Cholinergic and catecholaminergic afferents to the olfactory bulb in the Hamster: A neuroanatomical, biochemical, and histochemical investigation

Abstract

A series of neuroanatomical, biochemical, and histochemical studies have been conducted to determine the sources of cholinergic afferents to the main olfactory bulb (MOB) in the hamster. Following horseradish peroxidase (HRP) injections that are restricted to the MOB, retrograde neuronal labeling is observed bilaterally in the anterior olfactory nucleus, locus coeruleus, and raphe nuclei, and ipsilaterally in the ventral hippocampal rudiment, dorsal peduncular cortex, piriform cortex, nucleus of the lateral olfactory tract, anterior pole of the medial septal area and vertical limb of the diagonal band, nucleus of the horizontal limb of the diagonal band (HDB), and hypothalamus. Spread of HRP into the accessory olfactory bulb results in additional neuronal labeling ipsilaterally in the bed nucleus of the accessory olfactory tract, medial amygdaloid nucleus, and bed nucleus of the stria terminalis, and bilaterally in the posteromedial cortical amygdaloid nucleus. Retrograde tracing studies also have been conducted in cases with lesions in the basal forebrain or hypothalamus to assess the extent to which such lesions interrupt fibers of passage from other sources of centrifugal afferents, and the effects of such lesions on choline acetyltransferase (CAT) activity and catecholamine content in the MOB and on acetylcholinesterase (AChE) activity in the forebrain have been evaluated. Lesions in the basal forebrain reduce or eliminate CAT and AChE activity in the MOB in direct relationship to the extent of damage to the HDB. Norepinephrine (NE) content in the MOB also is reduced by basal forebrain lesions, but in relationship to damage of the medial forebrain bundle (MFB). The hypothalamic lesions have no effect on AChE activity in the forebrain or on CAT activity in the MOB, but they eliminate retrograde labeling in the locus coeruleus and raphe nuclei and reduce the NE content of the MOB to undetectable levels. The dopamine content of the MOB is not reduced by any of the lesions. Anterograde tracing studies have been conducted to compare the rostral projection patterns of the HDB with the distribution of AChE activity. Most of the rostrally directed axons travel in association with the MFB. A small component of axons travels in association with the lateral olfactory tract. Within the MOB, the axons terminate predominantly in the glomerular layer and in the vicinity of the internal plexiform layer. The projection and termination patterns of the HDB correspond well with the distribution of AChE activity. These various results indicate that the HDB is the major source of cholinergic afferents to the MOB.

Noradrenergic control of odor recognition in a nonassociative olfactory learning task in the mouse

“…The olfactory cortices, and specially the olfactory bulb, are densely innervated by other neuromodulatory systems including the basal forebrain cholinergic system (Macrides et al 1981;Le Jeune et al 1995), and the serotonergic system originating in the nucleus raphe dorsalis (McLean and Shipley 1987). These afferent systems could both interact with the LC-NA system and influence olfactory learning.…”

Early polysynaptic potentiation recorded in the dentate gyrus during an associative learning task

“…It is an all-or-none-like phenomenon because the potentiation appears only at the end of session 2 and not progressively. Indirectly, the hippocampus could influence the synaptic transmission in the olfactory bulb 22,23 and piriform cortex, 12,14 and the storage of information in both structures 20,31 via the horizontal diagonal band of Broca, which contains GABAergic 9,29 and cholinergic 17 cells.…”

Optogenetic Activation of Basal Forebrain Cholinergic Neurons Modulates Neuronal Excitability and Sensory Responses in the Main Olfactory Bulb

“…The MOB receives strong centrifugal inputs from the horizontal limb of the diagonal band of Broca (HDB), in which many cholinergic neurons are located (Macrides et al, 1981;Brashear et al, 1986;Salcedo et al, 2011). Although it is commonly believed that acetylcholine modulates signal processing in the MOB (Fletcher and Chen, 2010), its exact effects appear to be complex and different studies report seemingly opposite findings.…”