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71.
M. Goldermann W. Hanke W. R. Schlue 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》1994,174(2):231-237
Two types of potassium channels of identified (p-) neurones of the leech (Hirudo medicinalis) were investigated by using the patch-clamp technique. The openstate probability of these channels in cell-attached patches can be reduced by addition of 5-hydroxytryptamine to the bath solution. After excising the patches the application of alkaline phosphatase to the cytosolic face of the patch increases the open probability. The 5-HT1A-receptor agonist buspirone mimics the effect of 5-HT. Our experiments show that the effect of 5-HT might be due to a channel phosphorylation via a 5-HT1A-receptor subtype. 相似文献
72.
W. -M. Weber B. Dannenmaier W. Clauss 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》1993,163(2):153-159
The dorsal skin of the leech Hirudo medicinalis was used for electrophysiological measurements performed in Ussing chambers. The leech skin is a tight epithelium (transepithelial resistance = 10.5±0.5 k· cm-2) with an initial short-circuit current of 29.0±2.9 A·cm-2. Removal of Na+ from the apical bath medium reduced short-circuit current about 55%. Ouabain (50mol·l-1) added to the basolateral solution, depressed the short-circuit current completely. The Na+ current saturated at a concentration of 90 mmol Na+·l-1 in the apical solution (K
M=11.2±1.8 mmol·l-1). Amiloride (100 mol·l-1) on the apical side inhibited ca. 40% of the Na+ current and indicated the presence of Na+ channels. The dependence of Na+ current on the amiloride concentration followed Michaclis-Menten kinetics (K
i=2.9±0.4 mol·l-1). The amiloride analogue benzamil had a higher affinity to the Na+ channel (K
i=0.7±0.2 mol·l-1). Thus, Na+ channels in leech integument are less sensitive to amiloride than channels known from vertebrate epithelia. With 20 mmol Na+·l-1 in the mucosal solution the tissue showed an optimum amiloride-inhibitable current, and the amiloride-sensitive current under this condition was 86.8±2.3% of total short-circuit current. Higher Na+ concentrations lead to a decrease in amiloride-blockade short-circuit current. Sitmulation of the tissue with cyclic adenosine monophosphate (100 mol·l-1) and isobutylmethylxanthine (1 mmol·l-1) nearly doubled short-circuit current and increased amiloride-sensitive Na+ currents by 50%. By current fluctuation analysis we estimated single Na+ channel current (2.7±0.9 pA) and Na+ channel density (3.6±0.6 channels·m-2) under control conditions. After cyclic adenosine monophosphate stimulation Na+ channel density increased to 5.4±1.1 channels·m-2, whereas single Na+ channel current showed no significant change (1.9±0.2 pA). These data present a detailed investigation of an invertebrate epithelial Na+ channel, and show the similarities and differences to vertebrate Na+ channels. Whereas the channel properties are different from the classical vertebrate Na+ channel, the regulation by cyclic adenosine monophosphate seems similar. Stimulation of Na+ uptake by cyclic adenosine monophosphate is mediated by an increasing number of Na+ channels.Abbreviations
slope of the background noise component
- ADH
antidiuretic hormone
- cAMP
cyclic adenosine monophosphate
-
f
frequency
-
f
c
coner frequency of the Lorentzian noise component
- Hepes
N-hydroxyethylpiperazine-N-ethanesulphonic acid
- BMX
isobutyl-methylxanthine
-
i
Na
single Na+ channel current
-
I
Na
max, maximal inhibitable Na+ current
-
I
SC
short circuit current
-
K
i
half maximal blocker concentration
-
K
M
Michaelis constandard error of the mean
-
S
(f)
power density of the Lorentzian noise component
-
S
0
plateau value of the Lorentzian noise component
- TMA
tetramethylammonium
- Trizma
TRIS-hydroxymethyl-amino-methane
-
V
max
maximal reaction velocity
-
V
T
transepithelial potential
-
K
half maximal blocker concentration 相似文献
73.
The induction of long-term potentiation (LTP) is generally assumed to be triggered by Ca2+ entry into dendritic spines via NMDA receptor-gated channels. A previous computational model proposed that spines serve several functions in this process. First, they compartmentalize and amplify increases in [Ca2+]i. Second, they augment the nonlinear relationship between synaptic strength and the probability or magnitude of LTP induction. Third, they isolate the metabolic machinery responsible for LTP induction from increases in [Ca2+]i produced by voltage-gated Ca2+ channels in the dendritic shaft. Here we examine this last prediction of the model using methods that combine confocal microscopy with simultaneous neurophysiological recordings in hippocampal brain slices. Either of two Ca2+-sensitive dyes were injected into CA1 pyramidal neurons. Direct depolarization of the neurons via the somatic electrode produced clear increases in Ca2+ signals within the dendritic spines, a result that was not predicted by the previous spine model. Our new spine model suggests that some of this signal could theoretically result from Ca2+-bound dye diffusing from the dendritic shaft into the spine. Dye diffusion alone cannot, however, explain the numerous cases in which the Ca2+ signal in the spine was considerably larger than that in the adjacent dendritic shaft. The latter observations raise the possiblity of voltage-gated Ca2+ entry directly into the spine or else perhaps via Ca2+-dependent Ca2+release. The new spine model accommodates these observations as well as several other recent experimental results. 1994 John Wiley & Sons, Inc. 相似文献
74.
Arthur M. Brown 《The Journal of membrane biology》1993,131(2):93-104
Summary Ion channels are signaling molecules and by them-selves perform no work. In this regard they are un like the usual membrane
enzyme effectors for G proteins. The pathways of G protein receptor, G protein and ion channels are, therefore, purely infor
mational in function. Because a single G protein may have several ion channels as effectors, the effects should be coordinated
and this seems to be the case. Inhibition of Ca2+ current and stimulation of K+ currents would have a greater impact than either alone. Additional flexibility is provided by spontane ous noise in the complexes
of G protein receptor, G protein, and ion channel. By having a non-zero setpoint, the range of control is extended and the
responses become bi-directional. 相似文献
75.
76.
77.
Identification of a nucleo-cytoplasmic ionic pathway by osmotic shock in isolated mouse liver nuclei
Summary The observation that the nuclear envelope outer mem brane contains ion channels raises the question of whether these conductances
communicate between the cytosol and the nuclear envelope cisternae or between the cytosol and the cytoplasm. Failure to detect
large, nonselective holes using the patch-clamp technique has led to the speculation that ion channels and nuclear pores are
in fact the same.
In this paper we present evidence that the ionic channel, recorded in isolated liver nuclei with the patch-clamp configura
tion of “nucleus-attached,” spans the double membrane of the envelope, providing a direct contact between nucleoplasm and
cytoplasm. 相似文献
78.
Involvement of Calcium Channels in Depolarization-Evoked Release of Adenosine from Spinal Cord Synaptosomes 总被引:3,自引:1,他引:2
Abstract: The potential involvement of L- and N-type voltage-sensitive calcium (Ca2+ ) channels and a voltage-independent receptor-operated Ca2+ channel in the release of adenosine from dorsal spinal cord synaptosomes induced by depolarization with K+ and capsaicin was examined. Bay K 8644 (10 n M ) augmented release of adenosine in the presence of a partial depolarization with K+ (addition of 6 m M ) but not capsaicin (1 and 10 μ M ). This augmentation was dose dependent from 1 to 10 n M and was followed by inhibition of release from 30 to 100 n M . Nifedipine and nitrendipine inhibited the augmenting effect of Bay K 8644 in a dose-dependent manner, but neither antagonist had any effect on release of adenosine produced by K+ (24 m M ) or capsaicin (1 and 10 μ M ) ω-Conotoxin inhibited K+ -evoked release of adenosine in a dose-dependent manner but had no effect on capsaicin-evoked release. Ruthenium red blocked capsaicin-induced release of adenosine but had no effect on K+ -evoked release. Although L-type voltage-sensitive Ca2+ channels can modulate release of adenosine when synaptosomes are partially depolarized with K+ , N-type voltage-sensitive Ca2+ channels are primarily involved in K+ -evoked release of adenosine. Capsaicin-evoked release of adenosine does not involve either L- or N-type Ca2+ channels, but is dependent on a mechanism that is sensitive to ruthenium red. 相似文献
79.
80.
Ectopic ion channels developed locally at the injury site after nerve damage by light ligation around common sciatic nerve of the rats. Different channel types have different processes of formation, accumulation and degeneration. During the first three days after injury, mechanically activated channels that are modulated by Ca++ channel activities first appeared. As the nerve fibers begin to be excited by TEA, a blocker of K+ channels, suggesting that the accumulation of K+ channels, the responsibility of mechanically activated channels was declining. Onset of K+ channels was from the 3rd postoperative day and lasted up to the fiftieth day. This time course of K+ channel development was closely related to allodynia and hyperalgesia of neuropathic animal behaviour. The results suggest that chronic contraction injury induces a dynamic change in the ectopic mechanically activated channels and K+ channels at the injury site of nerve and there is an interchange in the development time courses of the mechanic 相似文献