Morphine withdrawal syndrome: differential participation of structures located within the amygdaloid complex and striatum of the rat.

The participation of amygdaloid and striatal structures in the various signs of morphine withdrawal syndrome (MWS) has been investigated using two complementary approaches: intracerebral application of naloxone in various nuclei of dependent rats and effects of various lesions and transections on systemically induced MWS. In morphine dependent rats local application of naloxone (10 micrograms in 0.1 microliter solution) in the vicinity of either the central nucleus of the amygdala or the lateral anterior nucleus but not in adjacent amygdaloid or striatal nuclei elicited the jump sign. Diarrhea was more frequently elicited by application of naloxone in the striatum or centromedial amygdala than the basolateral parts of the complex. In contrast, there was no specific anatomical correlates to the remaining signs including wet shakes, paw tremor, teeth chattering and chewing. Bilateral electrolytic lesion of the central amygdala or combined transection of the stria terminalis and so-called ventral amygdalofugal pathway eliminated the jump without affecting the remaining signs. In contrast a large bilateral destruction of the entire striatrum did not significantly affect the various signs. Bilateral transection of the stria terminalis reduced only the occurrence of the wet shakes. Also, a transection of the medial forebrain bundle considerably reduced the 3 main signs, i.e. jump, wet shakes and diarrhea. These results suggest that, in analogy to the acute actions of morphine, MWS should not be considered as a unitary phenomenon but as an ensemble of signs which probably reflect the intense activation induced by naloxone in a number of brain sites consequent to the abrupt interruption of opioid actions in a dependent animal. The significance of these results is discussed with reference to previous anatomical, biochemical and behavioural studies performed on the amygdala.