Journal articles: 'Rat locomotion/brain receptors'

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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 (August 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, Jessica Solorio, Mario G. Moreno, David Elias, Sidney A. Simon, and Ranier Gutierrez. "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 (July 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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BISOGNO, Tiziana, Dominique MELCK, Mikhail Yu BOBROV, Natalia M. GRETSKAYA, Vladimir V. BEZUGLOV, Luciano DE PETROCELLIS, and Vincenzo DI MARZO. "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 (October 24, 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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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 (June 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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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 (December 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 (June 1, 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, Pramod S. Terse, William B. Cafferty, Jeffery D. Kocsis, and Stephen M. Strittmatter. "Nogo receptor decoy promotes recovery and corticospinal growth in non-human primate spinal cord injury." Brain 143, no. 6 (May 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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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 (March 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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Mamiya, Keiko, Kevin Bay, R. D. Skinner, and E. Garcia-Rill. "Induction of long-lasting depolarization in medioventral medulla neurons by cholinergic input from the pedunculopontine nucleus." Journal of Applied Physiology 99, no. 3 (September 2005): 1127–37. http://dx.doi.org/10.1152/japplphysiol.00253.2005.

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Stimulation of the pedunculopontine nucleus (PPN) is known to induce changes in arousal and postural/locomotor states by activation of such descending targets as the caudal pons and the medioventral medulla (MED). Previously, PPN stimulation was reported to induce prolonged responses (PRs) in intracellularly recorded caudal pontine neurons in vitro. The present study used intracellular recordings in semihorizontal slices from rat brain stem (postnatal days 12–21) to determine responses in MED neurons following PPN stimulation. One-half (40/81) of MED neurons showed PRs after PPN stimulation. MED neurons with PRs had shorter duration action potential, longer duration afterhyperpolarization, and higher amplitude afterhyperpolarization than non-PR MED neurons. PR MED neurons were significantly larger (568 ± 44 μm2) than non-PR MED neurons (387 ± 32 μm2). The longest mean duration PRs and maximal firing rates during PRs were induced by PPN stimulation at 60 Hz compared with 10, 30, or 90 Hz. The muscarinic cholinergic agonist carbachol induced depolarization in all PR neurons tested, and the muscarinic cholinergic antagonist scopolamine reduced or blocked carbachol- and PPN stimulation-induced PRs in all MED neurons tested. These findings suggest that PPN stimulation-induced PRs may be due to activation of muscarinic receptor-sensitive channels, allowing MED neurons to respond to a transient, frequency-dependent depolarization with long-lasting stable states. PPN stimulation appears to induce PRs in large MED neurons using parameters known best to induce locomotion.

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Tang-Christensen, M., P. J. Larsen, R. Goke, A. Fink-Jensen, D. S. Jessop, M. Moller, and S. P. Sheikh. "Central administration of GLP-1-(7-36) amide inhibits food and water intake in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 4 (October 1, 1996): R848—R856. http://dx.doi.org/10.1152/ajpregu.1996.271.4.r848.

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Glucagon-like peptide (GLP)-1-(7-36) amide and its pancreatic receptors are important for control of blood glucose levels. However, rat GLP-1 receptors are also localized in the brain, in hypothalamus, and in areas without a blood-brain barrier. When rats were kept on a food restriction schedule, intracerebroventricular injection of GLP-1 just before food was offered inhibited food intake. However, peripheral GLP-1 administration by intraperitoneal injection had little effect. GLP-1 effects on water intake and output were also investigated. Intracerebroventricular GLP-1 profoundly inhibited angiotensin II-induced drinking behavior in rats, and water intake was suppressed by exogenous GLP-1 in rats habituated to a water restriction schedule. These effects were reproduced by intraperitoneal administration of GLP-1. Furthermore, intracerebroventricular GLP-1 stimulated urinary excretion of water and sodium. The centrally elicited effects were blocked by the GLP-1 antagonist exendin-(9-39) amide, whereas the N-terminally extended and inactive GLP-1-(1-36) amide had no effect on feeding and drinking. GLP-1 had no effect in behavioral assays measuring exploratory locomotor activity and conditioned taste aversion. In conclusion, GLP-1 may play a physiological role in regulation of both ingestion and the water and salt homeostasis.

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Blivis, D., G. Z. Mentis, M. J. O'Donovan, and A. Lev-Tov. "Differential Effects of Opioids on Sacrocaudal Afferent Pathways and Central Pattern Generators in the Neonatal Rat Spinal Cord." Journal of Neurophysiology 97, no. 4 (April 2007): 2875–86. http://dx.doi.org/10.1152/jn.01313.2006.

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The effects of opioids on sacrocaudal afferent (SCA) pathways and the pattern-generating circuitry of the thoracolumbar and sacrocaudal segments of the spinal cord were studied in isolated spinal cord and brain stem-spinal cord preparations of the neonatal rat. The locomotor and tail moving rhythm produced by activation of nociceptive and nonnociceptive sacrocaudal afferents was completely blocked by specific application of the μ-opioid receptor agonist [d-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin acetate salt (DAMGO) to the sacrocaudal but not the thoracolumbar segments of the spinal cord. The rhythmic activity could be restored after addition of the opioid receptor antagonist naloxone to the experimental chamber. The opioid block of the SCA-induced rhythm is not due to impaired rhythmogenic capacity of the spinal cord because a robust rhythmic activity could be initiated in the thoracolumbar and sacrocaudal segments in the presence of DAMGO, either by stimulation of the ventromedial medulla or by bath application of N-methyl-d-aspartate/serotonin. We suggest that the opioid block of the SCA-induced rhythm involves suppression of synaptic transmission through sacrocaudal interneurons interposed between SCA and the pattern-generating circuitry. The expression of μ opioid receptors in several groups of dorsal, intermediate and ventral horn interneurons in the sacrocaudal segments of the cord, documented in this study, provides an anatomical basis for this suggestion.

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Widdowson, PS, MJ Farnworth, R. Upton, and MG Simpson. "No changes in behaviour, nigro-striatal system neurochemistry or neuronal cell death following toxic multiple oral paraquat administration to rats." Human & Experimental Toxicology 15, no. 7 (July 1996): 583–91. http://dx.doi.org/10.1177/096032719601500706.

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We have examined whether the widely used herbicide, paraquat (1,1'-dimethyl-4,4'dipyridylium) may accumu late in rat brain following multiple oral dosing (5 mg paraquat ion/kg/day) for 14 days and whether this dosing regime may produce signs of neurotoxicity. This dosing regime may determine whether low dose exposure to mammals may be neurotoxic. Using [14C]paraquat to measure tissue and plasma paraquat concentrations, we observed significantly higher plasma and tissue paraquat concentrations in brain, liver, lungs and kidneys of rats which received multiple doses for 14 days, as compared to paraquat concentrations in tissues of rats which received only a single paraquat dose. Brain paraquat concentrations measured 24 h after dosing were tenfold higher in rats receiving 14 daily oral doses of paraquat, as compared to concentrations follow ing a single oral dose. A neuropathological study of the rat brain yielded no evidence that multiple paraquat dosing resulted in neuronal cell damage. Particular attention was paid to the nigrostriatal system. The paraquat treated rats gained approximately 10% less body weight over the 15 day experimental period as compared with controls demon strating that the dose of paraquat was toxic to the animals. Measurements of locomotor activity using open field tests or activity monitors did not reveal any statistically significant differences between control animals and those receiving paraquat. Fore- and hind-limb grip strength were not significantly different between the paraquat treated and control rats at any time point during the dosing regime, nor was there any evidence for locomotor co ordination deficits in any of the animals receiving paraquat. Densities of dopamine D1 and D2, NMDA, muscarinic and benzodiazepine receptors in the cerebral cortex and striatum were not significantly different between controls and rats which had received multiple paraquat doses. Concentrations of catecholamine neurotransmitters in the striatum, hypothalamus and frontal cerebral cortex were also measured to examine whether there was evidence for catecholamine depletion in these brain regions. We did not observe any significant reductions in dopamine, noradrenaline or DOPAC concentrations in any brain region of paraquat treated rats as compared with controls. On the contrary, dopamine concentrations in the striatim were significantly elevated in paraquat treated animals following a 15 day paraquat dosing regime. We attribute these changes in catecholamine concentrations to the general toxicity of paraquat which produces a stress response. In conclusion, we could not find any evidence that multiple paraquat dosing can lead to changes in locomotor activity or grip strength. In addition, the absence of neuropathology or changes in neurochemistry in the nigrostriatal tract demonstrates that paraquat does not behave like MPP+(N-methyl-4-phenylpyridinium), the neurotoxic metabolite of MPTP

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Weaver, SA, FX Aherne, MJ Meaney, AL Schaefer, and WT Dixon. "Neonatal handling permanently alters hypothalamic-pituitary- adrenal axis function, behaviour, and body weight in boars." Journal of Endocrinology 164, no. 3 (March 1, 2000): 349–59. http://dx.doi.org/10.1677/joe.0.1640349.

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Neonatal handling permanently alters hypothalamic- pituitary-adrenal axis (HPA) function in rats. In the rat, this treatment increases hippocampal glucocorticoid receptors (GR) and dampens plasma ACTH and corticosterone responses to stressors. The objectives of this study were to determine whether neonatal handling of pigs would effect permanent changes in plasma corticosteroid binding capacity (CBG), basal or stressor-induced plasma cortisol and ACTH concentrations, brain or pituitary GR levels, dexamethasone suppression of plasma cortisol and ACTH concentrations, behaviour in an open field-test pen, and body weights. Twelve litters of pigs were randomly assigned to either neonatal handling or no disturbance. Handled litters were removed from the farrowing crate for 10 min per day for the first 14 days of life. Male pigs were kept for the study and the boars were weighed monthly. At 7 months of age, boars were tested for locomotory behaviour in an open field-test pen. The boars were implanted with indwelling ear-vein catheters and blood samples were obtained basally, during and after application of a nose snare, and after 0.04 mg/kg dexamethasone. Boars were killed and blood samples were obtained and the brain and pituitary glands collected. Handled boars had greater (P<0.05) plasma CBG binding and lower basal total (P<0.05) and calculated free (P<0.03) plasma cortisol concentrations. No significant differences between treatments were found in plasma ACTH or cortisol responses to a nose-snare stressor; however, when killed, handled boars had greater (P<0.02) plasma ACTH concentrations. Handled and non-handled boars did not differ in plasma ACTH or cortisol responses to dexamethasone. There was no treatment effect on GR expression in the pituitary gland, frontal cortex, hippocampus, or hypothalamus. Behaviourally, the handled boars had higher (P<0.03) locomotor scores over inner squares and a lower (P<0.05) ratio of outer:inner squares entered in open field-tests. During the first 7 months of life, body weights were lower (P<0.004) for handled boars. In conclusion, neonatal handling permanently altered HPA function in pigs, but in a manner dissimilar to that found in the rat. These changes induced in the pig were not beneficial for commercial production with respect to body weight.

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Kobayashi, T., C. Good, K. Mamiya, R. D. Skinner, and E. Garcia-Rill. "Development of REM sleep drive and clinical implications." Journal of Applied Physiology 96, no. 2 (February 2004): 735–46. http://dx.doi.org/10.1152/japplphysiol.00908.2003.

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Rapid eye movement (REM) sleep in the human declines from ∼50% of total sleep time (∼8 h) in the newborn to ∼15% of total sleep time (∼1 h) in the adult, and this decrease takes place mainly between birth and the end of puberty. We hypothesize that without this developmental decrease in REM sleep drive, lifelong increases in REM sleep drive may ensue. In the rat, the developmental decrease in REM sleep occurs 10-30 days after birth, declining from >70% of total sleep time in the newborn to the adult level of ∼15% of sleep time during this period. Rats at 12-21 days of age were anesthetized with ketamine and decapitated, and brain stem slices were cut for intracellular recordings. We found that excitatory responses of pedunculopontine nucleus (PPN) neurons to N-methyl-d-aspartic acid decrease, while responses to kainic acid increase, over this critical period. During this developmental period, inhibitory responses to serotonergic type 1 agonists increase but responses to serotonergic type 2 agonists do not change. The results suggest that as PPN neurons develop, they are increasingly activated by kainic acid and increasingly inhibited by serotonergic type 1 receptors. These processes may be related to the developmental decrease in REM sleep. Developmental disturbances in each of these systems could induce differential increases in REM sleep drive, accounting for the postpubertal onset of a number of different disorders manifesting increases in REM sleep drive. Examination of modulation by PPN projections to ascending and descending targets revealed the presence of common signals modulating ascending arousal-related functions and descending postural/locomotor-related functions.

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Sławińska, Urszula, Henryk Majczyński, Anna Kwaśniewska, Krzysztof Miazga, Anna M. Cabaj, Marek Bekisz, Larry M. Jordan, and Małgorzata Zawadzka. "Unusual Quadrupedal Locomotion in Rat during Recovery from Lumbar Spinal Blockade of 5-HT7 Receptors." International Journal of Molecular Sciences 22, no. 11 (June 2, 2021): 6007. http://dx.doi.org/10.3390/ijms22116007.

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Coordination of four-limb movements during quadrupedal locomotion is controlled by supraspinal monoaminergic descending pathways, among which serotoninergic ones play a crucial role. Here we investigated the locomotor pattern during recovery from blockade of 5-HT7 or 5-HT2A receptors after intrathecal application of SB269970 or cyproheptadine in adult rats with chronic intrathecal cannula implanted in the lumbar spinal cord. The interlimb coordination was investigated based on electromyographic activity recorded from selected fore- and hindlimb muscles during rat locomotion on a treadmill. In the time of recovery after hindlimb transient paralysis, we noticed a presence of an unusual pattern of quadrupedal locomotion characterized by a doubling of forelimb stepping in relation to unaffected hindlimb stepping (2FL-1HL) after blockade of 5-HT7 receptors but not after blockade of 5-HT2A receptors. The 2FL-1HL pattern, although transient, was observed as a stable form of fore-hindlimb coupling during quadrupedal locomotion. We suggest that modulation of the 5-HT7 receptors on interneurons located in lamina VII with ascending projections to the forelimb spinal network can be responsible for the 2FL-1HL locomotor pattern. In support, our immunohistochemical analysis of the lumbar spinal cord demonstrated the presence of the 5-HT7 immunoreactive cells in the lamina VII, which were rarely 5-HT2A immunoreactive.

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Puymirat, Jack. "Thyroid receptors in the rat brain." Progress in Neurobiology 39, no. 3 (September 1992): 281–94. http://dx.doi.org/10.1016/0301-0082(92)90019-b.

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Li, Bo, Minjian Zhang, Yafei Liu, Dingyin Hu, Juan Zhao, Rongyu Tang, Yiran Lang, and Jiping He. "Rat Locomotion Detection Based on Brain Functional Directed Connectivity from Implanted Electroencephalography Signals." Brain Sciences 11, no. 3 (March 9, 2021): 345. http://dx.doi.org/10.3390/brainsci11030345.

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Previous findings have suggested that the cortex involved in walking control in freely locomotion rats. Moreover, the spectral characteristics of cortical activity showed significant differences in different walking conditions. However, whether brain connectivity presents a significant difference during rats walking under different behavior conditions has yet to be verified. Similarly, whether brain connectivity can be used in locomotion detection remains unknown. To address those concerns, we recorded locomotion and implanted electroencephalography signals in freely moving rats performing two kinds of task conditions (upslope and downslope walking). The Granger causality method was used to determine brain functional directed connectivity in rats during these processes. Machine learning algorithms were then used to categorize the two walking states, based on functional directed connectivity. We found significant differences in brain functional directed connectivity varied between upslope and downslope walking. Moreover, locomotion detection based on brain connectivity achieved the highest accuracy (91.45%), sensitivity (90.93%), specificity (91.3%), and F1-score (91.43%). Specifically, the classification results indicated that connectivity features in the high gamma band contained the most discriminative information with respect to locomotion detection in rats, with the support vector machine classifier exhibiting the most efficient performance. Our study not only suggests that brain functional directed connectivity in rats showed significant differences in various behavioral contexts but also proposed a method for classifying the locomotion states of rat walking, based on brain functional directed connectivity. These findings elucidate the characteristics of neural information interaction between various cortical areas in freely walking rats.

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20

Kohzuki, M., H. Onodera, M. Yasujima, Y. Itoyama, M. Kanazawa, T. Sato, and K. Abe. "Endothelin Receptors in Ischemic Rat Brain and Alzheimer Brain." Journal of Cardiovascular Pharmacology 26 (1995): S329–331. http://dx.doi.org/10.1097/00005344-199526003-00099.

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21

Kohzuki, M., H. Onodera, M. Yasujima, Y. Itoyama, M. Kanazawa, T. Sato, and K. Abe. "Endothelin Receptors in Ischemic Rat Brain and Alzheimer Brain." Journal of Cardiovascular Pharmacology 26 (1995): S329–331. http://dx.doi.org/10.1097/00005344-199506263-00099.

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22

Irifune, Masahiro, Tomoaki Sato, Takashige Nishikawa, Takashi Masuyama, Masahiro Nomoto, Takeo Fukuda, and Michio Kawahara. "Hyperlocomotion during Recovery from Isoflurane Anesthesia Is Associated with Increased Dopamine Turnover in the Nucleus Accumbens and Striatum in Mice." Anesthesiology 86, no. 2 (February 1, 1997): 464–75. http://dx.doi.org/10.1097/00000542-199702000-00022.

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Background It was recently reported that isoflurane increases dopamine release in the striatum in rats both in vivo and in vitro, and that isoflurane inhibits uptake of dopamine in the rat brain synaptosomes. However, the functional role of these effects of isoflurane on dopamine neurons is uncertain. Dopaminergic mechanisms within the nucleus accumbens and striatum play an important role in the control of locomotor activity, and a change in dopamine turnover depends essentially on a change in impulse flow in the dopamine neurons. In this study, the effects of isoflurane on locomotor activity and on dopamine turnover were investigated in discrete brain regions in mice. Methods Mice were placed in individual airtight clear plastic chambers and spontaneously breathed isoflurane in 25% oxygen and 75% nitrogen (fresh gas flow, 4 l/min). Locomotor activity was measured with an Animex activity meter. Animals were decapitated after treatments with or without isoflurane, and the concentrations of monoamines and their metabolites in different brain areas were measured by high-performance liquid chromatography. Results During the 10 min after the cessation of the 20-min exposure to isoflurane, there was a significant increase in locomotor activity in animals breathing 1.5% isoflurane but not 0.7% isoflurane. This increase in locomotor activity produced by 1.5% isoflurane was abolished by a low dose of haloperidol (0.1 mg/kg), a dopamine receptor antagonist. Regional brain monoamine assays revealed that 1.5% isoflurane significantly increased the 3,4-dihydroxyphenylacetic acid:dopamine ratio (one indicator of transmitter turnover) in the nucleus accumbens and striatum, but a concentration of 0.7% did not. This significant increase in dopamine turnover in these regions continued during 20 min after the cessation of the administration of 1.5% isoflurane. Conclusions These results suggest that isoflurane-induced hyperlocomotion during emergence may be associated with increased dopamine turnover in the nucleus accumbens and striatum.

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Phillips, Paddy A., Janice M. Kelly, Josephine M. Abrahams, Zbigniew Grzonka, George Paxinos, Frederick A. O. Mendelsohn, and Colin I. Johnston. "Vasopressin receptors in rat brain and kidney." Journal of Hypertension 6, no. 4 (December 1988): S550–553. http://dx.doi.org/10.1097/00004872-198812040-00173.

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Thoss, V. Silke, Dominique Duc, and Daniel Hoyer. "Somatostatin receptors in the developing rat brain." European Journal of Pharmacology 297, no. 1-2 (February 1996): 145–55. http://dx.doi.org/10.1016/0014-2999(95)00736-9.

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25

Haapaniemi, Helena, Minoru Tomita, Norio Tanahashi, Hidetaka Takeda, Masako Yokoyama, and Yasuo Fukuuchi. "Non-amoeboid locomotion of cultured microglia obtained from newborn rat brain." Neuroscience Letters 193, no. 2 (June 1995): 121–24. http://dx.doi.org/10.1016/0304-3940(95)11683-n.

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26

Cushman, Jesse, Jeannette Lo, Zhi Huang, Clive Wasserfall, and John M. Petitto. "Neurobehavioral Changes Resulting from Recombinase Activation Gene 1 Deletion." Clinical Diagnostic Laboratory Immunology 10, no. 1 (January 2003): 13–18. http://dx.doi.org/10.1128/cdli.10.1.13-18.2003.

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ABSTRACT Recombinase activation gene 1 (RAG-1) function is essential for V(D)J recombination in T-cell-receptor and immunoglobulin rearrangements whereby the immune system may encode memories of a vast array of antigens. The RAG-1 gene is also localized to neurons in the hippocampal formation and related limbic regions that are involved in spatial learning and memory as well as other parameters of neurobehavioral performance. Since the unique ability to encode memory is shared by the immune system and the brain, we tested the hypothesis that loss of the RAG-1 gene in the brain would influence learning and memory performance and examined several different domains of behavior in RAG-1-knockout and control mice. Compared to control mice, RAG-1-knockout mice exhibited increased locomotor activity in an open field under both dim and bright lighting conditions and decreased habituation (reduction in the expected decline in locomotor activity with increasing familiarity with the novel environment in a 1-h test session) in bright lighting. RAG-1-knockout mice also showed reduced levels of fearfulness for some measures of fear-motivated behavior in both the open-field behavior test and elevated-plus maze test. Contrary to our hypothesis, no differences in spatial learning and memory were found between the groups, although modest differences were observed visible-platform testing in the Morris water maze. Neither prepulse inhibition, a measure of sensorimotor gating, nor reflexive acoustic startle responses differed between the RAG-1-knockout and control mice. It remains to be determined if these changes are due to the loss of RAG-1 gene expression in the brain, are due to the absence of the gene in the immune system (e.g., the loss of cytokines with neuromodulatory activities), or are due to some combination of both effects. Study of the neurobiological actions of RAG-1 in the brain may provide new insights into important processes involved in normal brain function and disease.

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Shimizu, Yohei, Takahiro Shimizu, Suo Zou, Hideaki Ono, Yurika Hata, Masaki Yamamoto, Takaaki Aratake, et al. "Stimulation of brain α7-nicotinic acetylcholine receptors suppresses the rat micturition through brain GABAergic receptors." Biochemical and Biophysical Research Communications 548 (April 2021): 84–90. http://dx.doi.org/10.1016/j.bbrc.2021.02.051.

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Zhou, M. "Distribution of the sulphonylurea receptors in rat brain." Neuroscience Research 38 (2000): S81. http://dx.doi.org/10.1016/s0168-0102(00)81335-8.

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Imamura, Toru, Yoshihito Tokita, and Youji Mitsui. "Purification of basic FGF receptors from rat brain." Biochemical and Biophysical Research Communications 155, no. 2 (September 1988): 583–90. http://dx.doi.org/10.1016/s0006-291x(88)80534-5.

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Williams, Lynda M., Lisa T. Hannah, Michael H. Hastings, and Elizabeth S. Maywood. "Melatonin receptors in the rat brain and pituitary." Journal of Pineal Research 19, no. 4 (November 1995): 173–77. http://dx.doi.org/10.1111/j.1600-079x.1995.tb00186.x.

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31

KLOET, E. R. DE, J. M. H. M. REUL, F. R. VAN DEN BOSCH, J. A. D. M. TONNAER, and H. SAITO. "Ginsenoside RG1 and Corticosteroid Receptors in Rat Brain." Endocrinologia Japonica 34, no. 2 (1987): 213–20. http://dx.doi.org/10.1507/endocrj1954.34.213.

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32

Khan, Z. U., A. Gutiérrez, R. Martı́n, A. Peñafiel, A. Rivera, and A. de la Calle. "Dopamine D5 receptors of rat and human brain." Neuroscience 100, no. 4 (October 2000): 689–99. http://dx.doi.org/10.1016/s0306-4522(00)00274-8.

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33

Nukuda, Takashi, Koichiro Ozawa, and Tomio Segawa. "Solubilization of histamine H2-receptors from rat brain." Japanese Journal of Pharmacology 49 (1989): 85. http://dx.doi.org/10.1016/s0021-5198(19)56099-1.

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34

Gong, Jian-Ping, Emmanuel S. Onaivi, Hiroki Ishiguro, Qing-Rong Liu, Patricia A. Tagliaferro, Alicia Brusco, and George R. Uhl. "Cannabinoid CB2 receptors: Immunohistochemical localization in rat brain." Brain Research 1071, no. 1 (February 2006): 10–23. http://dx.doi.org/10.1016/j.brainres.2005.11.035.

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35

Martel, Jean-Claude, Serge St-Pierre, and Remi Quirion. "Neuropeptide Y receptors in rat brain: Autoradiographic localization." Peptides 7, no. 1 (January 1986): 55–60. http://dx.doi.org/10.1016/0196-9781(86)90061-6.

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36

Padua, Rodolfo A., James I. Nagy, and Jonathan D. Geiger. "Subcellular localization of ryanodine receptors in rat brain." European Journal of Pharmacology 298, no. 2 (March 1996): 185–89. http://dx.doi.org/10.1016/0014-2999(95)00797-0.

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37

Rimvall, Karin, F. Keller, and P. G. Waser. "Muscarinic receptors in slice cultures of rat brain." Neuropharmacology 25, no. 3 (March 1986): 221–26. http://dx.doi.org/10.1016/0028-3908(86)90243-1.

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Arrang, Jean-Michel, Nadia Defontaine, and Jean-Charles Schwartz. "Phencyclidine blocks histamine H3-receptors in rat brain." European Journal of Pharmacology 157, no. 1 (November 1988): 31–35. http://dx.doi.org/10.1016/0014-2999(88)90467-0.

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39

Cagnotto, Alfredo, Antonio Bastone, and Tiziana Mennini. "[3H](+)-Pentazocine binding to rat brain σ1 receptors." European Journal of Pharmacology: Molecular Pharmacology 266, no. 2 (January 1994): 131–38. http://dx.doi.org/10.1016/0922-4106(94)90102-3.

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40

Hoffman, Neil W., Arnold A. Gerall, and Peter W. Kalivas. "Sexual refractoriness and locomotion effects on brain monoamines in the male rat." Physiology & Behavior 41, no. 6 (January 1987): 563–69. http://dx.doi.org/10.1016/0031-9384(87)90312-x.

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41

Yang, Hui, Wei Li, Pan Meng, Zhuo Liu, Jian Liu, and Yuhong Wang. "Chronic Unpredictable Mild Stress Aggravates Mood Disorder, Cognitive Impairment, and Brain Insulin Resistance in Diabetic Rat." Evidence-Based Complementary and Alternative Medicine 2018 (December 3, 2018): 1–9. http://dx.doi.org/10.1155/2018/2901863.

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Diabetes-induced brain insulin resistance is associated with many mental diseases, including depression. Epidemiological evidences demonstrate the pathophysiologic link between stress, depression, and diabetes. This study was designed to determine whether chronic unpredictable mild stress- (CUMS-) induced changes in brain insulin resistance could contribute to deterioration in mood and cognitive functions in diabetic rats. Male SD rats were randomly assigned to three groups, including standard control group, the diabetes group, and the diabetes with CUMS group. After 7 weeks, emotional behaviors and memory performances as well as metabolic phenotypes were measured. In addition, we examined the changes in protein expression related to brain insulin signaling. Our results show that rats in diabetes with CUMS group displayed a decreased locomotor behavior in open-field test, an increased immobility time in forced swim test, and tail suspension test, and an impaired learning and memory in the Morris water maze when compared to animals in diabetes group. Further, diabetes with CUMS exhibited a significant decrease in phosphorylation of insulin receptor and an increase phosphorylation of IRS-1 in brain. These results suggest that the depression-like behaviors and cognitive function impairments in diabetic rats with CUMS were related to the changes of brain insulin signaling.

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42

Fouad, K., M. M. Rank, R. Vavrek, K. C. Murray, L. Sanelli, and D. J. Bennett. "Locomotion After Spinal Cord Injury Depends on Constitutive Activity in Serotonin Receptors." Journal of Neurophysiology 104, no. 6 (December 2010): 2975–84. http://dx.doi.org/10.1152/jn.00499.2010.

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Following spinal cord injury (SCI) neurons caudal to the injury are capable of rhythmic locomotor-related activity that can form the basis for substantial functional recovery of stepping despite the loss of crucial brain stem-derived neuromodulators like serotonin (5-HT). Here we investigated the contribution of constitutive 5-HT2 receptor activity (activity in the absence of 5-HT) to locomotion after SCI. We used a staggered hemisection injury model in rats to study this because these rats showed a robust recovery of locomotor function and yet a loss of most descending axons. Immunolabeling for 5-HT showed little remaining 5-HT below the injury, and locomotor ability was not correlated with the amount of residual 5-HT. Furthermore, blocking 5-HT2 receptors with an intrathecal (IT) application of the neutral antagonist SB242084 did not affect locomotion (locomotor score and kinematics were unaffected), further indicating that residual 5-HT below the injury did not contribute to generation of locomotion. As a positive control, we found that the same application of SB242084 completely antagonized the muscle activity induced by exogenous application of the 5-HT2 receptor agonists alpha-methyl-5-HT (IT). In contrast, blocking constitutive 5-HT2 receptor activity with the potent inverse agonist SB206553 (IT) severely impaired stepping as assessed with kinematic recordings, eliminating most hindlimb weight support and overall reducing the locomotor score in both hind legs. However, even in the most severely impaired animals, rhythmic sweeping movements of the hindlimb feet were still visible during forelimb locomotion, suggesting that SB206553 did not completely eliminate locomotor drive to the motoneurons or motoneuron excitability. The same application of SB206553 had no affect on stepping in normal rats. Thus while normal rats can compensate for loss of 5-HT2 receptor activity, after severe spinal cord injury rats require constitutive activity in these 5-HT2 receptors to produce locomotion.

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43

Atsuta, Y., E. Garcia-Rill, and R. D. Skinner. "Characteristics of electrically induced locomotion in rat in vitro brain stem-spinal cord preparation." Journal of Neurophysiology 64, no. 3 (September 1, 1990): 727–35. http://dx.doi.org/10.1152/jn.1990.64.3.727.

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1. Electrical stimulation of two brain stem regions in the decerebrate neonatal rat brain--the mesencephalic locomotor region (MLR) and the medioventral medulla (MED)--were found to elicit rhythmic limb movements in the hind-limb-attached, in vitro, brain stem-spinal cord preparation. 2. Electromyographic (EMG) analysis revealed locomotion similar to that observed during stepping in the adult rat. The step-cycle frequency could be increased by application of higher-amplitude currents; but, unlike the adult, alternation could not be driven to a gallop. 3. Threshold currents for inducing locomotion were significantly lower for stimulation of the MED compared with the MLR. Brain stem transections carried out at midpontine levels demonstrated that the presence of the MLR was not required for the expression of MED-stimulation-induced effects. 4. Substitution of the standard artificial cerebrospinal fluid (aCSF) by magnesium-free aCSF did not affect interlimb relationships and resulted in a significant decrease of the threshold currents for inducing locomotion. 5. Fixation of the limbs during electrical stimulation of brain stem sites altered the amplitude and duration of the EMG patterns, but the basic rhythm and timing of each muscle contraction during the step cycle was not affected. 6. These studies suggest that, although peripheral afferent modulation is evident in the neonatal locomotor control system, descending projections from brain stem-locomotor regions appear capable of modulating the activity of spinal pattern generators as early as the day of birth. However, there may be ceiling to the maximal frequency of stepping possible at this early age, perhaps suggesting a later-developing mechanism for galloping.

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44

Dourado, Margarida, Helder Cardoso-Cruz, Clara Monteiro, and Vasco Galhardo. "Effect of Motor Impairment on Analgesic Efficacy of Dopamine D2/3 Receptors in a Rat Model of Neuropathy." Journal of Experimental Neuroscience 10 (January 2016): JEN.S36492. http://dx.doi.org/10.4137/jen.s36492.

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Testing the clinical efficacy of drugs that also have important side effects on locomotion needs to be properly designed in order to avoid erroneous identification of positive effects when the evaluation depends on motor-related tests. One such example is the evaluation of analgesic role of drugs that act on dopaminergic receptors, since the pain perception tests used in animal models are based on motor responses that can also be compromised by the same substances. The apparent analgesic effect obtained by modulation of the dopaminergic system is still a highly disputed topic. There is a lack of acceptance of this effect in both preclinical and clinical settings, despite several studies showing that D2/3 agonists induce antinociception. Some authors raised the hypothesis that this antinociceptive effect is enhanced by dopamine-related changes in voluntary initiation of movement. However, the extent to which D2/3 modulation changes locomotion at analgesic effective doses is still an unresolved question. In the present work, we performed a detailed dose-dependent analysis of the changes that D2/3 systemic modulation have on voluntary locomotor activity and response to four separate tests of both thermal and mechanical pain sensitivity in adult rats. Using systemic administration of the dopamine D2/3 receptor agonist quinpirole, and of the D2/3 antagonist raclopride, we found that modulation of D2/3 receptors impairs locomotion and exploratory activity in a dose-dependent manner across the entire range of tested dosages. None of the drugs were able to consistently diminish either thermal or mechanical pain perception when administered at lower concentrations; on the other hand, the larger concentrations of raclopride (0.5–1.0 mg/kg) strongly abolished pain responses, and also caused severe motor impairment. Our results show that administration of both agonists and antagonists of dopaminergic D2/3 receptors affects sensorimotor behaviors, with the effect over locomotion and exploratory activity being stronger than the observed effect over pain responses.

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45

Brown, J., and A. Czarnecki. "Autoradiographic localization of atrial and brain natriuretic peptide receptors in rat brain." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 1 (January 1, 1990): R57—R63. http://dx.doi.org/10.1152/ajpregu.1990.258.1.r57.

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Displacement of bound 125I-labeled atrial natriuretic peptide-(1-28) [alpha 125I-ANP-(1-28)] by alpha-ANP-(5-28) and porcine brain natriuretic peptide (BNP) was used to map receptors common to these peptides in rat brain by in vitro autoradiography. alpha-125I-ANP bound reversibly to subfornical organ, area postrema, median preoptic, supraoptic and paraventricular nuclei, and arachnoid mater. Binding at these sites was displaced similarly by 1 microM unlabeled alpha-ANP, alpha-ANP-(5-28), and BNP. Binding dissociation constants in the subfornical organ and arachnoid were 4.40 +/- 1.15 and 3.99 +/- 0.86 nM, respectively, for alpha-ANP, and 2.41 +/- 1.11 and 2.23 +/- 1.06 nM, respectively, for BNP. alpha-125I-ANP also bound to choroid plexus. Here 1 microM unlabeled alpha-ANP displaced significantly more radioligand than did 1 microM BNP, and the concentration displacing 50% of bound radioligand was 2.23 +/- 0.78 nM for alpha-ANP and 1.51 +/- 0.67 nM for BNP. alpha-ANP-(5-28) also displaced alpha 125I-ANP at all sites with significantly greater affinity than did unlabeled alpha-ANP. alpha-125I-ANP was not displaced by completely unrelated peptides. Therefore, both atrial and brain natriuretic peptides may be high-affinity ligands at common receptors in some cerebral localities.

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46

Ninomiya, Haruaki, Shun Shimohama, Takashi Taniguchi, Soichi Miwa, and Motohatsu Fujiwara. "Effects of hypoxia on muscarinic receptors in rat brain." Japanese Journal of Pharmacology 43 (1987): 268. http://dx.doi.org/10.1016/s0021-5198(19)58609-7.

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47

Whitcomb, D. C., A. M. Puccio, S. R. Vigna, I. L. Taylor, and G. E. Hoffman. "Distribution of pancreatic polypeptide receptors in the rat brain." Brain Research 760, no. 1-2 (June 1997): 137–49. http://dx.doi.org/10.1016/s0006-8993(97)00295-3.

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48

Kidd, E. J., K. J. Miller, A. J. Sansum, and P. P. A. Humphrey. "Evidence for P2X3 receptors in the developing rat brain." Neuroscience 87, no. 3 (August 1998): 533–39. http://dx.doi.org/10.1016/s0306-4522(98)00294-2.

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49

Balcar, Vladimir J., Yi Li, Suzanne Killinger, and Maxwell R. Bennett. "Autoradiography of P2X ATP receptors in the rat brain." British Journal of Pharmacology 115, no. 2 (May 1995): 302–6. http://dx.doi.org/10.1111/j.1476-5381.1995.tb15877.x.

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50

Helmke, S. M., and D. M. F. Cooper. "Solubilization of stable adenosine A1 receptors from rat brain." Biochemical Journal 257, no. 2 (January 15, 1989): 413–18. http://dx.doi.org/10.1042/bj2570413.

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Abstract:

Despite numerous reports of solubilization of adenosine A1 receptors, little progress has been made in isolating or purifying the receptor, owing to the extreme lability of the preparations. The present solubilization strategies recognized the possible role of endogenous adenosine to produce adenosine-receptor-N-protein complexes, which are intrinsically unstable, and instead attempted to use caffeine to solubilize free adenosine receptors, which might be more stable. Endogenous adenosine was removed from membranes by using adenosine deaminase along with GTP to accelerate the release of receptor-bound adenosine. The receptors were then occupied with caffeine and solubilized with 3-[(3-cholamidopropyl)-dimethylammonio]-1-propanesulphonate (CHAPS) in the presence of glycerol. These soluble preparations exhibited the characteristics of free adenosine receptors. They bound the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPDPX) with high affinity to a single class of binding sites, which were insensitive to GTP. The binding activity was extremely stable, with a half-life of about 5 days at 4 degrees C; there was little change in either receptor number or affinity during 3 days at 4 degrees C. This methodology should greatly facilitate the characterization, isolation and purification of the adenosine A1 receptor.

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

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