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Author (up) Bi, L.-L.; Wang, J.; Luo, Z.-Y.; Chen, S.-P.; Geng, F.; Chen, Y.-hua; Li, S.-J.; Yuan, C.-hua; Lin, S.; Gao, T.-M. file  url
  Title Enhanced excitability in the infralimbic cortex produces anxiety-like behaviors Type Journal Article
  Year 2013 Publication Neuropharmacology Abbreviated Journal Neuropharmacology  
  Volume 72 Issue Pages 148-156  
  Keywords 6-Cyano-7-nitroquinoxaline-2,3-dione/pharmacology/therapeutic use; Animals; Animals, Newborn; Anxiety/chemically induced/drug therapy/*pathology; Bicuculline/toxicity; Disease Models, Animal; Excitatory Amino Acid Antagonists/pharmacology/therapeutic use; Excitatory Postsynaptic Potentials/drug effects/*physiology; Exploratory Behavior/drug effects; GABA-A Receptor Antagonists/toxicity; In Vitro Techniques; Inhibitory Postsynaptic Potentials/drug effects; Injections, Intraventricular; Male; Maze Learning/drug effects; Mice; Mice, Inbred C57BL; Patch-Clamp Techniques; Prefrontal Cortex/drug effects/*physiopathology  
  Abstract The medial prefrontal cortex (mPFC) has been implicated in modulating anxiety. However, it is unknown whether excitatory or inhibitory neurotransmission in the infralimbic (IL) subregion of the mPFC underlies the pathology of anxiety-related behavior. To address this issue, we infused the GABAA receptor (GABAAR) antagonist bicuculline to temporarily activate the IL cortex. IL cortex activation decreased the time spent in the center area in the open field test, decreased exploration of the open-arms in the elevated plus maze test, and increased the latency to bite food in the novelty-suppressed feeding test. These findings substantiate the GABAergic system's role in anxiety-related behaviors. IL cortex inactivation with the AMPA receptor (AMPAR) antagonist CNQX produced opposite, anxiolytic effects. However, infusion of the NMDA receptor (NMDAR) antagonist AP5 into the IL cortex had no significant effect. Additionally, we did not observe motor activity deficits or appetite deficits following inhibition of GABAergic or glutamatergic neurotransmission. Interestingly, we found parallel and corresponding electrophysiological changes in anxious mice; compared to mice with relatively low anxiety, the relatively high anxiety mice exhibited smaller evoked inhibitory postsynaptic currents (eIPSCs) and larger AMPA-mediated evoked excitatory postsynaptic currents (eEPSCs) in pyramidal neurons in the IL cortex. The changes of eIPSCs and eEPSCs were due to presynaptic mechanisms. Our results suggest that imbalances of neurotransmission in the IL cortex may cause a net increase in excitatory inputs onto pyramidal neurons, which may underlie the pathogenic mechanism of anxiety disorders.  
  Call Number Serial 1045  
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Author (up) Crider, M.E.; Cooper, R.L. file  url
  Title Importance of stimulation paradigm in determining facilitation and effects of neuromodulation Type Journal Article
  Year 1999 Publication Brain Research Abbreviated Journal Brain Res  
  Volume 842 Issue 2 Pages 324-331  
  Keywords Animals; Astacoidea; Axons/*physiology; Electric Stimulation; Electromyography; Evoked Potentials; In Vitro Techniques; Membrane Potentials; Muscle, Skeletal/innervation/physiology; Nerve Endings/physiology; Neuromuscular Junction/*physiology; Synaptic Transmission/physiology  
  Abstract Evoked synaptic activity within the CNS and at the neuromuscular junction in most in vivo preparations studied occurs not with single isolated stimuli, but with trains, or bursts, of stimuli. Although for ease in studying the mechanisms of vesicular synaptic transmission one often uses single discrete stimuli, the true mechanisms in the animal may be far more complex. When repetitive stimuli are present at a nerve terminal, often a heightened (i.e., facilitated) postsynaptic potential can be as a result. Facilitation is commonly used as an index of synaptic function and plasticity induced by chronic stimulation or by neuromodulation. The mechanisms that give rise to facilitation are thought to be the same that may underlie short-term learning and memory [C.H. Bailey, E.R. Kandel, Structural changes accompanying memory storage. Annu. Rev. Physiol. 55 (1993) 397-426.]. Differences in short term facilitation (STF) are seen depending on the conventional stimulation paradigm (twin pulse, train, or continuous) used to induce facilitation. Thus, a battery of paradigms should be used to characterize synaptic function to obtain a closer understanding of the possible in vivo conditions.  
  Call Number Serial 1593  
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Author (up) Edwards, R.G. file  url
  Title Maturation in vitro of mouse, sheep, cow, pig, rhesus monkey and human ovarian oocytes Type Journal Article
  Year 1965 Publication Nature Abbreviated Journal Nature  
  Volume 208 Issue 5008 Pages 349-351  
  Keywords Animals; Cattle; *Cell Division; Culture Media; Female; Haplorhini; Humans; In Vitro Techniques; Mice; *Ovum; Sheep; Swine  
  Abstract “The investigation of early development in many mammalian species is restricted by the difficulty of obtaining sufficient numbers of oocytes and embryos at particular stages of development.”  
  Call Number Serial 1159  
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Author (up) Hage, T.A.; Khaliq, Z.M. file  url
doi  openurl
  Title Tonic firing rate controls dendritic Ca2+ signaling and synaptic gain in substantia nigra dopamine neurons Type Journal Article
  Year 2015 Publication The Journal of Neuroscience : the Official Journal of the Society for Neuroscience Abbreviated Journal J Neurosci  
  Volume 35 Issue 14 Pages 5823-5836  
  Keywords Action Potentials/*physiology; Animals; Animals, Newborn; Calcium/*metabolism; Calcium Signaling/drug effects/*physiology; Dopaminergic Neurons/*cytology; Female; Glutamic Acid/pharmacology; In Vitro Techniques; Male; Mice; Microscopy, Confocal; Neurotransmitter Agents/pharmacology; Patch-Clamp Techniques; Substantia Nigra/*cytology; Synapses/drug effects/*physiology; action potential; backpropagation; calcium imaging; dendrite; dopamine; substantia nigra  
  Abstract Substantia nigra dopamine neurons fire tonically resulting in action potential backpropagation and dendritic Ca(2+) influx. Using Ca(2+) imaging in acute mouse brain slices, we find a surprisingly steep relationship between tonic firing rate and dendritic Ca(2+). Increasing the tonic rate from 1 to 6 Hz generated Ca(2+) signals up to fivefold greater than predicted by linear summation of single spike-evoked Ca(2+)-transients. This “Ca(2+) supralinearity” was produced largely by depolarization of the interspike voltage leading to activation of subthreshold Ca(2+) channels and was present throughout the proximal and distal dendrites. Two-photon glutamate uncaging experiments show somatic depolarization enhances NMDA receptor-mediated Ca(2+) signals >400 mum distal to the soma, due to unusually tight electrotonic coupling of the soma to distal dendrites. Consequently, we find that fast tonic firing intensifies synaptically driven burst firing output in dopamine neurons. These results show that modulation of background firing rate precisely tunes dendritic Ca(2+) signaling and provides a simple yet powerful mechanism to dynamically regulate the gain of synaptic input.  
  Call Number Serial 1135  
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Author (up) Sitdikova, G.F.; Islamov, R.R.; Mukhamedyarov, M.A.; Permyakova, V.V.; Zefirov, A.L.; Palotas, A. file  url
  Title Modulation of neurotransmitter release by carbon monoxide at the frog neuro-muscular junction Type Journal Article
  Year 2007 Publication Current Drug Metabolism Abbreviated Journal Curr Drug Metab  
  Volume 8 Issue 2 Pages 177-184  
  Keywords Acetylcholine/*metabolism; Animals; Carbon Monoxide/*pharmacology; Cyclic AMP/metabolism; Cyclic GMP/metabolism; Heme Oxygenase (Decyclizing)/metabolism; In Vitro Techniques; Muscle, Skeletal/metabolism; Neuromuscular Junction/*metabolism; Rana ridibunda; Synaptic Transmission/drug effects  
  Abstract Carbon monoxide (CO) is an endogenous gaseous messenger, which regulates numerous physiological functions in a wide variety of tissues. Using extracellular microelectrode recording from frog neuro-muscular preparation the mechanisms of exogenous and endogenous CO action on evoked quantal acetyl-choline (Ach) release were studied. It was shown that CO application increases Ach-release in dose-dependent manner without changes in pre-synaptic Na+ and K+ currents. The effect of exogenous CO on Ach-release was decreased by prior application of guanylate cyclase inhibitor ODQ and prevented by application of a cyclic guanylate monophosphate (cGMP) analog 8Br-cGMP. Pre-treatment of the preparation with adenylate cyclase inhibitor MDL-12330A has completely abolished the effect of CO, whereas elevation of intracellular level of cyclic adenosine monophosphate (cAMP) mimicked and eliminated CO action. Application of cGMP-activated phosphodiesterase-2 inhibitor EHNA did not prevent CO action, whereas inhibition of cGMP-inhibited phosphodiesterase-3 by quazinone has partially blocked the effect of CO. Utilizing immuno-histochemical methods CO-producing enzyme heme-oxygenase-2 (HO-2) was shown to be expressed in skeletal muscle fibers, mostly in sub-sarcolemmal region, karyolemma and sarcoplasmic reticulum. Zn-protoporphirin-IX, the selective HO-2 blocker, has depressed Ach-release, suggesting the tonic activating effect of endogenous CO on pre-synaptic function. These results suggest that facilitatory effect of CO on Ach-release is mediated by elevation of intracellular cAMP level due to activation of adenylate cyclase and decrease of cAMP breakdown. As such, endogenous skeletal muscle-derived CO mediates tonic retrograde up-regulation of neuro-transmitter release at the frog neuro-muscular junction.  
  Call Number Serial 1316  
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Author (up) Waring, M.J. file  url
  Title Complex formation between ethidium bromide and nucleic acids Type Journal Article
  Year 1965 Publication Journal of Molecular Biology Abbreviated Journal J Mol Biol  
  Volume 13 Issue 1 Pages 269-282  
  Keywords Animals; *Antiprotozoal Agents; Chemical Phenomena; Chemistry; Coliphages; *Dna; DNA, Bacterial; DNA, Viral; In Vitro Techniques; Ion Exchange Resins/cytology; Liver/chemically induced; Micrococcus; Rna; Rats; Ribosomes; Spectrophotometry  
  Abstract The interaction between ethidium bromide and nucleic acids shows a pronounced metachromatic effect which has been used to obtain quantitative data on the process of complex formation. Ethidium binds strongly to both DNA and RNA at sites which appear to be saturated when one drug molecule is bound for every 4 or 5 nucleotides. After the primary sites have been filled, a secondary binding process can occur, leading to the precipitation of a complex containing one drug molecule bound per nucleotide. The strong primary binding to DNA is not influenced by the base-composition or by denaturation of the DNA, but is sensitive to changes in the salt concentration, particularly when magnesium ions are present. Addition of magnesium chloride causes a marked reduction in the strength of the interaction without significantly affecting the number of sites available to bind the drug. The process of complex formation is shown to be reversible in solution by demonstrating an exchange reaction between free and bound ethidium. Complexes between ethidium and DNA can be dissociated by using a cation-exchange resin.

The binding of ethidium to DNA follows a similar pattern to that found with proflavine, suggesting that the forces involved in the binding of the two drugs may be similar.
  Call Number Serial 1559  
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