Fentanyl decreases catecholamine metabolism measured by in vivo voltammetry in the rat locus coeruleus

1989 ◽  
Vol 67 (5) ◽  
pp. 532-536 ◽  
Author(s):  
Brian Milne ◽  
Luc Quintin ◽  
Jean Yves Gillon ◽  
Jean-François Pujol

The objective of this study was to investigate under controlled conditions the effects of fentanyl on the rat locus coeruleus catechol oxidation current. Using differential normal pulse voltammetry combined with electrochemically treated carbon fiber electrodes to measure the catechol oxidation current, catecholamine metabolism can be reliably monitored. Male Sprague–Dawley rats weighing 500–600 g had carbon fiber electrodes implanted into the locus coeruleus under halothane – O2 – air anesthesia with controlled ventilation and muscle relaxation. Experiments consisted of four groups of rats given the following treatments: (A) saline (n = 6); (B) fentanyl, 10 μg∙kg−1 i.v. (n = 6); (C) naloxone, 800 μg∙kg−1 i.v. followed 2 min later by fentanyl, 10 μg∙kg−1 (n = 5); (D) clonidine, 200 μg∙kg−1 i.p. (n = 6). There was no significant change in the catechol oxidation current following saline. Fentanyl produced a significant (ANOVA, p < 0.05) decrease in the catechol oxidation current (maximum 32 min postinjection was 75.8 ± 4.6% of baseline). This decrease was prevented by a prior injection of naloxone. Clonidine produced a significant decrease in catechol oxidation current (maximum 40 min postinjection was 54.1 ± 7.0% of baseline). Systolic blood pressure was significantly decreased following clonidine and there were no significant changes in arterial blood gases throughout the experiments. The α2-adrenergic agonist clonidine and the opioid fentanyl produced a decrease in locus coeruleus catechol oxidation current measured by in vivo voltammetry, which monitors catecholamine turnover.Key words: catecholamine, clonidine, fentanyl, opiates, locus coeruleus, in vivo voltammetry.

2003 ◽  
pp. 321-384
Author(s):  
Nigel T. Maidment ◽  
Keith F. Martin ◽  
Anthony P. D. W. Ford ◽  
Charles A. Marsden

1988 ◽  
Vol 254 (2) ◽  
pp. R296-R301
Author(s):  
K. V. Thrivikraman ◽  
D. E. Carlson ◽  
D. S. Gann

Push-pull perfusion was used to determine monoaminergic activity in the locus coeruleus (LC) of alpha-chloralose-urethan-anesthetized cats after 20% hemorrhage. Blood was withdrawn from 0 to 3 min and reinfused from 10 to 13 min. Continuous 5-min interval samples of perfusate were collected from -5 to 15 min. Concentrations of the monoamines were determined using high-performance liquid chromatography with electrochemical detection. The perfusion sites (n = 21) were identified histologically. In a group of eight contiguous sites in the ventral LC (vLC), 4-hydroxy-3-methoxy-phenyl(ethylene)glycol (MHPG) increased significantly from 0.50 +/- 0.22 (control) to 1.19 +/- 0.42 pmol/5 min during the first 5 min after hemorrhage (P less than 0.05). This response differed significantly from that obtained at the remaining 13 sites. Other metabolites were not often detectable for many sites either within or outside vLC, and their responses to hemorrhage were not significant. The response of MHPG in the vLC indicates that norepinephrine (NE) turnover increases in this area selectively and implicates NE in the increase in the catecholamine oxidation current reported previously using in vivo voltammetry. Since the vLC was shown previously to facilitate adrenocorticotropin (ACTH) release, the increase in NE turnover after hemorrhage could induce ACTH release. This increase may also act locally to modulate the ascending hemodynamic signal.


1999 ◽  
Vol 90 (1) ◽  
pp. 165-173 ◽  
Author(s):  
Sean R. Hall ◽  
Brian Milne ◽  
Christopher Loomis

Background Blockade of spinal glycine receptors with intrathecal strychnine produces an allodynia-like state in the anesthetized rat. Innocuous hair deflection in the presence of intrathecal strychnine induces a nociceptive-like activation of catechol oxidation in the locus coeruleus and enhances cardiovascular responses. Because prostaglandins play a central role in augmenting pain, this study evaluated the effect of intrathecal nonsteroidal antiinflammatory drugs in strychnine-induced allodynia. Methods In urethane-anesthetized rats, changes in catechol oxidation in the locus coeruleus, measured using in vivo voltammetry, and cardiovascular parameters evoked by hair deflection of caudal dermatomes were determined after strychnine (40 microg) or saline were administered intrathecally. Subsequently, the effects of 30 microg ketorolac, 10 microg S(+)-ibuprofen, and 10 microg R(-)-ibuprofen administered intrathecally were evaluated. Results After strychnine was administered intrathecally, hair deflection evoked an increase in the locus coeruleus catechol oxidation (peak, 149.7+/-7.2% of baseline) and mean arterial blood pressure (peak, 127.5+/-3.8% of baseline). These responses were not observed after saline was administered intrathecally. All hair deflection-evoked, strychnine-dependent peak responses were attenuated significantly with intrathecally administered ketorolac and S(+)-ibuprofen but not with R(-)-ibuprofen. Conclusions Locus coeruleus catechol oxidation is a sensitive biochemical index of strychnine-induced allodynia and is correlated temporally with the cardiovascular responses evoked by hair deflection during spinal glycinergic inhibition. The ability of intrathecally administered ketorolac and S(+)-ibuprofen, but not R(-)-ibuprofen, to suppress the locus coeruleus catechol oxidation and cardiovascular peak responses evoked during strychnine-induced allodynia provide evidence that central prostaglandins play an important role in the abnormal sensory processing of strychnine-induced allodynia.


2017 ◽  
Vol 89 ◽  
pp. 400-410 ◽  
Author(s):  
I. Mitch Taylor ◽  
Elaine M. Robbins ◽  
Kasey A. Catt ◽  
Patrick A. Cody ◽  
Cassandra L. Happe ◽  
...  

1992 ◽  
Vol 25 (5) ◽  
pp. 795-805 ◽  
Author(s):  
Peng Tuzhi ◽  
Lu Honghuan ◽  
Liu Guoqing ◽  
Cao Tuping

Author(s):  
Yu Huan ◽  
Jeffrey P Gill ◽  
Johanna B Fritzinger ◽  
Paras R Patel ◽  
Julianna M Richie ◽  
...  

Abstract Objective. To understand neural circuit dynamics, it is critical to manipulate and record many individual neurons. Traditional recording methods, such as glass microelectrodes, can only control a small number of neurons. More recently, devices with high electrode density have been developed, but few of them can be used for intracellular recording or stimulation in intact nervous systems. Carbon fiber electrodes (CFEs) are 8 micron-diameter electrodes that can be assembled into dense arrays (pitches ≥ 80 µm). They have good signal-to-noise ratios (SNRs) and provide stable extracellular recording both acutely and chronically in neural tissue in vivo (e.g., rat motor cortex). The small fiber size suggests that arrays could be used for intracellular stimulation. Approach. We tested CFEs for intracellular stimulation using the large identified and electrically compact neurons of the marine mollusk Aplysia californica. Neuron cell bodies in Aplysia range from 30 µm to over 250 µm. We compared the efficacy of CFEs to glass microelectrodes by impaling the same neuron’s cell body with both electrodes and connecting them to a DC coupled amplifier. Main Results. We observed that intracellular waveforms were essentially identical, but the amplitude and SNR in the CFE were lower than in the glass microelectrode. CFE arrays could record from 3 to 8 neurons simultaneously for many hours, and many of these recordings were intracellular, as shown by simultaneous glass microelectrode recordings. CFEs coated with platinum-iridium could stimulate and had stable impedances over many hours. CFEs not within neurons could record local extracellular activity. Despite the lower SNR, the CFEs could record synaptic potentials. CFEs were less sensitive to mechanical perturbations than glass microelectrodes. Significance. The ability to do stable multi-channel recording while stimulating and recording intracellularly make CFEs a powerful new technology for studying neural circuit dynamics.


1989 ◽  
Vol 257 (2) ◽  
pp. R370-R376 ◽  
Author(s):  
K. V. Thrivikraman ◽  
D. A. Bereiter ◽  
D. S. Gann

Temporal changes in catecholamine activity within the paraventricular nucleus (PVN) of the hypothalamus were assessed using in vivo voltammetry after moderate hemorrhage in chloralose-anesthetized cats. Oxidation current was measured with carbon microelectrodes, and the change at +250 mV was used as an estimate of catecholamine activity. The magnitude and directional change in catecholamine activity was assessed for each site during the initial 3 min of blood loss. Of 62 recording sites, 45 sites were located along the rostrocaudal extent of the medial PVN. Fifteen of these 45 sites exhibited an increase, 15 others exhibited a decrease, and the remaining 15 sites exhibited no change in catecholamine activity. The magnitude of change in oxidation current was independent of the magnitude of the decrease in arterial pressure after hemorrhage. Twelve of the 15 sites that exhibited increases in catecholamine activity were located in the caudal PVN along its dorsomedial aspect, whereas the location of sites that exhibited decreases in catecholamine activity were more widely distributed throughout the nucleus. These data are consistent with the hypothesis that an increase in the release of catecholamines within the caudal PVN in response to hemorrhage is facilitatory for the release of adrenocorticotropin and/or vasopressin.


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