Anxiety-like behaviour in rats with mononeuropathy is reduced by the analgesic drugs morphine and gabapentin

Roeska, Kerstin; Doods, Henri; Arndt, Kirsten; Treede, Rolf‐Detlef; Ceci, Angelo

doi:10.1016/j.pain.2008.05.003

Cited by 110 publications

(89 citation statements)

References 30 publications

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“…Morphine is well recognized as an effective analgesic agent for pain control in an acute myocardial infarction in humans 49) and is known to reduce pain but also anxiety-like behavior in different neuropathic pain rodent models. 25,50,51) In this study, we did not encounter any differences between control rats and morphine-injected rats. The observed slight reduction in activity did not reach statistical signifi cance and is probably due to the concomitant sedation.…”

Section: Discussionmentioning

confidence: 59%

Behavioral Changes Following Experimentally-Induced Acute Myocardial Infarction in Rats

et al. 2014

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SummaryRats with experimentally-induced acute myocardial infarction (AMI) have proven to be a clinically relevant model for visceral pain. As there are no behavioral data available on rats in the postinfarction period, we aimed to identify specifi c pain-related behavioral changes following AMI to increase the validity of the model. AMI was induced by left coronary artery ligation and pain-related behavior was analyzed using the open fi eld test (OFT) and elevated plus maze (EPM). Morphine was applied following AMI induction to differentiate pain-related changes from those related to nonspecifi c global changes in responsiveness. AMI was histologically confi rmed.Hypolocomotion was consistently evident in all behavioral tests for both the infarcted group and sham group. In the OFT, both AMI and sham rats exhibited less exploratory behavior and less activity. A similar pattern of behavior was observed in EPM, where both surgical groups showed fewer entries to the open arms and spent less time in the open arms. The sham group with an intact pericardium showed the same pattern of activity as control rats. The reduction in activity and rearing observed following AMI was successfully reversed following morphine injection. This effect was abolished after naloxone application allowing us to attribute observed changes specifi cally to pain.This study demonstrates that pain-related behavior in the acute postinfarction period is generally characterized by reduced mobility and explorative behavior. Our results showed that cardiac ischemia as a consequence of experimentally-induced infarction is a less important source of pain behavior than manipulation of the pericardium. (Int Heart J 2014; 55: 169-177) Key words: Pericardium, Postoperative pain, Behavior C hest pain is the primary and the most prominent symptom leading to the hospitalization of patients with the diagnosis of acute myocardial infarction (AMI). 1)These patients account for 20% of patients in medical emergency departments.2) However, chest pain related to AMI varies signifi cantly both in its intensity 3,4) and incidence. 5,6) In addition, the pain severity does not seem to be a good predictor of the outcome of myocardial infarction. 7)While the evaluation of pain in humans is predominantly based on conscious perception, in animals it relies mainly on behavioral output. 8) Defined by the International Association for the Study of Pain (IASP) as an unpleasant sensory and emotional experience, 9) pain cannot be determined in animals, so proxy indicators are typically used. In order to increase the translational value of their studies, pain researchers working with experimental animals have focused more on complex behavioral responses and operant measures.10,11) Visceral pain models, eg, models of cardiac ischemia, delineate well these challenges. Pain elicited in these models is vague, with no specifi c region to focus pain measurements on, so broader behavioral and cognitive analysis is necessary to detect potential changes.12)The most commonly used stimuli i...

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Section: Discussionmentioning

confidence: 59%

Behavioral Changes Following Experimentally-Induced Acute Myocardial Infarction in Rats

et al. 2014

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“…In our hands, this positive allosteric modulator (PAM) of GABA A receptors did not induce any analgesic nor significant sedative actions at the selected dose in the CFA-induced arthritis pain model; although sedation was observed when diazepam was used at higher doses. In neuropathic pain models, a similar absence of analgesic actions was observed with etizolam [21] and midazolam [26], two selective benzodiazepine receptor agonists. Interestingly, a recent study by Munro and collaborators suggests that subtype-selective GABA A PAMs (i.e.…”

Section: Discussionmentioning

confidence: 66%

“…In fact, morphine has already been shown to decrease fear-and anxiety-related behaviors in rhesus monkeys [59] and in humans [60]. Furthermore, injection of morphine in healthy rats either has no effect [26] or induces anxiolytic effects [61,62] when tested in the EPM. Part of the explanation for this divergence in morphine effectiveness in relieving anxiety could involve the anxiety-like behavioral test employed, the dose used, the route of administration (systemic vs central vs local injection) and the injection protocol (acute vs sustained).…”

Section: Discussionmentioning

confidence: 99%

“…To date, very few preclinical studies have been conducted to investigate the co-morbidity between chronic pain and anxiety-like behaviors. For instance, only a few neuropathic pain studies have highlighted the development of anxiety-like behaviors in mice or rats using only a limited number of behavioral tests [21][22][23][24][25][26][27][28]. The aim of the present study was therefore to develop and validate a rat model of anxiety-like behaviors caused by chronic inflammatory pain, in line with the clinical reality.…”

Section: Introductionmentioning

confidence: 97%

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Increased anxiety-like behaviors in rats experiencing chronic inflammatory pain

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Beaudet

Beaudry

et al. 2012

Behavioural Brain Research

119

111

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For many patients, chronic pain is often accompanied, and sometimes amplified, by co-morbidities such as anxiety and depression. Although it represents important challenges, the establishment of appropriate preclinical behavioral models contributes to drug development for treating chronic inflammatory pain and associated psychopathologies. In this study, we investigated whether rats experiencing persistent inflammatory pain induced by intraplantar injection of complete Freund's adjuvant (CFA) developed anxiety-like behaviors, and whether clinically used analgesic and anxiolytic drugs were able to reverse CFA-induced anxiety-related phenotypes. These behaviors were evaluated over 28 days in both CFA-and saline-treated groups with a variety of behavioral tests. CFA-induced mechanical allodynia resulted in increased anxiety-like behaviors as evidenced by: 1) a significant decrease in percentage of time spent and number of entries in open arms of the elevated-plus maze (EPM), 2) a decrease in number of central squares visited in the open field (OF), and 3) a reduction in active social interactions in the social interaction test (SI). The number of entries in closed arms in the EPM and the distance travelled in the OF used as indicators of locomotor performance did not differ between treatments. Our results also reveal that in CFAtreated rats, acute administration of morphine (3 mg/kg, s.c.) abolished tactile allodynia and anxiety-like behaviors, whereas acute administration of diazepam (1 mg/kg, s.c) solely reversed anxiety-like behaviors. Therefore, pharmacological treatment of anxiety-like behaviors induced by chronic inflammatory pain can be objectively evaluated using multiple behavioral tests. Such a model could help identify/validate alternative potential targets that influence pain and cognitive dimensions of anxiety.

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“…For instance, the anti-nociceptive and anti-allodynic effectiveness of GBP has been widely supported by studies in animal models of many types of pain induced by peripheral nerve injury such as spinal nerve ligation [47][48][49][50], chronic compression injury [51][52][53][54][55][56] and spared nerve injury [57,58]. Moreover, GBP has also been demonstrated to have anti-allodynic and anti-hyperalgesic effects in animal models of diabetic neuropathy [29] and postherpetic neuralgia [59].…”

Section: Gabapentinoid Insensitivity In Central Neuropathic Pain Of Tmentioning

confidence: 99%

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

Yang

et al. 2016

Neurosci. Bull.

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The a 2 d-1 subunit of the voltage-gated Ca 2? channel (VGCC) is a molecular target of gabapentin (GBP), which has been used as a first-line drug for the relief of neuropathic pain. GBP exerts its anti-nociceptive effects by disrupting trafficking of the a 2 d-1 subunit to the presynaptic membrane, resulting in decreased neurotransmitter release. We previously showed that GBP has an antiallodynic effect in the first two weeks; but this is followed by insensitivity in the later stage after repeated administration in a rat model of central post-stroke pain (CPSP) hypersensitivity induced by intra-thalamic hemorrhage. To explore the mechanisms underlying GBP insensitivity, the cellular localization and time-course of expression of the a 2 d-1 subunit in both the thalamus and spinal dorsal horn were studied in the same model. We found that the a 2 d-1 subunit was mostly localized in neurons, but not astrocytes and microglia. The level of a 2 d-1 protein increased in the first two weeks after injury but then decreased in the third week, when GBP insensitivity occurred. Furthermore, the a 2 d-1 down-regulation was likely caused by later neuronal loss in the injured thalamus through a mechanism other than apoptosis. In summary, the present results suggest that the GBP receptor a 2 d-1 is mainly expressed in thalamic neurons in which it is up-regulated in the early stage of CPSP but this is followed by dramatic down-regulation, which is likely associated with GBP insensitivity after long-term use.Keywords Central post-stroke pain Á Calcium channel a 2 d subunit Á Gabapentinoid Á Thalamic hemorrhagic stroke Á Thalamus Á Spinal dorsal horn

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Anxiety-like behaviour in rats with mononeuropathy is reduced by the analgesic drugs morphine and gabapentin

Cited by 110 publications

References 30 publications

Behavioral Changes Following Experimentally-Induced Acute Myocardial Infarction in Rats

Behavioral Changes Following Experimentally-Induced Acute Myocardial Infarction in Rats

Increased anxiety-like behaviors in rats experiencing chronic inflammatory pain

Gabapentinoid Insensitivity after Repeated Administration is Associated with Down-Regulation of the α2δ-1 Subunit in Rats with Central Post-Stroke Pain Hypersensitivity

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