All rights reserved.”
“Purpose: We determined whether see more transcutaneous electrical foot stimulation combined with a low dose of tramadol (Sigma-Aldrich (R)) could completely suppress bladder overactivity.
Materials and Methods: Repeat cystometrograms were performed in 18 alpha-chloralose anesthetized cats by infusing the bladder with saline or 0.25% acetic acid. Transcutaneous electrical stimulation (5 Hz) of the cat hind foot at 2 to 4 times the threshold intensity needed to induce observable toe movement was applied to suppress acetic acid induced
bladder overactivity. Tramadol (1 to 3 mg/kg intravenously) was administered to enhance foot inhibition.
Results: Acetic acid irritated the bladder, induced bladder overactivity and significantly decreased bladder capacity to
a mean +/- SE of 26% +/- 5% of saline control capacity (p <0.01). Without tramadol, foot stimulation at 2 and 4 threshold intensity applied during acetic acid cystometrograms significantly increased Anlotinib solubility dmso bladder capacity to a mean of 47% +/- 5% and 62% +/- 6% of saline control capacity, respectively (p <0.05). Without foot stimulation, tramadol (1 mg/kg) only slightly changed bladder capacity to a mean of 39% +/- 2% of saline control capacity (p >0.05), while 3 mg/kg significantly increased capacity to 85% +/- 14% that of control (p <0.05). However, 1 mg/kg tramadol combined with foot stimulation increased bladder capacity to a mean of 71% +/- 18% (2 threshold intensity) and 84% +/- 14% (4 threshold intensity), respectively, which did not significantly differ from saline control capacity. In addition, long lasting (greater than 1.5 Cell press to 2 hours) post-stimulation inhibition was induced by foot stimulation combined with 3 mg/kg tramadol treatment.
Conclusions: This study suggests a new treatment strategy for overactive bladder by combining foot stimulation with a low dose of tramadol, which is noninvasive and has potentially high efficacy and fewer adverse effects.”
“Judgement bias has potential as a measure of affective state in animals.
The serotonergic system may be one mechanism involved with the formation of negative judgement biases. It was hypothesised that depletion of brain serotonin would induce negative judgement biases in sheep. A dose response trial established that 40 mg/kg of p-Chlorophenylalanine (pCPA) administered to sheep for 3 days did not affect feeding motivation or locomotion required for testing judgement biases. Thirty Merino ewes (10 months old) were trained to an operant task for 3 weeks. Sheep learnt to approach a bucket when it was placed in one corner of the testing facility to receive a feed reward (go response), and not approach it when in the alternate corner (no-go response) to avoid a negative reinforcer (exposure to a dog). Following training, 15 sheep were treated with pCPA (40 mg/kg daily) for an extended duration (5 days).