Bombesin injection into the central amygdala influences feeding behavior in the rat J. Vı ´gh a , L. Le ´na ´rd a,b, *, E ´ . Fekete a , I. Herna ´di a a Department of Zoology and Neurobiology, Faculty of Natural Sciences, Janus Pannonius University, H-7601 Pe ´cs, Ifju ´sa ´g str. 6, Hungary b Neurophysiology Research Group of the Hungarian Academy of Sciences at Institute of Physiology, Pe ´cs University Medical School, H-7643 Pe ´cs, Szigeti str. 12, Hungary Received 20 April 1998; accepted 16 November 1998 Abstract The present study was performed to determine whether low doses (10 or 40 ng) of bombesin microinjected into the amygdala could modify solid food intake. Forty ng of bombesin in 24 h deprived rats caused transient inhibition of food intake. This inhibitory effect was eliminated by prior bombesin antagonist treatment. A series of quantitative behavioral tests indicated that low doses of bombesin application specifically reduced food intake without altering the behavioral pattern or influencing the body temperature. The present results suggest, that bombesin-like peptides may act as a satiety signal in the central part of the amygdala. © 1999 Elsevier Science Inc. All rights reserved. Keywords: Bombesin; Amygdala; Feeding; Behavior; Body temperature 1. Introduction It has been shown that the neuropeptide bombesin (BN) and BN like peptides are involved in the mechanisms of satiety. BN originally extracted from the skin of Bombina bombina [2] consists of 14 amino acids. BN has a mamma- lian form [54], called gastrin-releasing peptide (GRP) iso- lated first from the porcine gastrointestinal tract [40,44]. The 27-amino acid containing GRP shares a similar C terminal peptide sequence with BN. Because BN repro- duces all the known effects of GRP, it is commonly used in mammalian experiments [39]. During eating GRP is released in the periphery [26] and it has been hypothesized that through its neuronal and hu- moral effects GRP acts as a satiety-signal evoking preab- sorptive satiety and responsible for the maintenance of post- prandial satiety [19]. Indeed, one significant action of intraperitoneally (IP) or intracerebroventricularly (ICV) ap- plied BN (or GRP) is the rapid and transient inhibition of feeding in either food-deprived, nondeprived, or sham-fed laboratory animals [9,16,18,27,38,43,50]. GRP receptors and BN-like immunoreactivity in the rat brain were found by immunhistochemical and autoradiographic investiga- tions with significant amounts in the hypothalamus and amygdala (AMY) [32,46,47,55]. The role of the hypothal- amus in feeding processes is well established [1,22,36]. As far as the AMY is concerned, the existence of a ‘hunger- center’ has been suggested in the dorsomedial-central part of this structure. Namely, in both dog and rat the destruction of the dorsomedial-central AMY caused aphagic and adip- sic symptoms similar to those seen after the lesion of the lateral hypothalamus (LH) [7,13–15,23,29]. It has also been shown that the amygdaloid ‘hunger-center’ exhibits only modulatory influences on the hypothalamic feeding mech- anisms [29]. The effects of BN have been tested on the central feed- ing-regulatory processes mainly by ICV applications. In these experiments, centrally applied BN reduced food in- take [4,5,10,17,31], increased grooming activity [4,5,10, 24], decreased exploration [10,24] and changes in body temperature have also been observed [25,52]. Local, intra- cerebral application of high doses of BN (1 g) into the paraventricular (PVN), dorsomedial (DMN) or ventrome- dial (VMH) nuclei of the hypothalamus, or the periaque- ductal gray (PAG) decreased food consumption with a si- multaneous increase of grooming [30]. These experiments, including lateral ventricular BN applications have been crit- icized suggesting that BN induces grooming activity and it * Corresponding author. Tel.: +36-72-324-122/1278 ext, fax: +36-72- 315-714. E-mail address: lenard@physiol.pote.hu (L. Le ´na ´rd) Peptides 20 (1999) 437– 444 0196-9781/99/$ – see front matter © 1999 Elsevier Science Inc. All rights reserved. PII: S0196-9781(99)00023-6