Spontaneous firing properties of rat medial vestibular nucleus neurons in brain slices by infrared visual patch clamp technique

2008 ◽  
Vol 2 (3) ◽  
pp. 264-268
Author(s):  
Jiao Xia ◽  
Weijia Kong ◽  
Yun Zhu ◽  
Yan Zhou ◽  
Yu Zhang ◽  
...  
Keyword(s):  
Patch Clamp ◽  
Vestibular Nucleus ◽  
Brain Slices ◽  
Medial Vestibular Nucleus ◽  
Spontaneous Firing ◽  
Patch Clamp Technique ◽  
Clamp Technique ◽  
Firing Properties

Plasticity of γ-aminobutyrate receptors in the medial vestibular nucleus of rat after inferior cerebellar peduncle transection

2002 ◽  
Vol 12 (1) ◽  
pp. 1-14
Author(s):  
Yizhe Sun ◽  
Donald A. Godfrey ◽  
Allan M. Rubin
Keyword(s):  
Vestibular Nucleus ◽  
Brain Slices ◽  
Medial Vestibular Nucleus ◽  
Grouped Data ◽  
Spontaneous Firing ◽  
Gaba A ◽  
Endogenous Gaba ◽  
Single Unit Recordings ◽  
Cerebellar Peduncle ◽  
Inferior Cerebellar Peduncle

Extracellular single unit recordings were made from regularly discharging medial vestibular nucleus neurons in brain slices from control rats and from rats surviving 7 days after bilateral transection of the inferior cerebellar peduncle. Decreases in firing rate during perfusion with the Îş-aminobutyric acid (GABA) agonists, muscimol (GABA A ) and baclofen (GABA B ), were greater in lesioned rats than in control rats. For the grouped data, the half-maximally-effective concentrations of muscimol and baclofen were 3.2 µM, as compared with 19.6 µM for control, and 0.8 µM, as compared with 2.7 µM for control, respectively. The antagonists bicuculline (GABA A ) and 2-OH-saclofen (GABA B ) only minimally affected the spontaneous firing rates of neurons in lesioned rats, significantly less than in control rats. The data suggest that the decreases of endogenous GABA levels in the medial vestibular nucleus after inferior cerebellar peduncle transection are accompanied by up-regulation of GABA A and, to a lesser extent, GABA B receptors.

Patch-Clamp Technique in Brain Slices

2003 ◽  
pp. 233-258 ◽  
Author(s):  
T. D. Plant ◽  
J. Eilers ◽  
A. Konnerth
Keyword(s):  
Patch Clamp ◽  
Brain Slices ◽  
Patch Clamp Technique ◽  
Clamp Technique

Ketamine blocks Ca2+-activated K+ channels in rabbit cerebral arterial smooth muscle cells

2003 ◽  
Vol 285 (3) ◽  
pp. H1347-H1355 ◽  
Author(s):  
Jin Han ◽  
Nari Kim ◽  
Hyun Joo ◽  
Euiyong Kim
Keyword(s):  
Smooth Muscle ◽  
Patch Clamp ◽  
Smooth Muscle Cells ◽  
Cerebral Arteries ◽  
Muscle Cells ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Arterial Smooth Muscle ◽  
Clamp Technique ◽  
Arterial Smooth Muscle Cells

Although ketamine and Ca2+-activated K+ (KCa) channels have been implicated in the contractile activity regulation of cerebral arteries, no studies have addressed the specific interactions between ketamine and the KCa channels in cerebral arteries. The purpose of this study was to examine the direct effects of ketamine on KCa channel activities using the patch-clamp technique in single-cell preparations of rabbit middle cerebral arterial smooth muscle. We tested the hypothesis that ketamine modulates the KCa channel activity of the cerebral arterial smooth muscle cells of the rabbit. Vascular myocytes were isolated from rabbit middle cerebral arteries using enzymatic dissociation. Single KCa channel activities of smooth muscle cells from rabbit cerebral arteries were recorded using the patch-clamp technique. In the inside-out patches, ketamine in the micromolar range inhibited channel activity with a half-maximal inhibition of the ketamine conentration value of 83.8 ± 12.9 μM. The Hill coefficient was 1.2 ± 0.3. The slope conductance of the current-voltage relationship was 320.1 ± 2.0 pS between 0 and +60 mV in the presence of ketamine and symmetrical 145 mM K+. Ketamine had little effect on either the voltage-dependency or open- and closed-time histograms of KCa channel. The present study clearly demonstrates that ketamine inhibits KCa channel activities in rabbit middle cerebral arterial smooth muscle cells. This inhibition of KCa channels may represent a mechanism for ketamine-induced cerebral vasoconstriction.

Molecular mechanisms of action for CFTR potentiators

2019 ◽  
Author(s):  
◽  
Han-I Yeh
Keyword(s):  
Cystic Fibrosis ◽  
Patch Clamp ◽  
Binding Site ◽  
Molecular Mechanisms ◽  
Mechanisms Of Action ◽  
Drug Binding ◽  
Patch Clamp Technique ◽  
Chemical Structures ◽  
Clamp Technique ◽  
Sites Of Action

[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] As the culprit behind cystic fibrosis (CF) is the dysfunction of the chloride channel cystic fibrosis transmembrane conductance regulator (CFTR), pharmacological reagents targeting CFTR may hold the key to the ultimate cure of CF. In this thesis, we present the studies in the mechanisms of action for CFTR potentiators, the small molecules that enhance the functions of CFTR. Using the patch-clamp technique, we demonstrated that the permeant anion nitrate modulates CFTR gating through a mechanism similar to the FDA-approved CFTR potentiator VX-770 (ivacaftor). Via separate sites of action, VX-770 and nitrate stabilize the open channel conformation of CFTR in an energetically additive manner. Next, we investigated the action of a novel CFTR potentiator, GLPG1837, and showed that despite their different chemical structures, GLPG1837 and VX-770 share the same mechanisms of action on CFTR gating and compete for a common binding site in the transmembrane domains of CFTR. An allosteric modulation model is further proposed to explain how the affinity and efficacy of both potentiators are determined by the energetic coupling between drug binding and channel gating. Finally, we combined molecular docking and patch-clamp technique to identify the binding site(s) for GLPG1837 and VX-770.

Sign in / Sign up

Export Citation Format

Share Document