Abstract
Background The neurotransmitter histamine is synthesized from histidine in histaminergic neurons. Later on it is taken up into synaptic vesicles by the vesicular monoamine transporter 2 and released into the synaptic cleft upon depolarization stimuli. The released neurotransmitter is metabolised by the enzyme histamine N-methyltransferase (HNMT) producing tele-methylhistamine (tMH). In order to be enzymatically degraded or possibly recycled, histamine must be transported either into the presynaptic neuron or into surrounding glial cells. Unlike other neurotransmitters, the mechanism and the transporters by which the histamine content within the brain is regulated is currently unresolved.
Highlights
The neurotransmitter histamine is synthesized from histidine in histaminergic neurons
The released neurotransmitter is metabolised by the enzyme histamine N-methyltransferase (HNMT) producing tele-methylhistamine
We investigated the influence of different antidepressants and organic cation transporter (OCT) inhibitors on histamine transport into astrocytes
Summary
The neurotransmitter histamine is synthesized from histidine in histaminergic neurons. Later on it is taken up into synaptic vesicles by the vesicular monoamine transporter 2 and released into the synaptic cleft upon depolarization stimuli. The released neurotransmitter is metabolised by the enzyme histamine N-methyltransferase (HNMT) producing tele-methylhistamine (tMH). In order to be enzymatically degraded or possibly recycled, histamine must be transported either into the presynaptic neuron or into surrounding glial cells. The mechanism and the transporters by which the histamine content within the brain is regulated is currently unresolved. Amitriptyline and desipramine, whereas the histamine metabolite tMH affected both histamine transport and reverse transport from cultured astrocytes. Neither decynium-22 nor corticosterone, known inhibitors of OCT, affected carrier-operated histamine transport
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