Studies on the Mechanism of Wet Dog Shakes Produced by Carbachol in Rats

Turski, Waldemar A.; Czuczwar, S.J.; Turski, Lechostaw; Sieklucka-Dziuba, M; Kleinrok, Z

doi:10.1159/000137951

Cited by 9 publications

(3 citation statements)

References 12 publications

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“…the hypothalamus (Maldonado et al, 1992), locus coereleus (Hoshi et al, 1987;Liu et al, 1999) hippocampus (Ohno et al, 1987) and ventral tegmental area (Wang et al, 2004)] and neurotransmitters [e.g. serotonin (Yap and Taylor, 1983;Fone et al, 1991), dopamine (David et al, 2005), acetylcholine (Turski et al, 1984)] in icilin-induced wet-dog shakes. In the future, it is imperative to investigate the role of multiple brain regions and neurotransmitters in icilin-evoked shaking behavior.…”

Section: Discussionmentioning

confidence: 99%

Nalfurafine, the kappa opioid agonist, inhibits icilin-induced wet-dog shakes in rats and antagonizes glutamate release in the dorsal striatum

Werkheiser¹,

Cowan²

2007

Neuropharmacology

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Icilin, a cooling compound, produces vigorous wet-dog shakes in rats. We have reported previously that icilin-induced wet-dog shakes are blocked by the kappa opioid receptor agonists, nalfurafine and U50,488H, and that icilin evokes a dose-and time-dependent increase in glutamate within the dorsal striatum. Since activation of kappa opioid receptors inhibits glutamate release intrastriatally, we targeted glutamate release within the dorsal striatum using nalfurafine and examined the role of the dorsal striatum in icilin-induced wet-dog shakes, more specifically, the effect that icilin-evoked intrastriatal glutamate release has on the overt stimulant behavior. We report that nalfurafine (0.04 mg/kg) inhibits icilin (0.50 mg/kg)-induced wet-dog shakes and that this inhibition is reversed by intrastriatal perfusion of the kappa opioid receptor antagonist, norbinaltorphimine (100 nM). Furthermore, we antagonized icilin-evoked glutamate release with nalfurafine (0.04 mg/kg), and reversed inhibition of glutamate release with intrastriatal norbinaltorphimine (100 nM). These findings support a central component in the behavioral response to icilin and suggest that activation of kappa opioid receptors antagonizes icilin-induced wet-dog shakes in rats by inhibiting glutamate release within the dorsal striatum.

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Section: Discussionmentioning

confidence: 99%

Nalfurafine, the kappa opioid agonist, inhibits icilin-induced wet-dog shakes in rats and antagonizes glutamate release in the dorsal striatum

Werkheiser¹,

Cowan²

2007

Neuropharmacology

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“…However, administration of carbachol, another muscarinic agonist, decreased the number and duration of SWD in Wag/Rij rats [58], indicating acetylcholine may play opposing roles in absence and partial epilepsies. Interestingly, carbachol can also be used to kindle motor seizures, and the wet dog shaking behavior associated with carbachol kindling may have muscarinic mechanisms [59]. In the SwLo rat, wet dog shaking was elevated during both hippocampal and amygdala kindling, pointing to possible muscarinic dysfunction in this model [27].…”

Section: Potential Mechanisms and Therapeutic Targetsmentioning

confidence: 99%

Rhythm and blues: Animal models of epilepsy and depression comorbidity

Epps

Weinshenker

2013

Biochemical Pharmacology

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Clinical evidence shows a strong, bidirectional comorbidity between depression and epilepsy that is associated with decreased quality of life and responsivity to pharmacotherapies. At present, the neurobiological underpinnings of this comorbidity remain hazy. To complicate matters, anticonvulsant drugs can cause mood disturbances, while antidepressant drugs can lower seizure threshold, making it difficult to treat patients suffering from both depression and epilepsy. Animal models have been created to untangle the mechanisms behind the relationship between these disorders and to serve as screening tools for new therapies targeted to treat both simultaneously. These animal models are based on chemical interventions (e.g. pentylenetetrazol, kainic acid, pilocarpine), electrical stimulations (e.g. kindling, electroshock), and genetic/selective breeding paradigms (e.g. Genetically Epilepsy-Prone Rats (GEPRs), Genetic Absence Epilepsy Rat from Strasbourg (GAERS), WAG/Rij rats, Swim Lo-Active rats (SwLo)). Studies on these animal models point to some potential mechanisms that could explain epilepsy and depression comorbidity, such as various components of the dopaminergic, noradrenergic, serotonergic, and GABAergic systems, as well as key brain regions, like the amygdala and hippocampus. These models have also been used to screen possible therapies. The purpose of the present review is to highlight the importance of animal models in research on comorbid epilepsy and depression and to explore the contributions of these models to our understanding of the mechanisms and potential treatments for these disorders.

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“…For example, we have shown in this study that SwLo rats are more susceptible to seizures and epileptogenesis induced by the muscarinic acetylcholine receptor agonist, pilocarpine. SwLo rats also have a higher incidence of wet dog shakes during kindling, and disturbances in the muscarinic system have been implicated in wet dog shakes induced by carbachol (Turski et al, 1984). These noradrenergic and cholinergic associations need to be tested empirically, and other neurotransmitter systems that modulate both mood and neuronal excitability (eg, serotonin, neuropeptides) could also be involved.…”

Section: Potential Mechanisms Underlying the Swlo Seizure Phenotypesmentioning

confidence: 99%

Seizure Susceptibility and Epileptogenesis in a Rat Model of Epilepsy and Depression Co-Morbidity

Epps

Tabb

Lin

et al. 2012

Neuropsychopharmacol

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Although a strong co-morbidity exists clinically between epilepsy and depression, the cause of this co-morbidity remains unknown, and a valid animal model is crucial for the identification of underlying mechanisms and the development of a screening tool for novel therapies. Although some rodent models of epilepsy have been reported to display behaviors relevant to affective disorders, the seizure susceptibility of animals prone to depression-like behavior has not been characterized. Toward this end, we assessed several forms of seizure sensitivity and epileptogenesis in rats selectively bred for vulnerability (Swim Lo-Active; SwLo) or resilience (Swim High-Active; SwHi) to depression-like phenotypes. The SwLo rats exhibit decreased motor activity in a swim test and other depression-like phenotypes, whereas the SwHi rats display increased motor activity in a swim test. SwLo rats exhibited a decreased latency to limbic motor seizures following acute pilocarpine administration in the absence of differences in pilocarpine pharmacokinetics, and also had a decreased threshold to tonic seizures induced by electroshock. Approximately half of the SwLo rats, but none of the SwHi rats, had spontaneous limbic motor seizures 5 weeks following pilocarpine-induced status epilepticus. While the number of stimulations required to achieve full amygdala and hippocampal electrical kindling were similar in the two rat lines, SwLo rats had a lower final hippocampal kindling threshold and more wet dog shakes during both amygdala and hippocampal kindling. Combined, these results indicate that SwLo rats are a model of epilepsy and depression co-morbidity that can be used for investigating underlying neurobiological and genetic mechanisms and screening novel therapeutics.

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Studies on the Mechanism of Wet Dog Shakes Produced by Carbachol in Rats

Cited by 9 publications

References 12 publications

Nalfurafine, the kappa opioid agonist, inhibits icilin-induced wet-dog shakes in rats and antagonizes glutamate release in the dorsal striatum

Nalfurafine, the kappa opioid agonist, inhibits icilin-induced wet-dog shakes in rats and antagonizes glutamate release in the dorsal striatum

Rhythm and blues: Animal models of epilepsy and depression comorbidity

Seizure Susceptibility and Epileptogenesis in a Rat Model of Epilepsy and Depression Co-Morbidity

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