ABSTRACT
Naloxone has been reported to affect pain and locomotor activity differently depending on the dose. The objective of the present investigation was to study the effects of low and high (6 micrograms and 3 mg/kg, s.c.) doses of naloxone (Nx) on formalin-induced pain (tonic pain) and spontaneous motor activity and any correlation between them. The experiments were conducted on adult male Wistar rats. Tonic pain and spontaneous motor activity were recorded by the formalin test and video monitoring respectively. An increase in spontaneous motor activity (locomotion, movements and distance) was observed following formalin injection as compared to basal activity (P < 0.05). Low dose of Nx reduced the pain intensity and also the spontaneous motor activity during the later phase (after 15 min of formalin injection) (P < 0.05). High dose of Nx on the other hand increased the pain intensity but still reduced motor activity (P < 0.05). Both doses of Nx initially produced hyperalgesia (5 min peak). The bidirectional effects of Nx on formalin pain were dissociated from the spontaneous motor behavior of rats. A direct correlation could not be established between pain intensity and spontaneous motor activity.
Subject(s)
Animals , Behavior, Animal/drug effects , Dose-Response Relationship, Drug , Formaldehyde , Male , Motor Activity/drug effects , Naloxone/pharmacology , Narcotic Antagonists/pharmacology , Nociceptors/drug effects , Pain/chemically induced , Rats , Rats, WistarABSTRACT
The limbic system has been implicated in the modulation of pain. The aim of this study was to determine the role of amygdala in different types of pain, viz., phasic and tonic. Unilateral stimulation of central nucleus of amygdala (CeA), basolateral nucleus (BL) and medial amygdaloid (MeA) in conscious rats resulted in the reduction of the tonic formalin-induced pain. The thresholds for simple vocalization (SV) and vocalization after-discharge (VA) were elevated during amygdalar stimulation in the tail-flick (phasic pain) test. However, the threshold for tail-flick (TF) evoked by electric shock was not affected. Tail-flick latency (TFL) to noxious heat was accentuated during amygdalar stimulation. These results suggest that amygdala had a modulatory role in the descending endogenous pain control mechanisms.