In the present brief overview we summarize results from several studies focusing on
two neuropeptides, galanin and neuropeptide Y (NPY) in discrete neuronal systems,
where they coexist with classic transmitters. On the basis of studies in different
animal models we propose that these peptides may be involved in regulation of certain
CNS functions and that drugs acting on their receptors may be of use in new therapeutic
strategies. At the spinal level galanin and NPY are regulated in DRG neurons by nerve injury and in dorsal horn neurons
by inflammation. It is possible that this leads to attenuation of pain sensitivity.
Moreover, both peptides may exert trophic effects, for example to enhance regeneration.
In the hypothalamic arcuate nucleus NPY and its receptors are part of the feeding circuitry, and we suggest that derangement
of these NPY neurons may at least in part underlay the lethal phenotype of anorectic
mice, which die 22 days postnatally after showing decreased food intake and growth
retardation. Expression of NPY and NPY receptors is changed in the hippocampus of mice comparatively early after prion inoculation, indicating that this peptide
system is affected in this spongiform degenerative disease in a region of importance
for learning and memory. Finally, galanin is co-localized with classic monoamine transmitters
in two central systems, the dorsal raphe serotonin neurons and the locus coeruleus noradrenergic neurons. In both cases galanin causes hyperpolarization (at high concentrations)
and prolongs monoamine-induced outward currents (at low concentrations), thus modulating
activity in two systems of importance for many brain functions including mood regulation.
It may therefore be interesting to analyse to what extent drugs affecting galaninergic
transmission also may be efficient in the treatment of, for example, depression.
Key words
Co-Existence - Depression - DRG Neurons - Feeding - Neuropeptides - Pain
