Evaluation of the anaesthetic effects of medetomidine and ketamine in rats and their reversal with atipamezole

Jang, Hwan Soo; Choi, Hyun-Soo; Lee, Sung Hee; Jang, Ki‐Hyo; Lee, Maan‐Gee

doi:10.1111/j.1467-2995.2009.00463.x

Cited by 33 publications

(27 citation statements)

References 24 publications

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“…Medetomidine is an agonist for central α 2 adrenoceptor, which is a mixture of sinistral medetomidine and DEX, and sinistral DEX has no pharmacological effects 15,16. DEX is a dextro isomer of medetomidine.…”

Section: Discussionmentioning

confidence: 99%

Effect of dexmedetomidine on hippocampal neuron development and BDNF-TrkB signal expression in neonatal rats

Zou

et al. 2016

NDT

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The study aimed to explore the effect of dexmedetomidine (DEX) on hippocampal neuron development process and on molecular expression of brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway in neonatal rats. The hippocampal neuron cells were isolated from newborn neonatal rats and cultured in vitro. One control group and three treated groups with 1, 10, and 100 μmol/L DEX were used for the study. Cell activity and apoptosis were detected by the MTT and terminal deoxynucleotidyl transferase-mediated biotinylated uridine triphosphate (UTP) nick end labeling assays. The synaptophysin (SYN) and postsynaptic density 95 (PSD95) were detected by quantitative polymerase chain reaction. There was no difference in the viability of neuron cells among the different dose groups of DEX and the control group during days 2–10 (P>0.05). Compared to the control group, there was no significant difference (P>0.05) in the expressions of SYN and PSD95 in the groups treated with 1 and 10 μmol/L DEX, whereas significant difference in the expression was observed in the group treated with 100 μmol/L DEX (P<0.01). Compared with the control group, the expression of BDNF was significantly upregulated (P<0.05) in the group treated with 100 μmol/L DEX. There were no significant differences in TrkB expression among the four groups. The expression of p-N-methyl-D-aspartate receptor increased with an increase in the concentration of DEX; however, only the high dose revealed a significant upregulation compared with the control group. The neuroprotective effect of DEX may be achieved by upregulating the expression of BDNF and phosphorylation level of N-methyl-D-aspartate receptor.

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Section: Discussionmentioning

confidence: 99%

Effect of dexmedetomidine on hippocampal neuron development and BDNF-TrkB signal expression in neonatal rats

Zou

et al. 2016

NDT

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“…Jang et al (2009) also found that SEF95 showed a strong correlation with the depth of anesthesia in rats. In contrast, other results insisted that spectral EEG parameters were not precise determinants to predict the level of anesthesia [24,33,34]. Prior to EEG evaluation, we considered that the central effects of tramadol, i.e., dose-dependent analgesia and seizure severity, significantly affected the EEG spectral parameters, especially on MPF or some low frequency band powers.…”

Section: Discussionmentioning

confidence: 99%

“…Surgery and EEG recording methods were similar to those in a previous study [24]. In brief, at least 7 days before starting the experiments, epidural screw electrodes (tip diameter 1.0 mm) for EEG recording were implanted under ketamine (60 mg/kg) and medetomidine (0.4 mg/kg) anesthesia.…”

Section: Methodsmentioning

confidence: 99%

The Effects of Tramadol on Electroencephalographic Spectral Parameters and Analgesia in Rats

Jang

Lee

2010

Korean J Physiol Pharmacol

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ABBREVIATIONS: EEG, electroencephalogram; TFL, tail-flick latency; NSS, numerical seizure score; %MPE, a percentage of maximal possible effect; MPF, median power frequency; SEF95, spectral edge frequency 95; SWD, spike-wave discharge.Received May 31, 2010, Revised June 10, 2010, Accepted June 20, 2010 Corresponding to: Maan-Gee Lee, Department of Pharmacology, School of Medicine, Kyungpook National University, 2-101, Dongindong, The effects of different doses of tramadol on analgesia and electroencephalographic (EEG) spectral parameters were compared in rats. Saline or tramadol 5, 10, 20 or 40 mg/kg was administered. The degree of analgesia was evaluated by tail-flick latency, and the degree of seizure was measured using numerical seizure score (NSS). Additionally, band powers, median power frequency and spectral edge frequency 95 were measured to quantify the EEG response. All doses of tramadol produced spike-wave discharge. Tramadol significantly and dose-dependently increased the analgesia, but these effects did not correspond with the changes in the EEG spectral parameters. NSS significantly increased in the Tramadol 20 and 40 mg/kg treatment groups compared to the Control and TRA5 groups, and two rats given 40 mg/kg had convulsions. In conclusion, tramadol dose-dependently increased the analgesic effect, and the 10 mg/kg dose appears to be a reliable clinical dose for analgesia in rats, but dose-dependent increases in analgesia and seizure severity did not correlate with EEG spectral parameters.

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“…Depth of anesthesia was noted every 30 min by recording reflex responses to toe web clamping. Anesthetic depth was scored according to criteria previously established by Zandieh et al and Jang et al [24,25], and a score < 2 was maintained in all experiments. In the pre-treatment period (Fig.…”

Section: B Treatmentsmentioning

confidence: 99%

Electronically induced contrast enhancement in whisker S1 cortical response fields

Kraus

Francis

2014

2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society

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The ability of an organism to specifically attend to relevant sensory information during learning and subsequent performance of a task is highly dependent on the release of the neurotransmitter Acetylcholine (ACh). Electrophysiological studies have shown that pairing endogenous ACh with specific visual or auditory stimuli induces long lasting enhancements of subsequent cortical responses to the previously paired stimulus. In this study we present data suggesting that similar effects can be elicited in the rat whisker sensory system. Specifically, we show that pairing whisker deflection with electrical stimulation of the magnocellular basal nucleus (BN: a natural source of cortical ACh) causes an increase in the center-surround contrast of the treated whisker's cortical response field (CRF). Meanwhile, deflections of whiskers distant from the treated whisker show overall increased response magnitudes, but non-significant changes in contrast between principle vs. surround barrel responses. Control trials, in which BN stimulation was not paired with whisker deflection, showed similar lack of contrast enhancement. These results indicate that BN stimulation, paired with incoming whisker information, selectively increases the paired whisker's CRF center-surround contrast, while unpaired BN stimulation causes a more general increases in S1 responsiveness, without contrast modulation. Enhanced control over whisker sensory pathway attentional mechanisms has the potential to facilitate a more effective transfer of desired information to the animal's neural processing circuitry, thereby allowing experimental evaluation of more complex behavior and cognition than was previously possible.

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Evaluation of the anaesthetic effects of medetomidine and ketamine in rats and their reversal with atipamezole

Cited by 33 publications

References 24 publications

Effect of dexmedetomidine on hippocampal neuron development and BDNF-TrkB signal expression in neonatal rats

Effect of dexmedetomidine on hippocampal neuron development and BDNF-TrkB signal expression in neonatal rats

The Effects of Tramadol on Electroencephalographic Spectral Parameters and Analgesia in Rats

Electronically induced contrast enhancement in whisker S1 cortical response fields

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