Blood platelets as a model for monoamine-containing neurones.

In recent years, it has become apparent that neurons have associated with them specific transport systems for the particular transmitter which they manufacture and release. Thus neurons that release norepinephrine (NE) possess a specific transport system capable of transporting NE from the external medium into the neurons. Similar uptake systems for dopamine and 5-HT are associated with neurons containing these transmitters (Iversen, 1967, 1970, 1971, 1973; Snyder et al., 1970). In cholinergic neurons, there is an uptake system for the precursor substance choline (Snyder et al., 1973). Apart from the transport of biogenic amines into the neurons themselves, other mechanisms exist to mediate the transport of these amines across the membranes of various nonneuronal cells which are associated with synapses using amine transmitters. Furthermore, within the neuronal cytoplasm there are other uptake systems to transfer the amines from the cytoplasm into synaptic vesicles, which act as concentrated amine storage reservoirs. The existence of these numerous amine transport systems is perhaps not surprising, since the biogenic amines are highly polar substances which do not readily penetrate biological membranes by simple diffusion.

Uptake Processes for Biogenic Amines

Mechanism of transmitter release.

1. The mechanism of efflux of (-)-[(3)H]-noradrenaline was examined in rabbit atria, which were pretreated with reserpine and pargyline.2. Between 40 and 100 min, efflux occurred predominantly from a single intraneuronal compartment.3. Efflux was rapidy increased by (-)- and (+)-noradrenaline, tyramine and (+/-)-metaraminol, but not by (+/-)-isopropylnoradrenaline or (+/-)-normetanephrine. The increase in efflux produced by (-)-noradrenaline was inhibited by cocaine and desipramine but not by lidocaine.4. Spontaneous effluxes, and those accelerated by (-)-noradrenaline, were temperature-sensitive.5. Efflux was increased by ouabain, omission of K(+), metabolic inhibition and lowering of the external Na(+) concentration. These effects were significantly reduced by cocaine and desipramine but not by lidocaine.6. These findings provide evidence that the efflux of [(3)H]-noradrenaline from adrenergic nerves occurs by a cocaine-sensitive, carrier-mediated process. The characteristics of the efflux process are compatible with, but not conclusive proof for, the Na(+)-gradient hypothesis.

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1476-5381.1973.tb08537.x

Mechanism of efflux of noradrenaline from adrenergic nerves in rabbit atria.

Role of sodium, potassium, quabain and reserpine in uptake, storage and metabolism of biogenic amines in synaptosomes

/pdf/cation-dependence-of-sympathetic-transmitter-retention-by-26l7jfcmnf.pdf

C. N. Gillts

Papers

Cation dependence of sympathetic transmitter retention by slices of rat ventricle