GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

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

Proceed reservation?

Export
Filter
  • Wiley  (2)
  • Rizzo, Valerio  (2)
  • Sardo, Pierangelo  (2)
Material
Publisher
  • Wiley  (2)
Person/Organisation
Language
Years
FID
  • 1
    Online Resource
    Online Resource
    Effects of nitric oxide‐active drugs on the discharge of subthalamic neurons: microiontophoretic evidence in the rat
    Wiley ; 2006
    In:  European Journal of Neuroscience Vol. 24, No. 7 ( 2006-10), p. 1995-2002
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 24, No. 7 ( 2006-10), p. 1995-2002
    Abstract: The presence of nitric oxide (NO) synthase and of soluble guanylyl cyclase, the main NO‐activated metabolic pathway, has been demonstrated in many cells of the subthalamic nucleus. In this study, the effects induced on the firing of 96 subthalamic neurons by microiontophoretically administering drugs modifying NO neurotransmission were explored in anaesthetized rats. Recorded neurons were classified into regularly and irregularly discharging on the basis of their firing pattern. Nω‐nitro‐ l ‐arginine methyl ester (L‐NAME; a NO synthase inhibitor), 3‐morpholino‐sydnonimin‐hydrocloride (SIN‐1; a NO donor), S‐nitroso‐glutathione (SNOG; another NO donor) and 8‐Br‐cGMP (a cell‐permeable analogue of cGMP, the main second‐messenger of NO neurotransmission) were iontophoretically applied while performing single‐unit extracellular recordings. The activity of most neurons was influenced in a statistically significant way: in particular, both current‐related inhibitory L‐NAME‐induced effects (20/39 tested cells) and excitatory effects of SIN‐1 (25/41 tested neurons), SNOG (19/32 tested cells) and 8‐Br‐cGMP (13/19 tested neurons) were demonstrated. Neither statistically significant differences between the responses of regularly and irregularly discharging cells, nor specific topographical clustering of responding neurons, were demonstrated. Neurons administered drugs oppositely modulating the NO neurotransmission often displayed responses to only one treatment. We hypothesize that NO neurotransmission could exert a modulatory influence upon subthalamic neurons, with a prevalent excitatory effect. However, in the light of the presence of some responses of opposite sign to the same drug displayed by different subthalamic neurons, more complex effects of NO neurotransmission could be suggested, probably due to interactions with other classical neurotransmitter systems.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    URL: Article
    DOI: 10.1111/ejn.2006.24.issue-7
    DOI: 10.1111/j.1460-9568.2006.05097.x
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2005178-5
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Intensity of GABA‐evoked responses is modified by nitric oxide‐active compounds in the subthalamic nucleus of the rat: A microiontophoretic study
    Wiley ; 2009
    In:  Journal of Neuroscience Research Vol. 87, No. 10 ( 2009-08), p. 2340-2350
    Details
    In: Journal of Neuroscience Research, Wiley, Vol. 87, No. 10 ( 2009-08), p. 2340-2350
    Abstract: We have previously described modulatory effects of nitric oxide (NO)–active drugs on subthalamic nucleus (STN) neurons. In this study, the effects of microiontophoretically applied NO‐active compounds on GABA‐evoked responses were investigated in subthalamic neurons extracellularly recorded from anesthetized rats: 45 of 62 cells were excited by S‐nitroso‐glutathione (SNOG), an NO donor, whereas 28 of 43 neurons were inhibited by N ω‐nitro‐ L ‐arginine methyl ester (L‐NAME), a NOS inhibitor. Nearly all neurons responding to SNOG and/or L‐NAME showed significant inhibitory responses to the administration of iontophoretic GABA. In these cells, the changes induced by NO‐active drugs in the magnitude of GABA‐evoked responses were used as indicators of NO modulation. In fact, when an NO‐active drug was co‐iontophoresed with GABA, significant changes in GABA‐induced responses were observed: generally, decreased magnitudes of GABA‐evoked responses were observed during continuous SNOG ejection, whereas the administration of L‐NAME enhanced GABA responses. In contrast, glutamate‐evoked responses were enhanced by SNOG and dampened by L‐NAME co‐iontophoresis. Furthermore, the iontophoretic administration of bicuculline (a GABA A receptor antagonist) completely abolished the GABA‐evoked inhibitory responses and reduced the magnitude of both the SNOG‐ and L‐NAME‐induced effects. The results suggest that the NO‐mediated modulation of subthalamic neurons could also be a result of an interaction between NO and GABA A neurotransmission. Increased NOS activity has been shown in the hyperactive STN neurons of parkinsonian patients; on the basis of our observations about the influence of NO‐active drugs on the baseline and GABA‐evoked activity of subthalamic cells, such hyperactivity suggests the involvement of increased NO levels and reduced sensitivity to GABA. © 2009 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0360-4012 , 1097-4547
    URL: Issue
    URL: Article
    DOI: 10.1002/jnr.v87:10
    DOI: 10.1002/jnr.22043
    Language: English
    Publisher: Wiley
    Publication Date: 2009
    detail.hit.zdb_id: 1474904-X
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...