Effect of VMH Lesion on Sucrose-Fed Analgesia in Formalin Pain.

Abstract

The ingestion of sucrose has been reported to produce analgesia in newly born rat [1], human [2,3], and adult rat models [4]. Sucrose ingestion in rat pups [1] immediately increases paw lift latency to thermal noxious stimulus, and in adult rats it decreases nociceptive behavioral rating to tonic formalin stimulus after 12 h [5]. In newborn infants, it reduces crying time, attenuates the increase in heart rate and blood pressure, and improves oxygen saturation, indicating analgesia [2,3,6]. This analgesic effect is clinically utilized to carry out minor surgical interventions such as immunization, circumcision, and venesection in newborn infants with no other anesthetic supplementation [2,3,6,7]. The analgesic action is possibly not secondary to distraction, but related to the hedonic qualities of sucrose [8]. The ingestion of palatable sweet substances such as candy is reported to decrease the levels of hypothalamic ␤-endorphin and opioid receptor binding probably because of increased utilization [9]. Moreover, the involvement of opioid peptide is further supported by abolition of the sucrose-fed analgesia in naloxone pretreated infants [2].Medial hypothalamus is involved in the modulation of pain, since its lesion produces hyperalgesia [10,11] and stimulation produces analgesia [12,13]; its neurons have opioid receptors [14][15][16]. These neurons also respond to iontophoretic application of glucose. These glucose-responsive neurons respond to both the peripheral noxious stimulation and micro iontophoretic application of opioid peptides by attenuating their firing rate [14][15][16]. There are therefore indirect indications of a link between opioid, analgesia, and food ingestion. It is not known whether the sucrose-fed analgesia is also neurally mediated. Similarly, the VMH also governs the preference for palatable food and is also influenced by palatable food [9]. The VMH therefore exerts a significant effect in pain modulation and carbohydrate preference, although its Japanese Journal of Physiology Vol. 51, No. 1, 2001 63Japanese Journal of Physiology, 51, 63-69, 2001 Key words: sucrose-fed analgesia, formalin pain, tonic pain, VMH. Abstract:The ingestion of sucrose (ad libitum) produces an immediate analgesic response to phasic noxious stimuli. The underlying mechanism for the analgesic effect of sucrose is attributed to its palatability, which mediates analgesia probably by the release of ␤-endorphin in the hypothalamus. The present study was designed to explore the role of ventromedial hypothalamus in the mediation of sucrose-fed analgesia. Adult male albino rats each received (20%) sucrose solution orally through a separate bottle until they had ingested 4-5 ml. Their behavioral responses to tonic noxious stimulus in a formalin test were studied in pre-and postsucrose-fed rats of control and in the VMH lesion groups . The average pain rating of a 60-min session significantly ( pϽ0.01) decreased after sucrose feeding in control rats, from 1.94Ϯ0.13 to 1.45Ϯ0.14, but sucrose feeding by the VMH lesion rat...

Threshold of Pain in Chronic Magnetic Field- (50 Hz, 17.9 μT) Exposed Rats: Effect of Sucrose Ingestion

“…On the one hand, ingestion of palatable food substances such as sucrose by adults or neonates immediately evokes analgesia in both human (Mercer and Holder, 1997;Bucher et al, 1995) and animal (Blass et al, 1987;Dutta et al, 2001) models, which was also reported from this laboratory and several other researchers. Taste stimulus initiates the cascade of information processing and transfer from tongue to medial hypothalamus including secretion of b-endorphins from arcuate nucleus (Mansour et al, 1988), action on VMH glucoresponsive neurons (Dutta et al, 2001;Pittman et al, 1979;Mukherjee et al, 2001b) translating it into behaviors such as pleasure, satiation, analgesia (Dutta et al, 2001;Schoenbaum et al, 1989), and alleviation of stress (Blass et al, 1987;Mukherjee et al, 2001a).…”

“…Ingestion of sucrose or any palatable substance has repeatedly been demonstrated to produce analgesia almost instantly (Blass et al, 1987;Dutta et al, 2001). A significant effect was attained within 5 min, which was maintained for 30-45 min post-sucrose ingestion in our rats.…”

“…Electrolytic lesion of ventromedial hypothalamus (VMH) abolishes the sucrose-fed analgesia to noxious stimuli (Dutta et al, 2001), thereby, supporting the inclusion of VMH as a key structure in the neural network of sucrose-fed analgesia. In addition, the critical role of VMH is highlighted by our previous reports of persistent reduction in the thresholds of TF, VD, and VA indicating hyperalgesia (Mukherjee et al, 2000) and abolition of sucrose-fed analgesia by VMH lesion (Dutta et al, 2001). VMH modulates the nociceptive behaviour through its glucoresponsive neurons (Mukherjee et al, 2001b).…”

“…A significant effect was attained within 5 min, which was maintained for 30-45 min post-sucrose ingestion in our rats. Sucrose fed analgesia is not alone exhibited during the experimental pain induced by tonic or phasic noxious stimuli in animals (Blass et al, 1987;Dutta et al, 2001;Mukherjee et al, 2001a) or humans (Bucher et al, 1995;Geyer et al, 2002;Miller et al, 1994) but also during the minor surgical interventions such as heel lancing (Bucher et al, 1995), immunization (Keith et al, 1996), venesection, or circumcision (Geyer et al, 2002). The distress in infants is significantly reduced in terms of infant behavior, biochemical, or endocrine parameters (Geyer et al, 2002;Keith et al, 1996).…”

“…Taste stimulus initiates the cascade of information processing and transfer from tongue to medial hypothalamus including secretion of b-endorphins from arcuate nucleus (Mansour et al, 1988), action on VMH glucoresponsive neurons (Dutta et al, 2001;Pittman et al, 1979;Mukherjee et al, 2001b) translating it into behaviors such as pleasure, satiation, analgesia (Dutta et al, 2001;Schoenbaum et al, 1989), and alleviation of stress (Blass et al, 1987;Mukherjee et al, 2001a). Both these above-mentioned factors viz.…”