Bilateral olfactory deprivation reveals a selective noradrenergic regulatory input to the olfactory bulb.
Unilateral olfactory deprivation in the rat induces changes in the catecholaminergic system of the olfactory bulb. Nevertheless, evidence suggests that unilateral deprivation does not fully prevent stimulation of the deprived bulb. The present report analyses the response of the catecholaminergic system of the olfactory bulb in fully deprived rats obtained by bilateral naris occlusion. The complete deprivation produces more rapid and dramatic changes in both the intrinsic and extrinsic catecholaminergic systems of the olfactory bulb. Intrinsic responses involve a rapid decrease in dopamine-containing cells to about 25% of controls, correlated with a decreased Fos expression in juxtaglomerular cells of all olfactory glomeruli, with the only exception of those of the atypical glomeruli which maintain unaltered expression of both markers. In parallel with these events, there is a progressive increase in the density of extrinsic noradrenergic axons arising from neurons in the locus coeruleus, which shows, in parallel, a progressive increase in Fos expression. This model demonstrates plastic changes in the catecholaminergic system of the olfactory bulb forming a valid morphological substrate for lowering thresholds in the processing of olfactory information. In addition to this generalized response, there is another one, directed to a specific subset of olfactory glomeruli (atypical glomeruli) involved in the processing of odor pheromone-like cues related to behavioral responses, that could be responsible for keeping active this reduced and selected group of glomeruli carrying crucial olfactory information. These results indicate the existence of adaptive changes in the catecholaminergic system of the olfactory bulb as a response to the lack of afferent peripheral stimulation. These changes involve dopamine- and noradrenaline-immunoreactive elements, in a strategy presumably directed at maintaining to the highest possible level the ability to detect olfactory signals.
Instituto de Neurociencias de Castilla y León (INCYL), Dipartmento Biología Celular y Patología, Facultad de Biología, Universidad de Salamanca, E-37007, Salamanca, Spain.
J G
JG
Briñón
C
C
Crespo
E
E
Weruaga
F J
FJ
Martínez-Guijarro
J
J
Aijón
J R
JR
Alonso
D000344:Afferent Pathways / Q000166:cytology / Q000293:injuries / Q000378:metabolism*; D000818:Animals; D001369:Axons / Q000378:metabolism* / Q000648:ultrastructure; D003714:Denervation / Q000009:adverse effects; D004298:Dopamine / Q000378:metabolism; D004299:Dopamine beta-Hydroxylase / Q000378:metabolism; D005260:Female; D008125:Locus Coeruleus / Q000166:cytology / Q000254:growth & development / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D009638:Norepinephrine / Q000378:metabolism*; D009830:Olfactory Bulb / Q000166:cytology / Q000254:growth & development* / Q000378:metabolism; D009832:Olfactory Nerve / Q000166:cytology / Q000378:metabolism*; D061219:Olfactory Nerve Injuries; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D012683:Sensory Deprivation / Q000502:physiology*; D012903:Smell / Q000502:physiology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D016760:Proto-Oncogene Proteins c-fos; D014446:Tyrosine 3-Monooxygenase; D004299:Dopamine beta-Hydroxylase; D004298:Dopamine; D009638:Norepinephrine