scholarly journals Muscarine increases cation conductance and decreases potassium conductance in rat locus coeruleus neurones.

1992 ◽  
Vol 455 (1) ◽  
pp. 471-485 ◽  
Author(s):  
K Z Shen ◽  
R A North
Keyword(s):  
Locus Coeruleus ◽  
Potassium Conductance ◽  
Cation Conductance

scholarly journals Nociceptin receptor coupling to a potassium conductance in rat locus coeruleus neurones in vitro

1996 ◽  
Vol 119 (8) ◽  
pp. 1614-1618 ◽  
Author(s):  
Mark Connor ◽  
Christopher W. Vaughan ◽  
Billy Chieng ◽  
Macdonald J. Christie
Keyword(s):  
Locus Coeruleus ◽  
Potassium Conductance ◽  
Receptor Coupling ◽  
Nociceptin Receptor

scholarly journals Cortistatin increase of a potassium conductance in rat locus coeruleus in vitro

1997 ◽  
Vol 122 (8) ◽  
pp. 1567-1572 ◽  
Author(s):  
Mark Connor ◽  
Susan L. Ingram ◽  
MacDonald J. Christie
Keyword(s):  
Locus Coeruleus ◽  
Potassium Conductance

Forskolin enhancement of opioid currents in rat locus coeruleus neurons

1996 ◽  
Vol 76 (3) ◽  
pp. 1559-1565 ◽  
Author(s):  
P. B. Osborne ◽  
J. T. Williams
Keyword(s):  
Locus Coeruleus ◽  
Adenylyl Cyclase ◽  
Cell Model ◽  
Brain Slices ◽  
Reversal Potential ◽  
Peak Effect ◽  
Extracellular Potassium ◽  
Potential Range ◽  
Extracellular Potassium Concentration ◽  
Cation Conductance

1. Opioids are known to hyperpolarize all neurons in the nucleus locus coeruleus (LC) and to inhibit adenylyl cyclase. Recent work has shown that activation of adenylyl cyclase with forskolin increased the amplitude of the opioid hyperpolarization in LC cells. The aim of the present study was to determine the mechanism of this augmented hyperpolarization. 2. Agonist-induced currents were studied in LC cells in brain slices using both intracellular and whole cell recordings. Forskolin increased the amplitude of mu-opioid- and alpha 2-adrenoceptor-mediated currents by approximately 30% of control measured at -60 mV. This effect of forskolin was dependent on the concentration having a threshold of approximately 1 microM and a peak effect at approximately 30 microM. Dideoxyforskolin (30 microM) caused a small reduction (-52 +/- 28 pA, mean +/- SE) in the amplitude of the opioid current. 3. Forskolin increased the agonist current in the outward direction over the entire potential range between -140 and -50 mV when recordings were made from neurons in cells recorded from slices cut in the horizontal plane. This augmented current produced a shift of the apparent reversal potential to more negative values. 4. Both the forskolin augmentation of the opioid current and the opoid current itself were reduced when the space clamp was improved by cutting the slice in the coronal plane, increasing the extracellular potassium concentration, and treating the slice with carbenoxolone. In addition, forskolin did not change the reversal potential of the opoid current. When expressed as a percentage change from control, forskolin had no significant effect on the opioid current in carbenoxolone (-13 +/- 13%) but produced a small augmentation in high extracellular potassium (15 +/- 4%) and coronoal slices (31 +/- 12%). 5. Two models were tested to explain the action of forskolin, one where cells are coupled electronically by a forskolin-sensitive conductance (coupled-cell model) and a second where opioids mediate an inhibition of a forskolin-induced cation conductance (2-conductance model). The experimental results were fit well only by the coupled-cell model, which predicted that the opioid/forskolin interaction is indirect and occurs primarily in response to forskolin increasing the degree of electrotonic coupling between LC neurons. The consequence of increased coupling would be to augment synchronous activity within the nucleus.

scholarly journals Cav1.2 and Cav1.3 L-type calcium channels operate in a similar voltage range but show different coupling to Ca2+-dependent conductances in hippocampal neurons

2014 ◽  
Vol 306 (12) ◽  
pp. C1200-C1213 ◽  
Author(s):  
Julia Hasreiter ◽  
Lena Goldnagl ◽  
Stefan Böhm ◽  
Helmut Kubista
Keyword(s):  
Calcium Channels ◽  
Knockout Mice ◽  
Hippocampal Neurons ◽  
Potassium Conductance ◽  
Voltage Range ◽  
Relative Contribution ◽  
Voltage Gated Calcium Channels ◽  
Cation Conductance ◽  
System L ◽  
The Central Nervous System

In the central nervous system, L-type voltage-gated calcium channels (LTCCs) come in two isoforms, namely Cav1.2 and Cav1.3 channels. It has been shown previously that these channels differ in biophysical properties, in subcellular localization, and in the coupling to the gene transcription machinery. In previous work on rat hippocampal neurons we have identified an excitatory cation conductance and an inhibitory potassium conductance as important LTCC coupling partners. Notably, a stimulus-dependent interplay of LTCC-mediated Ca2+ influx and activation of these Ca2+-dependent conductances was found to give rise to characteristic voltage responses. However, the contribution of Cav1.2 and Cav1.3 to these voltage responses remained unknown. Hence, the relative contribution of the LTCC isoforms therein was the focus of the current study on hippocampal neurons derived from genetically modified mice, which either lack a LTCC isoform (Cav1.3 knockout mice) or express a dihydropyridine-insensitive LTCC isoform (Cav1.2DHP−-knockin mice). We identified common and alternate ion channel couplings of Cav1.2 and Cav1.3 channels. Whereas hyperpolarizing Ca2+-dependent conductances were coupled to both Cav1.2 and Cav1.3 channels, an afterdepolarizing potential was only induced by the activity of Cav1.2 channels. Unexpectedly, the activity of Cav1.2 channels was found at relatively hyperpolarized membrane voltages. Our data add important information about the differences between Cav1.2 and Cav1.3 channels that furthers our understanding of the physiological and pathophysiological neuronal roles of these calcium channels. Moreover, our findings suggest that Cav1.3 knockout mice together with Cav1.2DHP−-knockin mice provide valuable models for future investigation of hippocampal LTCC-dependent afterdepolarizations.

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