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I t h a s been suggested t h a t alterations of monoamine receptor sensitivity in t h e c e n t r a l nervous system may b e associated with some f o r m s of a f f e c t i v e illness. I t h a s been observed by several investigators t h a t chronic t r e a t m e n t with antidepressant drugs causes down regulation of NE receptor coupled adenylate cyclase and b e t a adrenergic receptor binding in r a t brain. This observation h a s led to t h e suggestion t h a t t h e therapeutic e f f e c t s of antidepressant drugs may b e related to t h e changes in t h e responsivity of b e t a adrenergic receptors. In order to examine if depressive illness may be associated with a l t e r e d b e t a adrenergic function, we studied adenylate cyclase and i t s responsiveness to norepinephrine and isoproterenol in t h e leukocytes obtained from patients with psychiatric illness and normal controls as a n index of beta adrenergic receptor function. We also studied t h e e f f e c t s of antidepressant drugs, in vitro, on isoproterenol sensitive leukocyte adenylate cyclase. W e observed t h a t norepinephrine and isoproterenol sensitive leukocyte adenylate cyclase in depressed patients a r e significantly decreased as compared to normal controls. Our results appear to have been replicated by another group of investigators. W e also observed t h a t c e r t a i n antidepressnt drugs potentiate isoproterenol stimulated accumulation of cyclic AMP in human leukocytes. This potentiation w a s most pronounced in t h e case of iprindole. These results thus indicated a decreased beta adrenergic receptor function in patients with depressive illness.Whether or not such decreased receptor function is associated with depressive illness o r is a manifestation of s o m e other changes unrelated to t h e illness is not clear. Our results also indicate t h a t some antidepressant drugs may enhance adrenergic transmission by potentiating t h e e f f e c t s of neurotransmitters on b e t a adrenergic receptors.An abnormality of amine function in a f f e c t i v e illness may result due to changes in a m i n e biosynthesis, metabolism, uptake o r due to a n imbalance in neurotransmitter systems. I t is also possible t h a t amine dysfunction in a f f e c t i v e illness may b e associated with altered sensitivity of t h e c e n t r a l neurotransmitter receptors. Alterations in t h e neurotransmitter input from t h e presynaptic neuron may cause compensatory changes in t h e postsynaptic neurotransmitter receptor sensitivity o r response. In r e c e n t years, i t has been suggested t h a t in addition to t h e studies of monoamine metabolites and t h e e n z y m e s associated with t h e biosynthesis o r metabolism of t h e monoamines such as monoamineoxidase (MAO) or catechol-o-methyltransferase (COMT), t h e role of monoamine receptor sensitivity in a f f e c t i v e illness needs to b e examined as h a s been emphasized by Aschcroft et al. (1972).T h e observation by several groups of investigators t h a t chronic t r e a t m e n t with alm...

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House fly heads contain a site that binds alpha-bungarotoxin with high affinity. It is present at about 23 pmol/g of heads and binds alpha-bungarotoxin (labeled with [3H]pyridoxamine phosphate) reversibly with a Kd of 6 nM. The effects of 48 drugs have been compared on the alpha-bungarotoxin binding sites of house fly and Torpedo. The pharmacology of the house fly sites is similar to that previously reported for neuronal alpha-bungarotoxin binding sites in both vertebrates and invertebrates and is distinguishable from that of the classic nicotinic neuromuscular acetylcholine receptor, as exemplified by that of Torpedo electroplax. Differences between the house fly site and Torpedo include higher affinities of the Torpedo receptor for decamethonium, hexamethonium, carbamylcholine, and acetyl-beta-methylcholine, but lower affinities for nicotine, atropine, and dihydro-beta-erythroidine.