Abstract
The aim of the present study was to determine if phenobarbital affects the nociception threshold. Systemic (1-20 mg/kg) phenobarbital administration dose dependently induced hyperalgesia in the tail-flick, hot-plate and formalin tests in rats and in the abdominal constriction test in mice. Formalin and abdominal constriction tests were the most sensitive procedures for the detection of hyperalgesia in response to phenobarbital compared with the tail-flick and hot-plate tests. The hyperalgesia induced by systemic phenobarbital was blocked by previous administration of 1 mg/kg ip picrotoxin or either 1-2 mg/kg sc or 10 ng icv bicuculline. Intracerebroventricular phenobarbital administration (5 microg) induced hyperalgesia in the tail-flick test. In contrast, intrathecal phenobarbital administration (5 microg) induced antinociception and blocked systemic-induced hyperalgesia in this test. We suggest that phenobarbital may mediate hyperalgesia through GABA-A receptors at supraspinal levels and antinociception through the same kind of receptors at spinal levels.
Highlights
Barbiturates are drugs with the potential to reduce anxiety and promote sleep, to induce general anesthesia, and in special cases to inhibit tonic-clonic seizures [1]
Extending data from previous work [7], in the present study we showed that acute phenobarbital administration induced a dose-dependent hyperalgesia
Some barbiturates are still used today therapeutically as general anesthetics and anticonvulsants. These drugs essentially act at the central nervous system (CNS) level, facilitating GABAergic neurotransmission by binding at specific sites in the gammaaminobutyric acid (GABA)-A receptor [4]
Summary
Barbiturates are drugs with the potential to reduce anxiety and promote sleep, to induce general anesthesia, and in special cases to inhibit tonic-clonic seizures [1] In some of these conditions, they have been replaced with other drugs such as benzodiazepines and serotonin re-uptake inhibitors. Activation of the GABAA receptor has been associated with pain modulation in the central nervous system (CNS), essentially through the descending inhibitory system [5]. It is still a matter of discussion in the literature whether barbiturates increase [6,7] or decrease [8,9] the pain threshold
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