Publisher Summary This chapter takes a view of biogenic amines in the insect nervous system and to assess critically the evidence for their roles as neurotransmitters, neuromodulators and neurohormones. It attempts to answer several questions such as where biogenic amines are located in the insect nervous system; how are they synthesized and inactivated; and what physiological roles do they perform and how do they bring about their effects. Particular emphasis is placed on the correlation of biochemical, physiological, pharmacological and anatomical information from systems containing identified aminergic neurones. The chapter points out instances where data from one or more of the approaches is either missing or conflicts with that from another and suggests experiments to resolve these points. The function of biogenic amines in the insect nervous system has been compared with that in the vertebrate nervous system. In this context the chapter mentions the role of biogenic amines as chemical messengers in the vertebrate nervous system.

Biogenic Amines in the Insect Nervous System

Localization of transmitter candidates in the brain: the hippocampal formation as a model

Central dopaminergic neurons: Effects of alterations in impulse flow on the accumulation of dihydroxyphenylacetic acid

Summary

1
The administration of probenecid to mice increased the concentration of 4-hydroxy-3-methoxyphenylacetic acid (HVA) in the striatum, but did not raise the concentration of 3,4-dihydroxyphenylacetic acid (DOPAC)

2
After drug treatments which normally increase the concentration of HVA several-fold, inhibition of catechol-O-methyltransferase (COMT) by tropolone greatly reduced the concentration of HVA but resulted in only a small increase in the concentration of DOPAC in the striatum of the mouse

3
These results indicate that HVA and DOPAC do not occur at the same location in the tissue of the striatum and that DOPAC is not normally metabolized to HVA to any great extent in this tissue

4
When mice were treated with reserpine, which is thought to prevent the intraneuronal storage of dopamine, there was an increase in the striatal concentration of DOPAC which preceded an increase in the concentration of HVA Since non-cholinergic nerve endings of rat brain contain mitochondria and show monoamine oxidase activity, this result suggests that DOPAC is formed intraneuronally

5
It is concluded that the DOPAC in the striatum represents intraneuronal metabolism of dopamine and that only the HVA which is sensitive to the action of probenecid represents entirely extraneuronal metabolism of this amine Some of the HVA is not sensitive to the action of probenecid This suggests that part of the metabolism of dopamine involves both locations

6
A group of drugs which are chemically related to amphetamine were tested for their effects on the concentrations of DOPAC and HVA in the striatum It is suggested that d-amphetamine, 2-aminotetralin and 1,2,3,4-tetrahydroisoquinoline reduced the intraneuronal metabolism of dopamine whereas adamantanamine did not

3,4-dihydroxyphenylacetic acid and 4-hydroxy-3-methoxyphenylacetic acid in the mouse striatum: a reflection of intra- and extra-neuronal metabolism of dopamine?

The enzyme-catalyzed O-methylation of catecholamines was first described by Axelrod and coworkers in the late 1950’s [1–3]. They called the responsible enzyme catechol O-methyltransferase (COMT). During the subsequent 15 years the enzyme was partially purified, its distribution was established, several reaction mechanisms were proposed, and a number of inhibitors were described. The results of this study period were extensively reviewed by Guldberg and Marsden in 1975 [4].

H.C. Guldberg

Papers

On the mode of action of reserpine on dopamine metabolism in the rat striatum.

Effect of nigral and raphé lesions on the catechol-O-methyl transferase and monoamine oxidase activities in the rat striatum.

Catechol-O-methyl transferase and monoamine oxidase activities in rat submaxillary gland: Effects of ligation, sympathectomy and some drugs☆