Male mice from 14 standard inbred strains were exposed to morphine in a sustained released preparation injected subcutaneously. Five hours later withdrawal was precipitated by intraperitoneal injection of naloxone. Mice were tested from 0 to 15 min after naloxone for withdrawal jumping behavior, and then from minute 15-16 for other signs, including boli count, presence of soft stool, lacrimation, "wet dog" shakes, and air chewing. They were also assessed for change in body temperature 17 min after naloxone. Strains differed markedly in the severity of withdrawal for jumping, change in body temperature, and number of fecal boli. Strains also differed in percentage of animals displaying soft stool and air chewing behavior. The other two signs were seen at too low frequency for analysis. Correlations of strain mean withdrawal severity with other responses to morphine and other abused drugs showed that high morphine withdrawal jumping and low change in body temperature were both genetically related to high morphine consumption, but not generally to other measures of morphine withdrawal or morphine sensitivity.
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http://dx.doi.org/10.1016/j.drugalcdep.2008.07.006 | DOI Listing |
Front Vet Sci
December 2024
Experimental Surgery Facility, Experimental Animal Center, Faculty of Medicine, University of Bern, Bern, Switzerland.
Introduction: Use of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is still in the focus of research, in which pigs are commonly involved. During VA-ECMO, cardiovascular parameters are artificially manipulated and therefore not reliable indicators of nociception. Nociceptive withdrawal reflex (NWR) thresholds can be a suitable alternative in such a context.
View Article and Find Full Text PDFHeliyon
December 2024
Department of Biomedical Sciences, Pak Austria Fachhochschule: Institute of Applied Sciences and Technology, Haripur, Khyber Pakhtunkhwa, Pakistan.
Morphine belongs to the class of opioids and is known for its potential to cause dependence and addiction, particularly with prolonged use. Due to the associated risks, caution must be taken when prescribing and limiting its clinical use. Overexpression of N-methyl-D-aspartate (NMDA) receptors, nitric oxide and cGMP pathway has been implicated in exacerbate the development of morphine dependence and withdrawal.
View Article and Find Full Text PDFJ Neurosurg Anesthesiol
December 2024
Departments of Anaesthesiology, Pain Medicine and Critical Care.
Background: Smoking negatively impacts postoperative outcomes but acute abstinence from smoking during hospitalization can increase postoperative pain, lower pain thresholds, disrupt pain management, and trigger hyperalgesia due to abrupt nicotine withdrawal in tobacco users. Nicotine replacement therapy has been recommended to minimize these complications. We hypothesized that a high dose (21 mg/24 h) transdermal nicotine (TDN) patch would reduce postoperative pain and opioid requirements.
View Article and Find Full Text PDFBehav Pharmacol
December 2024
Department of Pharmacology, Biological Sciences Sector, Federal University of Paraná.
Opioid use disorder is a public health problem that includes symptoms such as withdrawal syndrome and opioid-induced hyperalgesia. Currently, drugs to treat side effects of opioids also have undesirable effects, which lead to limitations. This study investigated the effect of a treatment with cannabidiol in morphine-induced hyperalgesia and withdrawal behavior in morphine-dependent rats.
View Article and Find Full Text PDFBiochemistry (Mosc)
November 2024
Federal Research Center for Innovator and Emerging Biomedical and Pharmaceutical Technologies, Moscow, 125315, Russia.
The accumulated evidence suggests that varying levels of tyrosine kinase receptor signaling pathway activity may regulate opiate-associated neuroadaptation of noradrenergic system. Neurotrophin-3 (NT-3) interacts with tropomyosin receptor kinases (TRKs), binding mainly to TRKC receptors, which are expressed within noradrenergic neurons in the blue spot (, LC). Considering the difficulties in delivering full-length neurotrophins to the CNS after systemic administration, low-molecular mimetics of loop 4 in NT-3, hexamethylenediamide bis-(N-monosuccinyl-L-asparaginyl-L-asparagine) (GTS-301), and hexamethylenediamide bis-(N-γ-oxybutyryl-L-glutamyl-L-asparagine) (GTS-302), activating TRKC and TRKB receptors, were synthesized.
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