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Relevant bibliographies by topics / Rat locomotion/brain receptors

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Academic literature on the topic 'Rat locomotion/brain receptors'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "Rat locomotion/brain receptors"

1

Liu, Jun, and Larry M. Jordan. "Stimulation of the Parapyramidal Region of the Neonatal Rat Brain Stem Produces Locomotor-Like Activity Involving Spinal 5-HT7 and 5-HT2A Receptors." Journal of Neurophysiology 94, no. 2 (2005): 1392–404. http://dx.doi.org/10.1152/jn.00136.2005.

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Locomotion can be induced in rodents by direct application 5-hydroxytryptamine (5-HT) onto the spinal cord. Previous studies suggest important roles for 5-HT7 and 5-HT2A receptors in the locomotor effects of 5-HT. Here we show for the first time that activation of a discrete population of 5-HT neurons in the rodent brain stem produces locomotion and that the evoked locomotion requires 5-HT7 and 5-HT2A receptors. Cells localized in the parapyramidal region (PPR) of the mid-medulla produced locomotor-like activity as a result of either electrical or chemical stimulation, and PPR-evoked locomotor-like activity was blocked by antagonists to 5-HT2A and 5-HT7 receptors located on separate populations of neurons concentrated in different rostro-caudal regions. 5-HT7 receptor antagonists blocked locomotor-like activity when applied above the L3 segment; 5-HT2A receptor antagonists blocked locomotor-like activity only when applied below the L2 segment. 5-HT7 receptor antagonists decreased step cycle duration, consistent with an action on neurons involved in the rhythm-generating function of the central pattern generator (CPG) for locomotion. 5-HT2A antagonists reduced the amplitude of ventral root activity with only small effects on step cycle duration, suggesting an action directly on cells involved in the output stage of the pattern generator for locomotion, including motoneurons and premotor cells. Experiments with selective antagonists show that dopaminergic (D1, D2) and noradrenergic (α1, α2) receptors are not critical for PPR-evoked locomotor-like activity.

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Kalyanasundar, B., Claudia I. Perez, Alvaro Luna, et al. "D1 and D2 antagonists reverse the effects of appetite suppressants on weight loss, food intake, locomotion, and rebalance spiking inhibition in the rat NAc shell." Journal of Neurophysiology 114, no. 1 (2015): 585–607. http://dx.doi.org/10.1152/jn.00012.2015.

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Obesity is a worldwide health problem that has reached epidemic proportions. To ameliorate this problem, one approach is the use of appetite suppressants. These compounds are frequently amphetamine congeners such as diethylpropion (DEP), phentermine (PHEN), and bupropion (BUP), whose effects are mediated through serotonin, norepinephrine, and dopaminergic pathways. The nucleus accumbens (NAc) shell receives dopaminergic inputs and is involved in feeding and motor activity. However, little is known about how appetite suppressants modulate its activity. Therefore, we characterized behavioral and neuronal NAc shell responses to short-term treatments of DEP, PHEN, and BUP. These compounds caused a transient decrease in weight and food intake while increasing locomotion, stereotypy, and insomnia. They evoked a large inhibitory imbalance in NAc shell spiking activity that correlated with the onset of locomotion and stereotypy. Analysis of the local field potentials (LFPs) showed that all three drugs modulated beta, theta, and delta oscillations. These oscillations do not reflect an aversive-malaise brain state, as ascertained from taste aversion experiments, but tracked both the initial decrease in weight and food intake and the subsequent tolerance to these drugs. Importantly, the appetite suppressant-induced weight loss and locomotion were markedly reduced by intragastric (and intra-NAc shell) infusions of dopamine antagonists SCH-23390 (D1 receptor) or raclopride (D2 receptor). Furthermore, both antagonists attenuated appetite suppressant-induced LFP oscillations and partially restored the imbalance in NAc shell activity. These data reveal that appetite suppressant-induced behavioral and neuronal activity recorded in the NAc shell depend, to various extents, on dopaminergic activation and thus point to an important role for D1/D2-like receptors (in the NAc shell) in the mechanism of action for these anorexic compounds.

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3

BISOGNO, Tiziana, Dominique MELCK, Mikhail Yu BOBROV, et al. "N-acyl-dopamines: novel synthetic CB1 cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo." Biochemical Journal 351, no. 3 (2000): 817–24. http://dx.doi.org/10.1042/bj3510817.

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We reported previously that synthetic amides of polyunsaturated fatty acids with bioactive amines can result in substances that interact with proteins of the endogenous cannabinoid system (ECS). Here we synthesized a series of N-acyl-dopamines (NADAs) and studied their effects on the anandamide membrane transporter, the anandamide amidohydrolase (fatty acid amide hydrolase, FAAH) and the two cannabinoid receptor subtypes, CB1 and CB2. NADAs competitively inhibited FAAH from N18TG2 cells (IC50 = 19–100µM), as well as the binding of the selective CB1 receptor ligand, [3H]SR141716A, to rat brain membranes (Ki = 250–3900nM). The arachidonoyl (20:4 ω6), eicosapentaenoyl (20:5 ω3), docosapentaenoyl (22:5 ω3), α-linolenoyl (18:3 ω3) and pinolenoyl (5c,9c,12c 18:3 ω6) homologues were also found to inhibit the anandamide membrane transporter in RBL-2H3 basophilic leukaemia and C6 glioma cells (IC50 = 17.5–33µM). NADAs did not inhibit the binding of the CB1/CB2 receptor ligand, [3H]WIN55,212-2, to rat spleen membranes (Ki > 10µM). N-arachidonyl-dopamine (AA-DA) exhibited 40-fold selectivity for CB1 (Ki = 250nM) over CB2 receptors, and N-docosapentaenoyl-dopamine exhibited 4-fold selectivity for the anandamide transporter over FAAH. AA-DA (0.1–10µM) did not displace D1 and D2 dopamine-receptor high-affinity ligands from rat brain membranes, thus suggesting that this compound has little affinity for these receptors. AA-DA was more potent and efficacious than anandamide as a CB1 agonist, as assessed by measuring the stimulatory effect on intracellular Ca2+ mobilization in undifferentiated N18TG2 neuroblastoma cells. This effect of AA-DA was counteracted by the CB1 antagonist SR141716A. AA-DA behaved as a CB1 agonist in vivo by inducing hypothermia, hypo-locomotion, catalepsy and analgesia in mice (1–10mg/kg). Finally, AA-DA potently inhibited (IC50 = 0.25µM) the proliferation of human breast MCF-7 cancer cells, thus behaving like other CB1 agonists. Also this effect was counteracted by SR141716A but not by the D2 antagonist haloperidol. We conclude that NADAs, and AA-DA in particular, may be novel and useful probes for the study of the ECS.

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4

Zaporozhets, Eugene, Kristine C. Cowley, and Brian J. Schmidt. "Neurochemical excitation of propriospinal neurons facilitates locomotor command signal transmission in the lesioned spinal cord." Journal of Neurophysiology 105, no. 6 (2011): 2818–29. http://dx.doi.org/10.1152/jn.00917.2010.

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Previous studies of the in vitro neonatal rat brain stem-spinal cord showed that propriospinal relays contribute to descending transmission of a supraspinal command signal that is capable of activating locomotion. Using the same preparation, the present series examines whether enhanced excitation of thoracic propriospinal neurons facilitates propagation of the locomotor command signal in the lesioned spinal cord. First, we identified neurotransmitters contributing to normal endogenous propriospinal transmission of the locomotor command signal by testing the effect of receptor antagonists applied to cervicothoracic segments during brain stem-induced locomotor-like activity. Spinal cords were either intact or contained staggered bilateral hemisections located at right T1/T2 and left T10/T11 junctions designed to abolish direct long-projecting bulbospinal axons. Serotonergic, noradrenergic, dopaminergic, and glutamatergic, but not cholinergic, receptor antagonists blocked locomotor-like activity. Approximately 73% of preparations with staggered bilateral hemisections failed to generate locomotor-like activity in response to electrical stimulation of the brain stem alone; such preparations were used to test the effect of neuroactive substances applied to thoracic segments (bath barriers placed at T3 and T9) during brain stem stimulation. The percentage of preparations developing locomotor-like activity was as follows: 5-HT (43%), 5-HT/ N-methyl-d-aspartate (NMDA; 33%), quipazine (42%), 8-hydroxy-2-(di- n-propylamino)tetralin (20%), methoxamine (45%), and elevated bath K+ concentration (29%). Combined norepinephrine and dopamine increased the success rate (67%) compared with the use of either agent alone (4 and 7%, respectively). NMDA, Mg2+ ion removal, clonidine, and acetylcholine were ineffective. The results provide proof of principle that artificial excitation of thoracic propriospinal neurons can improve supraspinal control over hindlimb locomotor networks in the lesioned spinal cord.

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5

Cowley, Kristine C., Eugene Zaporozhets, Jason N. MacLean, and Brian J. Schmidt. "Is NMDA Receptor Activation Essential for the Production of Locomotor-Like Activity in the Neonatal Rat Spinal Cord?" Journal of Neurophysiology 94, no. 6 (2005): 3805–14. http://dx.doi.org/10.1152/jn.00016.2005.

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Previous work has established that in vitro bath application of N-methyl-d-aspartic acid (NMDA) promotes locomotor activity in a variety of vertebrate preparations including the neonatal rat spinal cord. In addition, NMDA receptor activation gives rise to active membrane properties that are postulated to contribute to the generation or stabilization of locomotor rhythm. However, earlier studies yielded conflicting evidence as to whether NMDA receptors are essential in this role. Therefore in this study, we examined the effect of NMDA receptor blockade, using d-2-amino-5-phosphono-valeric acid (AP5), on locomotor-like activity in the in vitro neonatal rat spinal cord. Locomotor-like activity was induced using 5-hydroxytryptamine (5-HT), acetylcholine, combined 5-HT and NMDA receptor activation, increased K+ concentration, or electrical stimulation of the brain stem and monitored using suction electrode recordings of left and right lumbar ventral root discharge. We also studied the effect on locomotor capacity of selectively suppressing NMDA receptor–mediated active membrane properties; this was achieved by removing Mg2+ ions from the bath, which in turn abolishes voltage-sensitive blockade of the NMDA receptor channel. The results show that, although NMDA receptor activation may seem essential for locomotor network operation under some experimental conditions, locomotor-like rhythms can nevertheless be generated in the presence of AP5 if spinal cord circuitry is exposed to appropriate levels of non–NMDA receptor–dependent excitation. Therefore neither NMDA receptor–mediated nonlinear membrane properties nor NMDA receptor activation in general is universally essential for locomotor network activation in the in vitro neonatal rat spinal cord.

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Guo, Chunmei, Yang Yang, Yun'ai Su, and Tianmei Si. "Postnatal BDNF Expression Profiles in Prefrontal Cortex and Hippocampus of a Rat Schizophrenia Model Induced by MK-801 Administration." Journal of Biomedicine and Biotechnology 2010 (2010): 1–5. http://dx.doi.org/10.1155/2010/783297.

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Neonatal blockade of N-methyl-D-aspartic acid (NMDA) receptors represents one of experimental animal models for schizophrenia. This study is to investigate the long-term brain-derived neurotrophic factor (BDNF) expression profiles in different regions and correlation with “schizophrenia-like” behaviors in the adolescence and adult of this rat model. The NMDA receptor antagonist MK801 was administered to female Sprague-Dawley rats on postnatal days (PND) 5 through 14. Open-field test was performed on PND 42, and PND 77 to examine the validity of the current model. BDNF protein levels in hippocampus and prefrontal cortex (PFC) were analyzed on PND 15, PND 42, and PND 77. Results showed that neonatal challenge with MK-801 persistently elevated locomotor activity as well as BDNF expression; the alterations in BDNF expression varied at different developing stages and among brain regions. However, these findings provide neurochemical evidence that the blockade of NMDA receptors during brain development results in long-lasting alterations in BDNF expression and might contribute to neurobehavioral pathology of the present animal model for schizophrenia. Further study in the mechanisms and roles of the BDNF may lead to better understanding of the pathophysiology of schizophrenia.

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Homma, Yutaka, R. D. Skinner, and E. Garcia-Rill. "Effects of Pedunculopontine Nucleus (PPN) Stimulation on Caudal Pontine Reticular Formation (PnC) Neurons In Vitro." Journal of Neurophysiology 87, no. 6 (2002): 3033–47. http://dx.doi.org/10.1152/jn.2002.87.6.3033.

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Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states. Previously, PPN stimulation was reported to induce prolonged responses (PRs) in extracellularly recorded PnC neurons in the decerebrate cat. The present study used intracellular recordings in semihorizontal slices from rat brain stem ( postnatal days 12–21) to determine responses in PnC neurons following PPN stimulation. Two-thirds (65%) of PnC neurons showed PRs after PPN stimulation. PnC neurons with PRs had higher amplitude afterhyperpolarizations (AHP) than non-PR (NPR) neurons. Both PR and NPR neurons were of mixed cell types characterized by “A” and/or “LTS,” or neither of these types of currents. PnC cells showed decreased AHP duration with age, due mostly to decreased AHP duration in NPR cells. The longest mean duration PRs were induced by stimulation at 60 and 90 Hz compared with 10 or 30 Hz. Maximal firing rates in PnC cells during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. BaCl2superfusion blocked PPN stimulation-induced PRs, suggesting that PRs may be mediated by blockade of potassium channels, in keeping with increased input resistance observed during PRs. Depolarizing pulses failed to elicit, and hyperpolarizing pulses failed to reset, PPN stimulation-induced PRs, suggesting that PRs may not be plateau potentials. Pharmacological testing revealed that nifedipine superfusion failed to block PPN stimulation-induced PRs; i.e., PRs may not be calcium channel-dependent. The muscarinic cholinergic agonist carbachol induced depolarization in most PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked PPN stimulation-induced PRs in some PnC neurons, suggesting that some PRs may be due to muscarinic receptor activation. The nonspecific ionotropic glutamate receptor antagonist kynurenic acid failed to block PPN stimulation-induced PRs, as did the metabotropic glutamate receptor antagonist (R, S)-αmethyl-4-carboxyphenylglycine, suggesting that PRs may not be mediated by glutamate receptors. These findings suggest that PPN stimulation-induced PRs may be due to increased excitability following closing of muscarinic receptor-sensitive potassium channels, allowing PnC neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs using parameters known best to induce locomotion. This mechanism may be related to switching from one state to another (e.g., locomotion vs. standing or sitting, waking vs. non-REM sleep or REM sleep).

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Chen, Gang, Yimin Liang, Fanghu Chen, Haifeng Wang, and Guoming Zhu. "The effect of lithium chloride on the motor function of spinal cord injury–controlled rat and the relevant mechanism." European Journal of Inflammation 17 (January 2019): 205873921985285. http://dx.doi.org/10.1177/2058739219852855.

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The objective of this study is to discuss the effect and mechanism of lithium chloride on the rehabilitation of locomotion post spinal cord injury (SCI) by observing the effect of lithium chloride on the expression of the brain-derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB) pathway. In total, 36 Sprague-Dawley (SD) rats were randomly divided into the sham operation group (n = 12), model group (n = 12), and lithium chloride group (n = 12). The sham operation group underwent laminectomy, while for the model group and the lithium chloride group with the NYU spinal cord impactor the SCI model was established. Basso, Beattie, and Bresnahan (BBB) score was used to evaluate locomotion after administration for 1, 3, 5, and 7 days, and the tissues were gathered for Nissl staining, transmission electron microscopy, immunofluorescence, and Western blot. With a statistical difference ( P < 0.05) on the 3rd day and significant difference ( P < 0.01) on the 5th day post administration, a higher BBB score was observed in the lithium chloride group indicating that lithium chloride improved the locomotion function after SCI. A better structure and morphology of neuron were observed by Nissl staining in the lithium chloride group. Lithium chloride promoted BDNF secretion from neurons in the spinal cord anterior horn with a significant difference compared to the model group ( P < 0.01). Compared with the model group, lithium chloride significantly promoted the expression of BDNF protein and phosphorylated TrkB protein ( P < 0.05), but no difference in the expression of TrkB was detected. Lithium chloride can alleviate the locomotion function after SCI with a mechanism that it can promote BDNF secretion from neurons in the spinal cord anterior horn and phosphorylation of TrkB to upregulate the BDNF/TrkB pathway supporting survival of neurons and regeneration and remyelination of axons.

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Wang, Xingxing, Tianna Zhou, George D. Maynard, et al. "Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury." Brain 143, no. 6 (2020): 1697–713. http://dx.doi.org/10.1093/brain/awaa116.

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Abstract After CNS trauma such as spinal cord injury, the ability of surviving neural elements to sprout axons, reorganize neural networks and support recovery of function is severely restricted, contributing to chronic neurological deficits. Among limitations on neural recovery are myelin-associated inhibitors functioning as ligands for neuronal Nogo receptor 1 (NgR1). A soluble decoy (NgR1-Fc, AXER-204) blocks these ligands and provides a means to promote recovery of function in multiple preclinical rodent models of spinal cord injury. However, the safety and efficacy of this reagent in non-human primate spinal cord injury and its toxicological profile have not been described. Here, we provide evidence that chronic intrathecal and intravenous administration of NgR1-Fc to cynomolgus monkey and to rat are without evident toxicity at doses of 20 mg and greater every other day (≥2.0 mg/kg/day), and far greater than the projected human dose. Adult female African green monkeys underwent right C5/6 lateral hemisection with evidence of persistent disuse of the right forelimb during feeding and right hindlimb during locomotion. At 1 month post-injury, the animals were randomized to treatment with vehicle (n = 6) or 0.10–0.17 mg/kg/day of NgR1-Fc (n = 8) delivered via intrathecal lumbar catheter and osmotic minipump for 4 months. One animal was removed from the study because of surgical complications of the catheter, but no treatment-related adverse events were noted in either group. Animal behaviour was evaluated at 6–7 months post-injury, i.e. 1–2 months after treatment cessation. The use of the impaired forelimb during spontaneous feeding and the impaired hindlimb during locomotion were both significantly greater in the treatment group. Tissue collected at 7–12 months post-injury showed no significant differences in lesion size, fibrotic scar, gliosis or neuroinflammation between groups. Serotoninergic raphespinal fibres below the lesion showed no deficit, with equal density on the lesioned and intact side below the level of the injury in both groups. Corticospinal axons traced from biotin-dextran-amine injections in the left motor cortex were equally labelled across groups and reduced caudal to the injury. The NgR1-Fc group tissue exhibited a significant 2–3-fold increased corticospinal axon density in the cervical cord below the level of the injury relative to the vehicle group. The data show that NgR1-Fc does not have preclinical toxicological issues in healthy animals or safety concerns in spinal cord injury animals. Thus, it presents as a potential therapeutic for spinal cord injury with evidence for behavioural improvement and growth of injured pathways in non-human primate spinal cord injury.

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10

Zarrindast, M. R., M. Nasehi, and M. Pournaghshband. "Effects of dopaminergic drugs in the dorsal hippocampus of rats in the MK801-induced anxiolytic-like behavior." European Psychiatry 26, S2 (2011): 441. http://dx.doi.org/10.1016/s0924-9338(11)72148-4.

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IntroductionExcitatory transmission through glutamate receptors constitutes the main mode of synaptic signaling in the brain regions that are critical for cognition such as learning and anxiety.ObjectivesThe possible involvement of dorsal hippocampal (intra-CA1) dopaminergic receptor mechanism on the anxiolytic-like response induced by NMDA receptor antagonist, MK801 has been investigated in the present study.MethodsThe male wistar rats were used and the elevated plus maze apparatus has been used to test parameters (%OAT, %OAE, locomotor activity, grooming, rereading and defection) of anxiety-like behaviors in the present study.ResultsThe data indicated that intra-CA1 administration of MK801 (2 μg/rat, intra-CA1) increased %OAT and %OAE but not other exploratory behaviors, indicating an anxiolytic-like response. Moreover, intra-CA1injection SCH23390 (0.25, 0.5 and 1 μg/rat) and sulpiride (0.25, 0.5 and 0.75 μg/rat) by itselves, 5 min before testing have no effect on exploratory behaviors. On the other hand, co-administration of ineffective dose of SCH23390 (0.5 μg/rat) with ineffective dose of MK801 (1 g/rat) increased %OAT but not other exploratory behaviors, suggestion anxiolytic-like behaviors. Furthermore, intra-CA1 administration of different doses of sulpiride (0.12, 0.5 and 0.75 μg/rat) 5 min before injection of effective dose of MK801 (2 μg/rat) decreased %OAT and %OAE but did not other exploratory behaviors induced by MK801.ConclusionThe results may indicate modulatory effect dopaminergic system of CA1 in the anxiolytic-like response induced by MK801.

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Dissertations / Theses on the topic "Rat locomotion/brain receptors"

1

Coles, S. K. "Controls of the locomotor system in the rat." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233493.

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Boulay, Denis. "Etude chez le rat des modifications comportementales et neurochimiques après administrations répétées d'agonistes dopaminergiques indirects : la cocaïne ou le GBR12783." Rouen, 1995. http://www.theses.fr/1995ROUE5042.

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Nous avons recherché si un blocage répété du système de capture de la dopamine par un inhibiteur spécifique de la capture neuronale de dopamine, le GBR12783, pouvait mimer les sensibilisations observées après administrations de cocaïne, inhibiteur non sélectif de la recapture des monoamines. Des administrations répétées de GBR12783 ont induit une sensibilisation à ses effets stimulants moteurs, se développant au cours du temps et pouvant persister plusieurs semaines après la dernière administration. L'expression de cette sensibilisation dépend en partie de la durée des traitements chroniques ; elle est favorisée par le contexte environnemental. Les traitements chroniques par le GBR12783 ne modifient pas les taux tissulaires ni de la dopamine, ni de ses métabolites mesurés 48 heures ou 15 jours après l'arrêt des traitements dans le noyau accumbens et le striatum. Un traitement répété de 15 jours par le GBR12783 ou par la cocaïne diminue la densité du transporteur neuronal de la DA dans la partie coque du noyau accumbens. Cette diminution n'apparaît que 15 jours après l'arrêt des traitements ; elle pourrait participer à la sensibilisation des effets moteurs de ces substances. Des administrations répétées de GBR12783 induisant chez le rat une sensibilisation aux effets moteurs de cet inhibiteur de capture de la dopamine ont sensibilisé également les effets stimulants moteurs d'un dérivé de la neurotensine (résistant à la dégradation par les peptidases): la D tryptophane-11-neurotensine injectée par voie i. C. V. , Sans pour autant modifier la densité des récepteurs de la neurotensine

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Cohen, Ricky Israel. "Rat brain oligodendrocytes express muscarinic and adrenergic receptors." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42006.

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The aim of the studies underlying this thesis was to characterize the muscarinic and adrenergic receptors expressed in rat brain oligodendrocytes' (OLs); determine if ligand binding alters second messenger levels classically associated with these families of receptors, such as inositol phosphates (InsP), intracellular calcium ( (Ca$ rm sp{2+} rbrack sb{i}),$ and cyclic AMP (cAMP); and the role of neurotransmitters, acetylcholine (Ach) or norepinephrine (NE) on oligodendrocyte growth.<br>CCH (carbachol), a stable Ach analog, caused a concentration and time dependent increase in the accumulation of InsPs and the mobilization of (Ca$ rm sp{2+} rbrack sb{i},$ which was inhibited by atropine, a specific muscarinic antagonist, and was negatively regulated by acute activation of protein kinase C by the phorbol ester TPA. CCH also negatively regulated the $ beta$-adrenergic-stimulated increase in cAMP levels. Using subtype m1 and m2 specific muscarinic receptor oligonucleotide primers RT-PCR confirmed the presence of, at least, these two muscarinic receptor subtypes. CCH caused a time and concentration-dependent increase in c-fos proto-oncogene mRNA levels as determined by Northern blot analysis. The CCH-stimulated c-fos increase was mediated through a non-phorbol ester sensitive PKC isozyme, and was dependent upon intra and extracellular calcium. Moreover, CCH stimulated DNA synthesis in OLPs, as measured by both ($ sp3$H) -thymidine and BrdU incorporation.<br>Lastly, the NE-stimulated signal transduction pathway was characterized in developing OLPs. Using selective agonists and antagonists, we determined that NE increased the formation of InsPs through $ alpha sb1$ adrenoceptors. We further subclassified the $ alpha sb1$ receptor to the $ rm alpha sb{1A}$ subtype using more selective reagents; WB4101, a selective antagonist for $ rm alpha sb{1A}$ receptors blocked the response to NE, while chloroethylclonidine, an $ rm alpha sb{1B}$ antagonist had no effect. Furthermore, Pertussis toxin, a bacterial toxin that ADP-ribosylates and inactivates certain G-proteins, EGTA, a calcium chelator, or CdCl$ sb2,$ an inorganic calcium channel blocker, all significantly blocked the NE-stimulated InsP formation. Together these results suggest that OLPs express $ alpha sb1$-adrenoceptors characteristic of the $ rm alpha sb{1A}$ subtype.<br>In toto, these studies demonstrate that developing OLs express functional muscariaic and adrenergic receptors, and suggest that Ach may function as a trophic factor. These results help to define a mechanism whereby neurons, and OLs may use neurotransmitters to communicate both during development and in the mature central nervous system.

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Cohen, Ricky Israel. "Rat brain oligodendrocytes express muscarinic and adrenergic receptors." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0022/NQ29913.pdf.

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Mahalekam, Malani. "Natriuretic peptide receptors in developing and adult rat brain." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368618.

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Howard, Helen Clare. "The pharmacological characterisation of oxytocin receptors in the rat brain." Thesis, University of Bristol, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299594.

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Pasquini, Filoteo. "High resolution radioautographic visualization of delta opioid receptors in rat brain." Thesis, McGill University, 1988. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=64051.

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Smith, Steven Andrew. "The role of Peroxisome proliferator-activated receptors in the rat brain /." St. Lucia, Qld, 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe17982.pdf.

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Gibbins, Jonathan Martin. "The purification of corticotropin-releasing factor (CRF) receptors from rat brain." Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260813.

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Schindler, Marcus. "The distribution of somatostatin receptors in the rat and human brain." Thesis, University of Cambridge, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627298.

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Books on the topic "Rat locomotion/brain receptors"

1

Bowlby, Deborah Anne. Regulation of wstrogen receptors in the rat brain. National Library of Canada, 1994.

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Cao, Chenglong. Immunological screening of a rat brain cDNA library for genes encoding potential novel glutamate receptors. National Library of Canada, 1993.

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Billinton, Andrew. Brain GABA[Beta] receptors and GBR1 mRNA in rat seizure models and human temporal lobe epilepsy. University of Birmingham, 1999.

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Clarke, Wendy Elizabeth. Intracellular compartmentalisation of fibroblast growth factor-2 and associated high and low affinity receptors after cerebral injury to the adult rat brain. University of Birmingham, 1999.

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Seale, J. V. A quantitative immunohistochemical analysis of the distribution of insulin receptors in the rat brain for regions associated with memory compared to regions not associated with memory. University of Surrey Roehampton, 2001.

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Grove, Kevin Lyle. Angiotensin II receptors in the hypothalamus of the adult and developing female rat brain. 1994.

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Autoradiographic localization of insulin receptors in rat brain: Prominence in olfactory and limbic areas. National Institute of Arithitis, Diabetes, and Digestive and Kidney Diseases], 1986.

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Cao, Chenglong. Immunological screening of a rat brain cDNA library for genes encoding potential novel glutamate receptors. 1994.

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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.

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Bird, Mark F., and David G. Lambert. Deorphanization of ORL-1/LC132 by reverse pharmacology in two landmark studies. Edited by Paul Farquhar-Smith, Pierre Beaulieu, and Sian Jagger. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198834359.003.0026.

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Abstract:

Deorphanization of ORL-1/LC132 in 1995 by reverse pharmacology in two simultaneously published landmark studies added a new member to the opioid family of G-protein coupled receptors. Meunier and Reinscheid used cells expressing recombinant ORL-1 (human) or LC132 (rat) and the presumed intracellular inhibition of cyclic AMP formation to ‘fish’ for endogenous peptide ligands in rat whole-brain and pig hypothalamic extracts. Both studies reported the isolation of a 17-amino-acid peptide, which was named nociceptin and orphanin FQ by the two authors, respectively. The behaviour of the isolated peptide was a complete surprise, as a general hyperalgesia was observed when the peptide was administered at supraspinal sites. We now know that this peptide has, in fact, anti-opioid action, particularly in the medulla. The endogenous peptide exerts a multitude of effects both in the nervous system and, unlike classical opioids, has efficacy in neuropathic pain.

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Book chapters on the topic "Rat locomotion/brain receptors"

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Wood, P. L., L. L. Martin, and C. A. Altar. "[3H]Tryptamine Receptors in Rat Brain." In Neuropsychopharmacology of the Trace Amines. Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5010-4_9.

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Clarke, P. B. S., and A. Pert. "Autoradiographical Evidence of Nicotinic Receptors in Rat Brain." In Tobacco Smoking and Nicotine. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1911-5_11.

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Mendelsohn, Laurane G. "Visualization of IGF-2 Receptors in Rat Brain." In Insulin, Insulin-like Growth Factors, and Their Receptors in the Central Nervous System. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-5380-5_21.

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Chabot, Jean-Guy, Satyabrata Kar, and Rémi Quirion. "Ontogenic Profile of Epidermal Growth Factor Receptors in Rat Brain." In Receptors in the Developing Nervous System. Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1540-7_5.

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Ben-Shachar, Dorit, and Moussa B. H. Youdim. "Brain Iron and Dopamine D2 Receptors in the Rat." In Advances in Behavioral Biology. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4613-2179-8_33.

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Taylor, J. E. "Binding of Neuromediators to Their Receptors in Rat Brain." In Rökan. Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73686-5_11.

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Ikezaki, Kiyonobu, T. Nomura, M. Takahashi, B. F. Zieroth, and M. Fukui. "MRI Contrast Enhancement by Mn-TPPS in Experimental Rat Brain Tumor with Peripheral Benzodiazepine Receptors." In Brain Edema IX. Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9334-1_95.

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Scharfman, Helen E. "Presynaptic and Postsynaptic Actions of Somatostatin in Area CA1 and the Dentate Gyrus of Rat and Rabbit Hippocampal Slices." In Presynaptic Receptors in the Mammalian Brain. Birkhäuser Boston, 1993. http://dx.doi.org/10.1007/978-1-4684-6825-0_4.

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Winkler, T., H. S. Sharma, E. Stålberg, and J. Westman. "Benzodiazepine Receptors Influence Spinal Cord Evoked Potentials and Edema Following Trauma to the Rat Spinal Cord." In Brain Edema X. Springer Vienna, 1997. http://dx.doi.org/10.1007/978-3-7091-6837-0_66.

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Kitabgi, Patrick, and Jean-Pierre Vincent. "Effects of Cations and Nucleotides on Neurotensin Binding to Rat Brain Synaptic Membranes." In Neural and Endocrine Peptides and Receptors. Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-5152-8_21.

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Conference papers on the topic "Rat locomotion/brain receptors"

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Fukayama, Osamu, Noriyuki Taniguchi, Takafumi Suzuki, and Kunihiko Mabuchi. "RatCar system for estimating locomotion states using neural signals with parameter monitoring: Vehicle-formed brain-machine interfaces for rat." In 2008 30th Annual International Conference of the IEEE Engineering in Medicine and Biology Society. IEEE, 2008. http://dx.doi.org/10.1109/iembs.2008.4650416.

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