Activation of Locus Coeruleus Enhances the Responses of Olfactory Bulb Mitral Cells to Weak Olfactory Nerve Input

Abstract

The main olfactory bulb (MOB) receives a dense projection from the pontine nucleus locus coeruleus (LC), the largest collection of norepinephrine (NE)-containing cells in the brain. LC is the sole source of NE innervation of MOB. Previous studies of the actions of exogenously applied NE on mitral cells, the principal output neurons of MOB, are contradictory. The effect of synaptically released NE on mitral cell activity is not known, nor is the influence of NE on responses of mitral cells to olfactory nerve inputs. The goal of the present study was to assess the influence of LC activation on spontaneous and olfactory nerve-evoked activity of mitral cells. In methoxyflurane-anesthetized rats, intracoerulear microinfusions of acetyicholine (ACh) (200 mM; 90-120 nl) evoked a four- to fivefold increase in LC neuronal discharge, and a transient EEG desynchronization and decrease in mitral cell discharge. LC activation increased excitatory responses of mitral cells evoked by weak (i.e., perithreshold) nasal epithelium shocks (1.0 Hz) in 17/18 cells (mean Increase = 67%). The discharge rate of mitral cells at the time that epithelium-evoked responses were increased did not differ significantly from pre-LC activation baseline values. Thus, changes in mitral baseline activity do not account for the increased response to epithelium stimulation. These findings suggest that increased activity in LC-NE projections to MOB may enhance detection of relatively weak odors.

Gabrb3 gene deficient mice exhibit increased risk assessment behavior, hypotonia and expansion of the plexus of locus coeruleus dendrites

“…The LC and the locus subcoeruleus (SC) belong to the descending pathway that regulates nociceptive neurons in the dorsal horn of the spinal cord with the norepinephrine produced in the LC being involved in the suppression of nociceptive neuronal activity (Jones and Gebhart, 1986;Mokha et al, 1985). In addition, increased activity in LC-NE projections to the olfactory bulb results in enhanced detection of relatively weak odors (Jiang et al, 1996). Consequently, the semi-quantitative finding that the pericoerulear dendritic zone of the LC in gabrb3 -/-mice is significantly larger than in control mice, may underlie the previously reported enhanced responsiveness to low intensity thermal stimuli in the tail flick and hot-plate test (Ugarte et al, 2000) and to altered odor discrimination (Nusser et al, 2001).…”

“…These behaviors are modulated, in part, by the noradrenergic nuclei, the locus coeruleus (LC), which regulates a broad spectrum of physiological and behavioral processes that include anxiety, attention, muscle tone, arousal, neophobia, emotionality and stress (Aston- Jones and Cohen, 2005;Berridge and Waterhouse, 2003;Jiang et al, 1996;Kiyashchenko et al, 2001;Priolo et al, 1991). Consequently, deficits in LC function have been implicated in several neurological disorders such as attention deficit hyperactivity disorder, depression and epilepsy (Berridge and Waterhouse, 2003).…”

Coordinate Synaptic Mechanisms Contributing to Olfactory Cortical Adaptation

“…␤-adrenergic receptors have been demonstrated in layer I and II within aPCX , and norepinephrine (NE) can modulate afferent input to the piriform cortex in vitro, although to a lesser extent than the effect of norepinephrine on association fiber synapses (Hasselmo et al, 1997). NE release and LC activity are known to increase during arousal, vigilance, and exposure to novelty (Vankov et al, 1995) and also increase both mitral/tufted cell responses to olfactory nerve input and aPCX responses to odors (Jiang et al, 1996). We thus examined whether NE modulators alter cortical adaptation.…”

α2-Adrenergic receptor activation promotes long-term potentiation at excitatory synapses in the mouse accessory olfactory bulb

“…LC activation enhances MC responses to weak olfactory nerve input (Jiang et al 1996). This may be due to a transient reduction of the recurrent inhibition of MCs by LC activation (Okutani et al 1998).…”