pI,pHAi ADRENERGIC AND HI GH STRF.PTO OTOCININDUCED D ^I3ETI CHANGES IN THE BRAIN STEM C RATS

the state. while EPI content remained increased as in die diabetic B,, for a]pha2 adrenergic receptors slw^nificantly while Unlabelled clonidine inhibited [31-I]NE binding in BS of control, diabetic and insulin treated ulations bindi diabetic rats showed that alpha2 adrenergicre^ punks cojnidiabetic animal the ligand bound sites with Hill slopes significantly away from unity. weaker to the low affinity site than in controls. Insulin treatment reversed[ this allumbmn to control levels. The displacement analysis using (-)-epinephrine age in control and diabetic animals revealed two populations of receptor affind ityo=tat ss. In control animals, when GTP analogue added with epinephrine, the curve ngle affinity and contro S model; but in the diabetic BS this effect `not aobserved. In bintact oth the diabetic data thus showlthat the effects of monovalent cations on affinity alphaz adrenergic receptors have a reduced affinity v due in stem ialtered Itscppeomson(5regulation. The serotonin (5-HT) coat hydroxy) tryptophan (5-HTP) showed an increase and its breakdown metabolite (5-hydroxy) indoleacetic acid (5-I{IAA) showed a significant decrease. This showed that in serotonergic which l nerves there is a disturbance in both synthetic and breakdown a numbers pretma'med an increased 5-HT. The high affinity serotonin receptor um ese serotonerg decrease in the receptor affinity. The insulin ^treatment sturtiy showsha decreased serotonergic receptor kinetic parameters to control level. receptor function. These changes in adrenergic and serotonergic receptor function were