Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Dynorphins directly inhibit neuronal nicotinic acetylcholine receptors in PC12 cells (2000)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 12 (2000), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The authors have previously reported that dynorphin A (1–17), an endogenous kappa opioid agonist, inhibits the current mediated through neuronal nicotinic acetylcholine receptors (nAChRs) without the involvement of opioid receptors or G-proteins. We have further characterized this action to elucidate the mechanisms. The nicotine-induced current was studied in PC12 cells using patch-clamp techniques. In the whole-cell configuration, four kinds of dynorphins with different lengths, dynorphin A (1–17) (1–13) (2–13) and (1–8), similarly inhibited the nicotine-induced inward current at 1 μm and accelerated the current decay. The inhibition by dynorphin A (1–17) was not antagonized by the increasing concentrations of nicotine. The current–voltage relationship revealed that dynorphin's inhibition was voltage independent at the membrane potentials from −30 to −70 mV. The inhibition was not affected by pretreatment with pertussis toxin (PTX) or inclusion of staurosporine into the pipette solution. The inhibitory effect of dynorphin A (1–17) was well preserved in the outside-out patch configuration. Analysis of the nicotine-induced noise and single-channel kinetics revealed that dynorphin A(1–17) reduced open time without changing the amplitude of the unitary current. We found that the inhibitory effect on neuronal nAChRs is shared by all four dynorphins studied. The inhibition appears to be non-competitive and voltage independent. The outside-out recording together with other experiments indicated that a major part of this inhibition is not mediated through cytoplasmic messengers, but based on the direct action of dynorphins on neuronal nAChRs leading to the reduction of open time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.2000.00012.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of continuous negative extrathoracic pressure ventilation on left ventricular dimensions and hemodynamics in dogs (1993)
    Springer
    Journal of anesthesia 7 (1993), S. 308-315 
    Details
    ISSN: 1438-8359
    Keywords: Negative pressure ventilation ; Hemodynamics ; Preload ; Transesophageal echocardiography
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract It has been reported that continuous negative extrathoracic pressure ventilation (CNETPV) depresses cardiac output less than continuous positive pressure ventilation (CPPV) does, and this difference may be related to the different effects of two ventilatory modes on preload. We performed simultaneous measurements of hemodynamics and left ventricular short axis dimensions by transesophageal echocardiography (TEE) to evaluate left ventricular preload and function during CNETPV and CPPV in normal dogs. Hemodynamic measurements and simultaneous TEE recording were performed at 5 successive periods; 1) the first control period of intermittent positive pressure ventilation (IPPV1), 2) CNETPV with negative end-expiratory pressure (NEEP) of −10 cmH2O (CNET10), 3) CNETPV with NEEP of −15 cmH2O (CNET15), 4) the second control period of IPPV (IPPV2), and 5) CPPV with PEEP of 15 cmH2O (CPPV15). Left ventricular end-systolic and end-diastolic dimension (LVESD and LVEDD), ejection fraction (EF) and fractional shortening (FS) were measured from TEE recordings. Both CNET10 and CNET15 induced no significant changes in hemodynamics and left ventricular dimensions, compared with those during IPPV1. However, CPPV15 reduced cardiac output and stroke volume (SV) and increased heart rate significantly, compared with IPPV2. CPPV15 significantly decreased LVEDD compared with IPPV2. Neither EF nor FS showed any significant change throughout the experiment. These results indicate that CNETPV preserved cardiac output because it maintained the preload and the left ventricular function. (Andoh T, Doi H, Kudoh I, et al.: Effects of continuous negative extrathoracic pressure ventilation on left ventricular dimensions and hemodynamics in dogs. J Anesth 7: 308–315, 1993)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054030070308
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...