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Author (up) Andersson, D.R.; Bjornsson, E.; Bergquist, F.; Nissbrandt, H. file  url
openurl 
  Title Motor activity-induced dopamine release in the substantia nigra is regulated by muscarinic receptors Type Journal Article
  Year 2010 Publication Experimental Neurology Abbreviated Journal Exp Neurol  
  Volume 221 Issue 1 Pages 251-259  
  Keywords Analysis of Variance; Animals; Area Under Curve; Brain Injuries/chemically induced/*pathology; Chromatography, High Pressure Liquid/methods; Dendrites/drug effects/metabolism; Disease Models, Animal; Dopamine/*metabolism; Dose-Response Relationship, Drug; Electrochemistry/methods; Female; Functional Laterality; Mecamylamine/pharmacology; Microdialysis/methods; Motor Activity/drug effects/*physiology; Muscarinic Antagonists/pharmacology; Nicotinic Antagonists/pharmacology; Oxidopamine; Rats; Rats, Sprague-Dawley; Receptors, Muscarinic/*physiology; Rotarod Performance Test/methods; Scopolamine Hydrobromide/pharmacology; Substantia Nigra/drug effects/*metabolism/pathology; gamma-Aminobutyric Acid/metabolism  
  Abstract Nigro-striatal neurons release dopamine not only from their axon terminals in the striatum, but also from somata and dendrites in the substantia nigra. Somatodendritic dopamine release in the substantia nigra can facilitate motor function by mechanisms that may act independently of axon terminal dopamine release in the striatum. The dopamine neurons in the substantia nigra receive a cholinergic input from the pedunculopontine nucleus. Despite recent efforts to introduce this nucleus as a potential target for deep brain stimulation to treat motor symptoms in Parkinson's disease; and the well-known antiparkinsonian effects of anticholinergic drugs; the cholinergic influence on somatodendritic dopamine release is not well understood. The aim of this study was to investigate the possible regulation of locomotor-induced dopamine release in the substantia nigra by endogenous acetylcholine release. In intact and 6-OHDA hemi-lesioned animals alike, the muscarinic antagonist scopolamine, when perfused in the substantia nigra, amplified the locomotor-induced somatodendritic dopamine release to approximately 200% of baseline, compared to 120-130% of baseline in vehicle-treated animals. A functional importance of nigral muscarinic receptor activation was demonstrated in hemi-lesioned animals, where motor performance was significantly improved by scopolamine to 82% of pre-lesion performance, as compared to 56% in vehicle-treated controls. The results indicate that muscarinic activity in the substantia nigra is of functional importance in an animal Parkinson's disease model, and strengthen the notion that nigral dopaminergic regulation of motor activity/performance is independent of striatal dopamine release.  
  Call Number Serial 308  
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Author (up) Arias-Carrion, O.; Palomero-Rivero, M.; Millan-Aldaco, D.; Haro, R.; Drucker-Colin, R.; Murillo-Rodriguez, E. file  url
doi  openurl
  Title Infusion of modafinil into anterior hypothalamus or pedunculopontine tegmental nucleus at different time-points enhances waking and blocks the expression of recovery sleep in rats after sleep deprivation Type Journal Article
  Year 2011 Publication Experimental Neurology Abbreviated Journal Exp Neurol  
  Volume 229 Issue 2 Pages 358-363  
  Keywords Analysis of Variance; Animals; Benzhydryl Compounds/pharmacology/*therapeutic use; Central Nervous System Stimulants/pharmacology/*therapeutic use; Electroencephalography; Hypothalamus, Anterior/*drug effects; Microinjections; Pedunculopontine Tegmental Nucleus/*drug effects; Rats; Sleep/*drug effects; Sleep Deprivation/*drug therapy; Wakefulness/*drug effects  
  Abstract Clinical studies have indicated that the primary pharmacological activity of modafinil (MOD) is inducing wakefulness; however, the brain targets that underlie its wake-promoting activity have not been described. In the present study, we show that MOD injected into sleep-wake related brain areas promoted alertness. If administered (10, 20, or 30 mug/1 muL) into either anterior hypothalamus (AH) or pedunculopontine tegmental nucleus (PPTg) at 08:00, 12:00 or 16:00 h, MOD enhanced wakefulness whereas diminished slow wave sleep as well as rapid eye movement sleep. In addition, microinjection of MOD (10, 20, or 30 mug/1 muL) either into AH or PPTg after total sleep deprivation prevented the sleep rebound. Taken together, these observations suggest that AH and PPTg play a key role in the wake-inducing effects of MOD and encourage further experimentation to draw a possible mechanism of action.  
  Call Number Serial 330  
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Author (up) Arolfo, M.P.; Brioni, J.D. file  url
openurl 
  Title Diazepam impairs place learning in the Morris water maze Type Journal Article
  Year 1991 Publication Behavioral and Neural Biology Abbreviated Journal Behav Neural Biol  
  Volume 55 Issue 1 Pages 131-136  
  Keywords Animals; Diazepam/*pharmacology; Discrimination Learning/*drug effects; Dose-Response Relationship, Drug; Escape Reaction/*drug effects; Male; Mental Recall/drug effects; Orientation/*drug effects; Rats; Rats, Inbred Strains; Reaction Time/drug effects; Retention (Psychology)/*drug effects  
  Abstract The effect of diazepam (0.3, 1.0, and 3.0 mg/kg) on the acquisition and retention of place learning was evaluated. The analysis of escape latencies indicates that 1.0 and 3.0 mg/kg diazepam significantly impaired the retention of spatial information. When a free swim trial was carried out only control animals showed spatial bias to the target quadrant. The absence of spatial bias in the group that received 0.3 mg/kg suggests that the amnesic effect of diazepam can be seen at doses similar to or even lower than the anxiolytic ones, and that the GABA/benzodiazepine receptor complex is highly sensitive to the cognitive impairment induced by diazepam in spatial tasks.  
  Call Number Serial 249  
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Author (up) Arrant, A.E.; Schramm-Sapyta, N.L.; Kuhn, C.M. file  url
openurl 
  Title Use of the light/dark test for anxiety in adult and adolescent male rats Type Journal Article
  Year 2013 Publication Behavioural Brain Research Abbreviated Journal Behav Brain Res  
  Volume 256 Issue Pages 119-127  
  Keywords Adrenergic alpha-2 Receptor Antagonists/pharmacology; Age Factors; Animals; Antidepressive Agents/pharmacology; Anxiety/*diagnosis/drug therapy; Carbolines/pharmacology; Exploratory Behavior/drug effects; Factor Analysis, Statistical; *Light; Male; Motor Activity/drug effects; *Neuropsychological Tests; Rats, Sprague-Dawley; Regression Analysis; Risk-Taking; Time Factors; Yohimbine/pharmacology; Adolescence; Anxiety; Fg-7142; Factor analysis; Light/dark test; Yohimbine  
  Abstract The light/dark (LD) test is a commonly used rodent test of unconditioned anxiety-like behavior that is based on an approach/avoidance conflict between the drive to explore novel areas and an aversion to brightly lit, open spaces. We used the LD test to investigate developmental differences in behavior between adolescent (postnatal day (PN) 28-34) and adult (PN67-74) male rats. We investigated whether LD behavioral measures reflect anxiety-like behavior similarly in each age group using factor analysis and multiple regression. These analyses showed that time in the light compartment, percent distance in the light, rearing, and latency to emerge into the light compartment were measures of anxiety-like behavior in each age group, while total distance traveled and distance in the dark compartment provided indices of locomotor activity. We then used these measures to assess developmental differences in baseline LD behavior and the response to anxiogenic drugs. Adolescent rats emerged into the light compartment more quickly than adults and made fewer pokes into the light compartment. These age differences could reflect greater risk taking and less risk assessment in adolescent rats than adults. Adolescent rats were less sensitive than adults to the anxiogenic effects of the benzodiazepine inverse agonist N-methyl-beta-carboline-3-carboxamide (FG-7142) and the alpha(2) adrenergic antagonist yohimbine on anxiety-like behaviors validated by factor analysis, but locomotor variables were similarly affected. These data support the results of the factor analysis and indicate that GABAergic and noradrenergic modulation of LD anxiety-like behavior may be immature during adolescence.  
  Call Number Serial 1614  
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Author (up) Atherton, P.J.; Babraj, J.; Smith, K.; Singh, J.; Rennie, M.J.; Wackerhage, H. file  url
openurl 
  Title Selective activation of AMPK-PGC-1alpha or PKB-TSC2-mTOR signaling can explain specific adaptive responses to endurance or resistance training-like electrical muscle stimulation Type Journal Article
  Year 2005 Publication FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology Abbreviated Journal Faseb J  
  Volume 19 Issue 7 Pages 786-788  
  Keywords Adaptation, Physiological; Adenylate Kinase/*metabolism; Animals; Electric Stimulation; Enzyme Activation; Male; Mitogen-Activated Protein Kinases/metabolism; Muscle Contraction; Muscle Proteins/biosynthesis; Muscle, Skeletal/*physiology; Myofibrils/metabolism; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Phosphorylation; Physical Conditioning, Animal; Physical Endurance/physiology; Physical Exertion; Protein Kinases/*metabolism; Proto-Oncogene Proteins c-akt/*metabolism; RNA-Binding Proteins/*metabolism; Rats; Rats, Wistar; Sarcoplasmic Reticulum/metabolism; Signal Transduction; TOR Serine-Threonine Kinases; Transcription Factors/*metabolism; Tumor Suppressor Proteins/*metabolism  
  Abstract Endurance training induces a partial fast-to-slow muscle phenotype transformation and mitochondrial biogenesis but no growth. In contrast, resistance training mainly stimulates muscle protein synthesis resulting in hypertrophy. The aim of this study was to identify signaling events that may mediate the specific adaptations to these types of exercise. Isolated rat muscles were electrically stimulated with either high frequency (HFS; 6x10 repetitions of 3 s-bursts at 100 Hz to mimic resistance training) or low frequency (LFS; 3 h at 10 Hz to mimic endurance training). HFS significantly increased myofibrillar and sarcoplasmic protein synthesis 3 h after stimulation 5.3- and 2.7-fold, respectively. LFS had no significant effect on protein synthesis 3 h after stimulation but increased UCP3 mRNA 11.7-fold, whereas HFS had no significant effect on UCP3 mRNA. Only LFS increased AMPK phosphorylation significantly at Thr172 by approximately 2-fold and increased PGC-1alpha protein to 1.3 times of control. LFS had no effect on PKB phosphorylation but reduced TSC2 phosphorylation at Thr1462 and deactivated translational regulators. In contrast, HFS acutely increased phosphorylation of PKB at Ser473 5.3-fold and the phosphorylation of TSC2, mTOR, GSK-3beta at PKB-sensitive sites. HFS also caused a prolonged activation of the translational regulators p70 S6k, 4E-BP1, eIF-2B, and eEF2. These data suggest that a specific signaling response to LFS is a specific activation of the AMPK-PGC-1alpha signaling pathway which may explain some endurance training adaptations. HFS selectively activates the PKB-TSC2-mTOR cascade causing a prolonged activation of translational regulators, which is consistent with increased protein synthesis and muscle growth. We term this behavior the “AMPK-PKB switch.” We hypothesize that the AMPK-PKB switch is a mechanism that partially mediates specific adaptations to endurance and resistance training, respectively.  
  Call Number Serial 2075  
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