The locus coeruleus noradrenergic system — evidence against a role in attention, habituation, anxiety and motor activity

Crow, Timothy J.; Deakin, J.F.W.; File, Sandra E.; Longden, A.; Wendlandt, S

doi:10.1016/0006-8993(78)91021-1

Cited by 134 publications

(21 citation statements)

References 33 publications

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“…In contrast with these findings, ablation of the LC in rodents leads to an increase in fear responses to novelty (Delini-Stula, et al, 1984; Koob, et al, 1984; Itoi and Sugimoto, 2010; Mason and Fibiger, 1979), or no change in social contacts during novelty (Crow, et al, 1978), and increasing LC activation decreases anxious behavior in the open field test (Weiss et al, 1994). These findings suggest that LC activity may help reduce anxiety in at least some contexts.…”

Section: Discussionmentioning

confidence: 80%

Higher locus coeruleus MRI contrast is associated with lower parasympathetic influence over heart rate variability

et al. 2017

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The locus coeruleus (LC) is a key node of the sympathetic nervous system and suppresses parasympathetic activity that would otherwise increase heart rate variability. In the current study, we examined whether LC-MRI contrast reflecting neuromelanin accumulation in the LC was associated with high-frequency heart rate variability (HF-HRV), a measure reflecting parasympathetic influences on the heart. Recent evidence indicates that neuromelanin, a byproduct of catecholamine metabolism, accumulates in the LC through young and mid adulthood, suggesting that LC-MRI contrast may be a useful biomarker of individual differences in habitual LC activation. We found that, across younger and older adults, greater LC-MRI contrast was negatively associated with HF-HRV during fear conditioning and spatial detection tasks. This correlation was not accounted for by individual differences in age or anxiety. These findings indicate that individual differences in LC structure relate to key cardiovascular parameters.

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Section: Discussionmentioning

confidence: 80%

Higher locus coeruleus MRI contrast is associated with lower parasympathetic influence over heart rate variability

et al. 2017

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“…While disruption of the NE systems in the brain or stimulation of these systems by various means can affect such behaviors as motor activity (Stone and Mendlinger, 1974;Geyer et al, 1972;Carey, 1976), investigatory activity (Delini-Stula et al, 1984), social interaction (Eison et al, 1977), and sleep (Kaitin et al, 1986), the effects seen are generally small, variable, and depend on specific testing conditions (see, for example, Amaral and Sinnamon, 1977;Mason, 1981;Robinson et al, 1977;Crow et al, 1978;Carli et al, 1983;Robbins et al, 1985). To some extent, this conclusion may be influenced by less-than-optimal methodology (i.e., the most-utilized technique is the making of lesions [including use of neurotoxins] which does not produce altered N E activity but produces nonphysiological destruction of the system); nevertheless, the overall conclusion indicated by a considerable body of work is that experimental manipulation of brain N E does not influence depression-related responses profoundly or directly.…”

Section: Problemmentioning

confidence: 99%

Hypothesis linking the noradrenergic and dopaminergic systems in depression

et al. 1995

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A hypothesis is presented that attempts to describe the mechanism by which noradrenergic neurons in the brain influence dopaminergic neurons to produce behavioral changes seen in depression. The historical background pointing to a norepinephrine (NE)‐dopamine (DA) interaction in depression is described. This interaction is suggested by numerous observations indicating that whereas NE is important in therapy and pathogenesis of depression, basic research implicates DA in depression‐related behavioral responses (motor activity changes, hedonic response) much more so than NE. The hypothesized NE‐DA interaction is introduced in relation to an animal model (stress‐induced behavioral depression) that has traced depressive symptomatology to abnormal activity (hyperresponsivity) of locus coeruleus (LC) neurons. Based on recent data by Grenhoff et al. (1993; J Neural Transm 93:11–25), it is suggested that the augmented burst firing of LC neurons found in behavioral depression releases galanin from LC axon terminals, and this inhibits (hyper‐polarizes) DA neurons in the ventral tegmentum (VTA) to mediate depression‐related behavioral changes. Initial results showing that microinfusion of galanin into the VTA decreases spontaneous and swim‐test motor activity of animals are described. Depression 3:225–245 (1995/1996). © 1996 Wiley‐Liss, Inc.

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“…Reviewing basic research relating symptoms of depression to changes in noradrenergic activity in the brain reveals that experimental alterations in brain NE can affect behaviors such as motor activity, investigatory behavior, social interaction, and sleep (e.g., Stone and Medlinger, 1974; Carey, 1976; Delini-Stula et al, 1984; Eison et al, 1977; Kaitin et al, 1986), but the changes in these behaviors resulting from profound perturbations of NE are often small, variable, and depend upon specific testing conditions for changes to be seen (e.g., Amaral and Sinnamon, 1977; Carli et al, 1983; Crow et al, 1978; Robbins et al, 1989; Robinson et al, 1977). In contrast, alteration of brain dopamine (DA) appears to have much more impact on behaviors related to depression.…”

Section: Introductionmentioning

confidence: 99%

Influence of chronic administration of antidepressant drugs on mRNA for galanin, galanin receptors, and tyrosine hydroxylase in catecholaminergic and serotonergic cell-body regions in rat brain

Rovin¹,

Boss-Williams²,

Alisch³

et al. 2012

Neuropeptides

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Activity of locus coeruleus (LC) neurons and release of the peptide galanin (GAL), which is colocalized with norepinephrine (NE) in LC neurons, has been implicated in depression and, conversely, in antidepressant action. The present study examined the influence of chronic administration (for 14 days, via subcutaneously-implanted minipump) of antidepressant (AD) drugs representing three different classes (tricyclic [desipramine], selective serotonin reuptake inhibitor [SSRI] [paroxetine], and monoamine oxidase inhibitor [MAOI] [phenelzine]) on mRNA for GAL, GAL receptors (GalR1, R2, and R3), and tyrosine hydroxylase (TH), the rate-limiting enzyme for NE synthesis, in four brain regions – LC, A1/C1, dorsal raphe (DRN), and ventral tegmentum (VTA) of rats. Consistent with previous findings that chronic administration of AD drugs decreases activity of LC neurons, administration of AD drugs reduced mRNA for both GAL and TH in LC neurons. GAL and TH mRNA in LC neurons was highly correlated. AD drugs also reduced GAL and TH mRNA in A1/C1 and VTA but effects were smaller than in LC. The largest change in mRNA for GAL receptors produced by AD administration was to decrease mRNA for GalR2 receptors in the VTA region. Also, mRNA for GalR2 and GalR3 receptors was significantly (positively) correlated in all three predominantly catecholaminergic brain regions (LC, A1/C1, and VTA). Relative to these three brain regions, unique effects were seen in the DRN region, with the SSRI elevating GAL mRNA and with mRNA for GalR1 and GalR3 being highly correlated in this brain region. The findings show that chronic administration of AD drugs, which produces effective antidepressant action, results in changes in mRNA for GAL, GAL receptors, and TH in brain regions that likely participate in depression and antidepressant effects.

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The locus coeruleus noradrenergic system — evidence against a role in attention, habituation, anxiety and motor activity

Cited by 134 publications

References 33 publications

Higher locus coeruleus MRI contrast is associated with lower parasympathetic influence over heart rate variability

Higher locus coeruleus MRI contrast is associated with lower parasympathetic influence over heart rate variability

Hypothesis linking the noradrenergic and dopaminergic systems in depression

Influence of chronic administration of antidepressant drugs on mRNA for galanin, galanin receptors, and tyrosine hydroxylase in catecholaminergic and serotonergic cell-body regions in rat brain

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