more information
Search within Results:

Select All    Deselect All
 |   | 
Details
   print
  Records Links
Author (up) Amici, M.; Eusebi, F.; Miledi, R. file  url
openurl 
  Title Effects of the antibiotic gentamicin on nicotinic acetylcholine receptors Type Journal Article
  Year 2005 Publication Neuropharmacology Abbreviated Journal Neuropharmacology  
  Volume 49 Issue 5 Pages 627-637  
  Keywords Animals; Anti-Bacterial Agents--pharmacology; Cochlea--drug effects; DNA, Complementary--biosynthesis; Electrophysiology; Gentamicins--pharmacology; Humans; Membrane Potentials--drug effects, physiology; Mice; Nicotinic Antagonists; Oocytes--metabolism; Patch-Clamp Techniques; RNA, Complementary--biosynthesis; Receptors, Nicotinic--biosynthesis, drug effects, genetics; Torpedo; Vestibule, Labyrinth--drug effects; Xenopus; alpha7 Nicotinic Acetylcholine Receptor  
  Abstract Medical treatment with the aminoglycosidic antibiotic gentamicin may produce side effects that include neuromuscular blockage and ototoxicity; which are believed to result from a dysfunction of nicotinic acetylcholine receptors (AChRs). Gentamicin is known to reversibly block ACh-currents generated by the activation of muscle-type alphabetagammadelta-AChR and neuronal alpha9-AChR. We studied the effects of gentamicin on heteromeric alphabetagammadelta-AChR and homomeric alpha7-AChR expressed in Xenopus oocytes. Prolonged treatment with gentamicin, and other antibiotics, differentially altered alphabetagammadelta- and alpha7-AChR responses. Specifically, gentamicin accelerated desensitization and did not reduce ACh-currents in oocytes expressing alphabetagammadelta-AChRs, whereas ACh-currents were reduced and desensitization was unaltered in oocytes expressing alpha7-AChRs. Moreover, acutely applied gentamicin acted as a competitive antagonist on both types of receptors and increased the rate of desensitization in alphabetagammadelta-AChR while reducing the rate of desensitization in alpha7-AChR. This data helps to better understand the action of gentamicin on muscle and nervous tissues, providing mechanistic insights that could eventually lead to improving the medical use of aminoglycosides.  
  Call Number Serial 445  
Permanent link to this record
 

 
Author (up) Bayer, L.; Eggermann, E.; Serafin, M.; Grivel, J.; Machard, D.; Muhlethaler, M.; Jones, B.E. file  url
doi  openurl
  Title Opposite effects of noradrenaline and acetylcholine upon hypocretin/orexin versus melanin concentrating hormone neurons in rat hypothalamic slices Type Journal Article
  Year 2005 Publication Neuroscience Abbreviated Journal Neuroscience  
  Volume 130 Issue 4 Pages 807-811  
  Keywords Acetylcholine/pharmacology/*physiology; Action Potentials/drug effects/physiology; Animals; Arousal/drug effects/physiology; Cholinergic Agonists/pharmacology; Hypothalamic Area, Lateral/cytology/drug effects/*metabolism; Hypothalamic Hormones/*metabolism; Intracellular Signaling Peptides and Proteins/*metabolism; Locus Coeruleus/physiology; Melanins/*metabolism; Models, Neurological; Neural Inhibition/drug effects/physiology; Neural Pathways/cytology/drug effects/metabolism; Neurons/drug effects/*metabolism; Neuropeptides/*metabolism; Norepinephrine/pharmacology/*physiology; Organ Culture Techniques; Patch-Clamp Techniques; Pedunculopontine Tegmental Nucleus/physiology; Pituitary Hormones/*metabolism; Rats; Rats, Sprague-Dawley; Sleep/physiology; Synaptic Transmission/drug effects/physiology  
  Abstract Hypocretin/orexin (Hcrt/Orx) and melanin concentrating hormone (MCH) are peptides contained in overlapping cell groups of the lateral hypothalamus and commonly involved in regulating sleep-wake states and energy balance, though likely in different ways. To see if these neurons are similarly or differentially modulated by neurotransmitters of the major brainstem arousal systems, the effects of noradrenaline (NA) and carbachol, a cholinergic agonist, were examined on identified Hcrt/Orx and MCH neurons in rat hypothalamic slices. Whereas both agonists depolarized and excited Hcrt/Orx neurons, they both hyperpolarized MCH neurons by direct postsynaptic actions. According to the activity profiles of the noradrenergic locus coeruleus and cholinergic pontomesencephalic neurons across the sleep-waking cycle, the Hcrt/Orx neurons would be excited by NA and acetylcholine (ACh) and thus active during arousal, whereas the MCH neurons would be inhibited by NA and ACh and thus inactive during arousal while disinhibited and possibly active during slow wave sleep. According to the present pharmacological results, Hcrt/Orx neurons may thus stimulate arousal in tandem with other arousal systems, whereas MCH neurons may function in opposition with other arousal systems and thus potentially dampen arousal to promote sleep.  
  Call Number Serial 331  
Permanent link to this record
 

 
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
openurl 
  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  
Permanent link to this record
 

 
Author (up) Conrad, K.L.; Louderback, K.M.; Gessner, C.P.; Winder, D.G. file  url
doi  openurl
  Title Stress-induced alterations in anxiety-like behavior and adaptations in plasticity in the bed nucleus of the stria terminalis Type Journal Article
  Year 2011 Publication Physiology & Behavior Abbreviated Journal Physiol Behav  
  Volume 104 Issue 2 Pages 248-256  
  Keywords Adaptation, Physiological/drug effects/*physiology; Analysis of Variance; Animals; Anxiety/*etiology/*pathology; Behavior, Animal/drug effects; Biophysics; Corticosterone/adverse effects; Disease Models, Animal; Electric Stimulation; Exploratory Behavior/drug effects/physiology; Long-Term Potentiation/drug effects/*physiology; Male; Maze Learning/drug effects; Mice; Mice, Inbred C57BL; Patch-Clamp Techniques/methods; Septal Nuclei/drug effects/*physiopathology; Social Isolation/psychology; Time Factors  
  Abstract In vulnerable individuals, exposure to stressors can result in chronic disorders such as generalized anxiety disorder (GAD), major depressive disorder (MDD), and post-traumatic stress disorder (PTSD). The extended amygdala is critically implicated in mediating acute and chronic stress responsivity and anxiety-like behaviors. The bed nucleus of the stria terminalis (BNST), a subregion of the extended amygdala, serves as a relay of corticolimbic information to the paraventricular nucleus of the hypothalamus (PVN) to directly influence the stress response. To investigate the influence of the corticosteroid milieu and housing conditions on BNST function, adult C57Bl/6J were either acutely or chronically administered corticosterone (CORT, 25mg/kg in sesame oil) or vehicle (sesame oil) or were group housed or socially isolated for 1 day (acute) or 6-8 weeks (chronic). To ascertain whether these stressors could influence anxiety-like behavior, studies were performed using the novel open-field (NOF) and the elevated zero maze (EZM) tests. To investigate potential associated changes in plasticity, alterations in BNST function were assessed using ex vivo extracellular field potential recordings in the (dorsal-lateral) dlBNST and a high frequency stimulus protocol to induce long-term potentiation (LTP). Our results suggest that chronic CORT injections and chronic social isolation housing conditions lead to an increase in anxiety-like behavior on the EZM and NOF. Chronically stressed mice also displayed a parallel blunting of LTP in the dlBNST. Conversely, acute social isolation housing had no effect on anxiety-like behavior but still resulted in a blunting of LTP in the dlBNST. Collectively, our results suggest acute and chronic stressors can have a distinct profile on plasticity in the BNST that is not uniformly associated with an increase in anxiety-like behavior.  
  Call Number Serial 85  
Permanent link to this record
 

 
Author (up) de Groat, W.C.; Yoshimura, N. file  url
openurl 
  Title Changes in afferent activity after spinal cord injury Type Journal Article
  Year 2010 Publication Neurourology and Urodynamics Abbreviated Journal Neurourol Urodyn  
  Volume 29 Issue 1 Pages 63-76  
  Keywords Afferent Pathways/metabolism/*physiopathology; Animals; Central Nervous System/metabolism/*physiopathology; Ganglia, Spinal/metabolism/*physiopathology; Genetic Therapy/methods; Humans; Mechanotransduction, Cellular; Nerve Fibers, Myelinated; Nerve Fibers, Unmyelinated; Nerve Growth Factor/metabolism; Neuroanatomical Tract-Tracing Techniques; Neuronal Plasticity; Patch-Clamp Techniques; Pituitary Adenylate Cyclase-Activating Polypeptide/metabolism; Potassium Channels/metabolism; Recovery of Function; Reflex; Sodium Channels/metabolism; Spinal Cord Injuries/complications/metabolism/*physiopathology/therapy; Urinary Bladder/*innervation; Urinary Bladder, Neurogenic/etiology/metabolism/*physiopathology/therapy; *Urination; gamma-Aminobutyric Acid/metabolism  
  Abstract AIMS: To summarize the changes that occur in the properties of bladder afferent neurons following spinal cord injury. METHODS: Literature review of anatomical, immunohistochemical, and pharmacologic studies of normal and dysfunctional bladder afferent pathways. RESULTS: Studies in animals indicate that the micturition reflex is mediated by a spinobulbospinal pathway passing through coordination centers (periaqueductal gray and pontine micturition center) located in the rostral brain stem. This reflex pathway, which is activated by small myelinated (Adelta) bladder afferent nerves, is in turn modulated by higher centers in the cerebral cortex involved in the voluntary control of micturition. Spinal cord injury at cervical or thoracic levels disrupts voluntary voiding, as well as the normal reflex pathways that coordinate bladder and sphincter function. Following spinal cord injury, the bladder is initially areflexic but then becomes hyperreflexic due to the emergence of a spinal micturition reflex pathway. The recovery of bladder function after spinal cord injury is dependent in part on the plasticity of bladder afferent pathways and the unmasking of reflexes triggered by unmyelinated, capsaicin-sensitive, C-fiber bladder afferent neurons. Plasticity is associated with morphologic, chemical, and electrical changes in bladder afferent neurons and appears to be mediated in part by neurotrophic factors released in the spinal cord and the peripheral target organs. CONCLUSIONS: Spinal cord injury at sites remote from the lumbosacral spinal cord can indirectly influence properties of bladder afferent neurons by altering the function and chemical environment in the bladder or the spinal cord.  
  Call Number Serial 2147  
Permanent link to this record
Select All    Deselect All
 |   | 
Details
   print

Save Citations: