001): 1312–20. http://dx.doi.org/10.1152/jn.2001.86.3.1312.

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The deposition of amyloid β-protein (Aβ) in the brain and the loss of cholinergic neurons in the basal forebrain are two pathological hallmarks of Alzheimer's disease (AD). Although the mechanism of Aβ neurotoxicity is unknown, these cholinergic neurons display a selective vulnerability when exposed to this peptide. In this study, application of Aβ25–35 or Aβ1–40 to acutely dissociated rat neurons from the basal forebrain nucleus diagonal band of Broca (DBB), caused a decrease in whole cell voltage-activated currents in a majority of cells. This reduction in whole cell currents occurs through a modulation of a suite of potassium conductances including calcium-activated potassium ( I C), the delayed rectifier ( I K), and transient outward potassium ( I A) conductances, but not calcium or sodium currents. Under current-clamp conditions, Aβ evoked an increase in excitability and a loss of accommodation in cholinergic DBB neurons. Using single-cell RT-PCR technique, we determined that Aβ actions were specific to cholinergic, but not GABAergic DBB neurons. Aβ effects on whole cell currents were occluded in the presence of membrane-permeable protein tyrosine kinase inhibitors, genistein and tyrphostin B-44. Our data indicate that the Aβ actions on specific potassium conductances are modulated through a protein tyrosine kinase pathway and that these effects are selective to cholinergic but not GABAergic cells. These observations provide a cellular basis for the selectivity of Aβ neurotoxicity toward cholinergic basal forebrain neurons that are at the epicenter of AD pathology.

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Griffith, William H., Dustin W. DuBois, Annette Fincher, Kathryn A. Peebles, Jennifer L. Bizon, and David Murchison. "Characterization of age-related changes in synaptic transmission onto F344 rat basal forebrain cholinergic neurons using a reduced synaptic preparation." Journal of Neurophysiology 111, no. 2 (January 15, 2014): 273–86. http://dx.doi.org/10.1152/jn.00129.2013.

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Basal forebrain (BF) cholinergic neurons participate in a number of cognitive processes that become impaired during aging. We previously found that age-related enhancement of Ca2+ buffering in rat cholinergic BF neurons was associated with impaired performance in the water maze spatial learning task (Murchison D, McDermott AN, Lasarge CL, Peebles KA, Bizon JL, and Griffith WH. J Neurophysiol 102: 2194–2207, 2009). One way that altered Ca2+ buffering could contribute to cognitive impairment involves synaptic function. In this report we show that synaptic transmission in the BF is altered with age and cognitive status. We have examined the properties of spontaneous postsynaptic currents (sPSCs) in cholinergic BF neurons that have been mechanically dissociated without enzymes from behaviorally characterized F344 rats. These isolated neurons retain functional presynaptic terminals on their somata and proximal dendrites. Using whole cell patch-clamp recording, we show that sPSCs and miniature PSCs are predominately GABAergic (bicuculline sensitive) and in all ways closely resemble PSCs recorded in a BF in vitro slice preparation. Adult (4–7 mo) and aged (22–24 mo) male rats were cognitively assessed using the water maze. Neuronal phenotype was identified post hoc using single-cell RT-PCR. The frequency of sPSCs was reduced during aging, and this was most pronounced in cognitively impaired subjects. This is the same population that demonstrated increased intracellular Ca2+ buffering. We also show that increasing Ca2+ buffering in the synaptic terminals of young BF neurons can mimic the reduced frequency of sPSCs observed in aged BF neurons.

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Hill, Elisa L., Thierry Gallopin, Isabelle Férézou, Bruno Cauli, Jean Rossier, Paul Schweitzer, and Bertrand Lambolez. "Functional CB1 Receptors Are Broadly Expressed in Neocortical GABAergic and Glutamatergic Neurons." Journal of Neurophysiology 97, no. 4 (April 2007): 2580–89. http://dx.doi.org/10.1152/jn.00603.2006.

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The cannabinoid receptor CB1 is found in abundance in brain neurons, whereas CB2 is essentially expressed outside the brain. In the neocortex, CB1 is observed predominantly on large cholecystokinin (CCK)-expressing interneurons. However, physiological evidence suggests that functional CB1 are present on other neocortical neuronal types. We investigated the expression of CB1 and CB2 in identified neurons of rat neocortical slices using single-cell RT-PCR. We found that 63% of somatostatin (SST)-expressing and 69% of vasoactive intestinal polypeptide (VIP)-expressing interneurons co-expressed CB1. As much as 49% of pyramidal neurons expressed CB1. In contrast, CB2 was observed in a small proportion of neocortical neurons. We performed whole cell recordings of pyramidal neurons to corroborate our molecular findings. Inhibitory postsynaptic currents (IPSCs) induced by a mixed muscarinic/nicotinic cholinergic agonist showed depolarization-induced suppression of inhibition and were decreased by the CB1 agonist WIN-55212-2 (WIN-2), suggesting that interneurons excited by cholinergic agonists (mainly SST and VIP neurons) possess CB1. IPSCs elicited by a nicotinic receptor agonist were also reduced in the presence of WIN-2, suggesting that neurons excited by nicotinic agonists (mainly VIP neurons) indeed possess CB1. WIN-2 largely decreased excitatory postsynaptic currents evoked by intracortical electrical stimulation, pointing at the presence of CB1 on glutamatergic pyramidal neurons. All WIN-2 effects were strongly reduced by the CB1 antagonist AM 251. We conclude that CB1 is expressed in various neocortical neuronal populations, including glutamatergic neurons. Our combined molecular and physiological data suggest that CB1 widely mediates endocannabinoid effects on glutamatergic and GABAergic transmission to modulate cortical networks.

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Momiyama, Toshihiko, and Laszlo Zaborszky. "Somatostatin Presynaptically Inhibits Both GABA and Glutamate Release Onto Rat Basal Forebrain Cholinergic Neurons." Journal of Neurophysiology 96, no. 2 (August 2006): 686–94. http://dx.doi.org/10.1152/jn.00507.2005.

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A whole cell patch-clamp study was carried out in slices obtained from young rat brain to elucidate the roles of somatostatin in the modulation of synaptic transmission onto cholinergic neurons in the basal forebrain (BF), a region that contains cholinergic and GABAergic corticopetal neurons and somatostatin (SS)-containing local circuit neurons. Cholinergic neurons within the BF were identified by in vivo prelabeling with Cy3 IgG. Because in many cases SS is contained in GABAergic neurons in the CNS, we investigated whether exogenously applied SS can influence GABAergic transmission onto cholinergic neurons. Bath application of somatostatin (1 μM) reduced the amplitude of the evoked GABAergic inhibitory presynaptic currents (IPSCs) in cholinergic neurons. SS also reduced the frequency of miniature IPSCs (mIPSCs) without affecting their amplitude distribution. SS-induced effect on the mIPSC frequency was significantly larger in the solution containing 7.2 mM Ca2+ than in the standard (2.4 mM Ca2+) external solution. Similar effects were observed in the case of non-NMDA glutamatergic excitatory postsynaptic currents (EPSCs). SS inhibited the amplitude of evoked EPSCs and reduced the frequency of miniature EPSCs dependent on the external Ca2+ concentration with no effect on their amplitude distribution. Pharmacological analyses using SS-receptor subtype–specific drugs suggest that SS-induced action of the IPSCs is mediated mostly by the sst2 subtype, whereas sst subtypes mediating SS-induced inhibition of EPSCs are mainly sst1 or sst4. These findings suggest that SS presynaptically inhibits both GABA and glutamate release onto BF cholinergic neurons in a Ca2+-dependent way, and that SS-induced effect on IPSCs and EPSCs are mediated by different sst subtypes.

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Sander, Guy R., Simon J. H. Brookes, and Barry C. Powell. "Expression of Notch1 and Jagged2 in the Enteric Nervous System." Journal of Histochemistry & Cytochemistry 51, no. 7 (July 2003): 969–72. http://dx.doi.org/10.1177/002215540305100712.

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The Notch signaling pathway is a vitally important pathway in regulating brain development. To explore the involvement of the Notch pathway in neuronal cells of adult rat gut, we investigated the expression of Notch1 and Jagged2 by in situ hybridization (ISH) and immunohistochemistry (IHC). In the enteric nervous system, Notch1 and Jagged2 were expressed in ganglia of the submucosal and myenteric plexus. Notch1 was preferentially expressed in cholinergic neurons lacking calretinin or nitric oxide synthase (NOS), whereas Jagged2 was present in most neuron subtypes. We propose that Notch1 and Jagged2 have a continuing role in the maintenance and function of neuronal cells in the adult enteric nervous system.

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Serbinek, Daniela, Celine Ullrich, Michael Pirchl, Tanja Hochstrasser, Rainald Schmidt-Kastner, and Christian Humpel. "S100b Counteracts Neurodegeneration of Rat Cholinergic Neurons in Brain Slices after Oxygen-Glucose Deprivation." Cardiovascular Psychiatry and Neurology 2010 (May 24, 2010): 1–7. http://dx.doi.org/10.1155/2010/106123.

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Alzheimer's disease is a severe chronic neurodegenerative disorder characterized by beta-amyloid plaques, tau pathology, cerebrovascular damage, inflammation, reactive gliosis, and cell death of cholinergic neurons. The aim of the present study is to test whether the glia-derived molecule S100b can counteract neurodegeneration of cholinergic neurons after oxygen-glucose deprivation (OGD) in organotypic brain slices of basal nucleus of Meynert. Our data showed that 3 days of OGD induced a marked decrease of cholinergic neurons (60% of control), which could be counteracted by 50 μg/mL recombinant S100b. The effect was dose and time dependent. Application of nerve growth factor or fibroblast growth factor-2 was less protective. C-fos-like immunoreactivity was enhanced 3 hours after OGD indicating metabolic stress. We conclude that S100b is a potent neuroprotective factor for cholinergic neurons during ischemic events.

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Ichimiya, Toshifumi, Shinichi Kohsaka, and Kazuyuki Nakajima. "Cholinergic neurons in rat facial nucleus." Neuroscience Research 68 (January 2010): e225. http://dx.doi.org/10.1016/j.neures.2010.07.992.

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Chiocchetti, R., T. Hitrec, F. Giancola, J. Sadeghinezhad, F. Squarcio, G. Galiazzo, E. Piscitiello, et al. "Phosphorylated Tau protein in the myenteric plexus of the ileum and colon of normothermic rats and during synthetic torpor." Cell and Tissue Research 384, no. 2 (January 29, 2021): 287–99. http://dx.doi.org/10.1007/s00441-020-03328-0.

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AbstractTau protein is of primary importance for neuronal homeostasis and when hyperphosphorylated (PP-Tau), it tends to aggregate in neurofibrillary tangles, as is the case with tauopathies, a class of neurodegenerative disorders. Reversible PP-Tau accumulation occurs in the brain of hibernating rodents and it was recently observed in rats (a non-hibernator) during synthetic torpor (ST), a pharmacological-induced torpor-like condition. To date, the expression of PP-Tau in the rat enteric nervous system (ENS) is still unknown. The present study immunohistochemically investigates the PP-Tau expression in the myenteric plexus of the ileum and colon of normothermic rats (CTRL) and during ST, focusing on the two major subclasses of enteric neurons, i.e., cholinergic and nitrergic.Results showed that both groups of rats expressed PP-Tau, with a significantly increased percentage of PP-Tau immunoreactive (IR) neurons in ST vs. CTRL. In all rats, the majority of PP-Tau-IR neurons were cholinergic. In ST rats, the percentage of PP-Tau-IR neurons expressing a nitrergic phenotype increased, although with no significant differences between groups. In addition, the ileum of ST rats showed a significant decrease in the percentage of nitrergic neurons. In conclusion, our findings suggest an adaptive response of ENS to very low core body temperatures, with changes involving PP-tau expression in enteric neurons, especially the ileal nitrergic subpopulation. In addition, the high presence of PP-Tau in cholinergic neurons, specifically, is very interesting and deserves further investigation. Altogether, these data strengthen the hypothesis of a common cellular mechanism triggered by ST, natural hibernation and tauopathies occurring in ENS neurons.

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Apartis, Emmanuelle, Frederique R. Poindessous-Jazat, Yvon A. Lamour, and Marie H. Bassant. "Loss of Rhythmically Bursting Neurons in Rat Medial Septum Following Selective Lesion of Septohippocampal Cholinergic System." Journal of Neurophysiology 79, no. 4 (April 1, 1998): 1633–42. http://dx.doi.org/10.1152/jn.1998.79.4.1633.

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Apartis, Emmanuelle, Frederique R. Poindessous-Jazat, Yvon A. Lamour, and Marie H. Bassant. Loss of rhythmically bursting neurons in rat medial septum following selective lesion of septohippocampal cholinergic system. J. Neurophysiol. 79: 1633–1642, 1998. The medial septum contains cholinergic and GABAergic neurons that project to the hippocampal formation. A significant proportion of the septohippocampal neurons (SHN) exhibit a rhythmically bursting (RB) activity that is involved in the generation of the hippocampal theta rhythm. The neurochemical nature of septal RB neurons is not firmly established. To address this question, the septal unit activity has been recorded in rats after selective destruction of the cholinergic septal neurons by the immunotoxin 192 IgG-saporin. Experiments have been performed in urethan-anesthetized and unanesthetized rats, 14–21 days after lesion. Acetylcholinesterase (AChE) histochemistry revealed a near-complete loss of cholinergic septal neurons and of cholinergic fibers in the hippocampus. The recorded neurons were located in the medial septum-diagonal band of Broca area. A number of these neurons were identified as projecting to the hippocampus (SHN) by their antidromic response to the electrical stimulation of the fimbria-fornix. In urethan-anesthetized lesioned rats, the percentage of RB neurons decreased significantly as compared with controls (17 vs. 41% for SHNs and 5 vs. 19% for unidentified septal neurons). The axonal conduction velocity and the burst frequency of the SHNs that retained a RB activity were higher in lesioned as compared with control rats. The number of spikes per burst was lower and the burst duration was shorter in lesioned rats as compared with controls. The urethan-resistant hippocampal theta was altered both in terms of frequency and amplitude. In unanesthetized lesioned rats, no RB septal neurons were found during arousal, as compared with 25% in controls. Their number was also markedly reduced during paradoxical sleep (9.7 vs. 38.5%). Histochemistry in 192 IgG-saporin–treated rats showed that RB neurons were found in areas devoid of AChE-positive neurons but containing parvalbumine-positive (presumably GABAergic) neurons. These data show that RB activity is considerably reduced after selective lesion of the cholinergic medial septal neurons. They suggested that the large majority of the RB septal neurons are cholinergic and that the few neurons that display RB activity in lesioned rats are GABAergic.

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Takazawa, Tomonori, Yasuhiko Saito, Keisuke Tsuzuki, and Seiji Ozawa. "Membrane and Firing Properties of Glutamatergic and GABAergic Neurons in the Rat Medial Vestibular Nucleus." Journal of Neurophysiology 92, no. 5 (November 2004): 3106–20. http://dx.doi.org/10.1152/jn.00494.2004.

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In previous studies, neurons in the medial vestibular nucleus (MVN) were classified mainly into 2 types according to their intrinsic membrane properties in in vitro slice preparations. However, it has not been determined whether the classified neurons are excitatory or inhibitory ones. In the present study, to clarify the relationship between the chemical and electrophysiological properties of MVN neurons, we explored mRNAs of cellular markers for GABAergic (glutamic acid decarboxylase 65, 67, and neuronal GABA transporter), glutamatergic (vesicular glutamate transporter 1 and 2), glycinergic (glycine transporter 2), and cholinergic neurons (choline acetyltransferase and vesicular acetylcholine transporter) expressed in electrophysiologically characterized MVN neurons in rat brain stem slice preparations. For this purpose, we combined whole cell patch-clamp recording analysis with single-cell reverse transcription–polymerase chain reaction (RT-PCR) analysis. We examined the membrane properties such as afterhyperpolarization (AHP), firing pattern, and response to hyperpolarizing current pulse to classify MVN neurons. From the single-cell RT-PCR analysis, we found that GABAergic neurons consisted of heterogeneous populations with different membrane properties. Comparison of the membrane properties of GABAergic neurons with those of other neurons revealed that AHPs without slow components and a firing pattern with delayed spike generation (late spiking) were preferential properties of GABAergic neurons. On the other hand, most glutamatergic neurons formed a homogeneous subclass of neurons exhibiting AHPs with slow components, repetitive firings with constant interspike intervals (continuous spiking), and time-dependent inward rectification in response to hyperpolarizing current pulses. We also found a small number of cholinergic neurons with various membrane properties. These findings clarify the electrophysiological properties of excitatory and inhibitory neurons in the MVN, and the information about the preferential membrane properties may be useful for identifying GABAergic and glutamatergic MVN neurons electrophysiologically.

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