Microinjection of NMDA Receptor Agents into the Central Nucleus of the Amygdale Alters Food Intake in Rats

Introduction A great deal of evidence indicates that the Limbic areas such as amygdala plays an important role in the control of food and water intake [1].Glutamatergic mechanisms are present in all brain regions regulating feeding, including the nucleus accumbens, hypothalamus, and amygdala. A limbic forebrain region strongly implicated in the motivational mechanisms for feeding [2]. For years, the main effects of glutamate were thought to be exclusively mediated by ion channel mechanisms. However, glutamate receptors can now be categorised into two major groups; (I) ionotropic and (II) metabotropic receptors. This categorisation is based on intracellular/extracellular coupling and on different pharmacological and biochemical characteristics. Ionotropic receptors Abstract Food intake is the primary factor for body weight regulation in animals. Eating behavior is known to be modulated by various neurotransmitters and receptors. The central nucleus of the amygdala (CeA) is the forebrain structures which are important in regulation of ingestive behavior. There is direct and circumstantial evidence to indicate that some circuits involved with feeding behavior include glutamatergic elements. The present study examined whether administration of NMA or MK801 in the CeA alters food intake under deprivation. Animals were deprived for 24 h before tested for food intake. NMDA glutamatergic receptor agonist, NMA (N-Methyl-DL-aspartic acid) and its antagonist, MK801 (Dizocilpine hydrogen maleate) were infused bilaterally, and food intakes were measured for 12 h post-injection. The intra-CeA injection of NMDA glutamatergic agonist NMA (0.25, 0.5 and 0.75 μg/ rat) showed no effect on cumulative food intake. However, administration of NMDA glutamatergic antagonist, MK801 (0.25, 0.5 and 1 μg/rat) increased food intake in the deprived rats. The finding suggest that NMDA receptors in the CeA are responsible for the glutamatergic modulation of feeding in this nucleus.