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1

KOÇ, Gizem Gül. "Ergonomi ve Locus Coeruleus." Arşiv Kaynak Tarama Dergisi 31, no. 4 (December 30, 2022): 284–92. http://dx.doi.org/10.17827/aktd.1220966.

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Pons ta tüp şeklinde bir anatomik şekle sahip olan locus coeruleus küçük yapısına rağmen nerdeyse tüm merkezi sinir sistemini (M.S.S’yi) etkilemektedir. Yaklaşık iki yüzyıl önce fark edilen locus coeruleus, noradrenalin kaynağı olup hücrelerinin içerdiği nöromelanin pigmentinden kaynaklı koyu mavi olarak görülmektedir. Bu nedenle, Latince’de coeruleus (gökyüzü mavisi) olarak isimlendirilmiştir. Ponsta bilateral olarak yerleşim gösteren bu hücre grubu yaklaşık olarak 45,000 ile 50,000 hücre içermektedir. Son yıllarda gelişen teknoloji ve optogenetik çalışmalar, fonksiyonel manyetik rezonans görüntüleme (MRG) teknikleri ile locus coeruleus ile ilgili pek çok bilginin elde edilmesini sağlamıştır. Bu anatomik yapının dikkat, uyanıklık, stress gibi bilişsel özelliklerde anahtar rol oynadığı bilinmektedir. Okülomotor fonksiyonların zihinsel işlevleri yansıtması nedeniyle özellikle ergonomi alanında çalışan mühendislerin ilgi odağı olmuştur. Sunulan bu derleme çalışmasında locus coeruleusun anatomik yapısı, fizyolojik özellikleri ve nöroergonomi alanında klinik öneminin ortaya konması amaçlanmıştır. Ayrıca, nörobilim ve beyin görüntüleme konusunda meydana gelen gelişmeler ışığında bu anatomik yapının nöroergonomide de ele alınması gerektiğini ve bu alanda yapılacak çalışmaların artması görüşündeyiz.
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2

Benarroch, Eduardo E. "Locus coeruleus." Cell and Tissue Research 373, no. 1 (July 7, 2017): 221–32. http://dx.doi.org/10.1007/s00441-017-2649-1.

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3

Bouret, Sebastien, and Susan Sara. "Locus coeruleus." Scholarpedia 5, no. 3 (2010): 2845. http://dx.doi.org/10.4249/scholarpedia.2845.

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4

Betts, Matthew J., Evgeniya Kirilina, Maria C. G. Otaduy, Dimo Ivanov, Julio Acosta-Cabronero, Martina F. Callaghan, Christian Lambert, et al. "Locus coeruleus imaging as a biomarker for noradrenergic dysfunction in neurodegenerative diseases." Brain 142, no. 9 (July 20, 2019): 2558–71. http://dx.doi.org/10.1093/brain/awz193.

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Abstract Pathological alterations to the locus coeruleus, the major source of noradrenaline in the brain, are histologically evident in early stages of neurodegenerative diseases. Novel MRI approaches now provide an opportunity to quantify structural features of the locus coeruleus in vivo during disease progression. In combination with neuropathological biomarkers, in vivo locus coeruleus imaging could help to understand the contribution of locus coeruleus neurodegeneration to clinical and pathological manifestations in Alzheimer’s disease, atypical neurodegenerative dementias and Parkinson’s disease. Moreover, as the functional sensitivity of the noradrenergic system is likely to change with disease progression, in vivo measures of locus coeruleus integrity could provide new pathophysiological insights into cognitive and behavioural symptoms. Locus coeruleus imaging also holds the promise to stratify patients into clinical trials according to noradrenergic dysfunction. In this article, we present a consensus on how non-invasive in vivo assessment of locus coeruleus integrity can be used for clinical research in neurodegenerative diseases. We outline the next steps for in vivo, post-mortem and clinical studies that can lay the groundwork to evaluate the potential of locus coeruleus imaging as a biomarker for neurodegenerative diseases.
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5

Morris, Laurel S., Jordan G. McCall, Dennis S. Charney, and James W. Murrough. "The role of the locus coeruleus in the generation of pathological anxiety." Brain and Neuroscience Advances 4 (January 2020): 239821282093032. http://dx.doi.org/10.1177/2398212820930321.

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This review aims to synthesise a large pre-clinical and clinical literature related to a hypothesised role of the locus coeruleus norepinephrine system in responses to acute and chronic threat, as well as the emergence of pathological anxiety. The locus coeruleus has widespread norepinephrine projections throughout the central nervous system, which act to globally modulate arousal states and adaptive behavior, crucially positioned to play a significant role in modulating both ascending visceral and descending cortical neurocognitive information. In response to threat or a stressor, the locus coeruleus–norepinephrine system globally modulates arousal, alerting and orienting functions and can have a powerful effect on the regulation of multiple memory systems. Chronic stress leads to amplification of locus coeruleus reactivity to subsequent stressors, which is coupled with the emergence of pathological anxiety-like behaviors in rodents. While direct in vivo evidence for locus coeruleus dysfunction in humans with pathological anxiety remains limited, recent advances in high-resolution 7-T magnetic resonance imaging and computational modeling approaches are starting to provide new insights into locus coeruleus characteristics.
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6

Hansen, Niels. "The Longevity of Hippocampus-Dependent Memory Is Orchestrated by the Locus Coeruleus-Noradrenergic System." Neural Plasticity 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/2727602.

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The locus coeruleus is connected to the dorsal hippocampus via strong fiber projections. It becomes activated after arousal and novelty, whereupon noradrenaline is released in the hippocampus. Noradrenaline from the locus coeruleus is involved in modulating the encoding, consolidation, retrieval, and reversal of hippocampus-based memory. Memory storage can be modified by the activation of the locus coeruleus and subsequent facilitation of hippocampal long-term plasticity in the forms of long-term depression and long-term potentiation. Recent evidence indicates that noradrenaline and dopamine are coreleased in the hippocampus from locus coeruleus terminals, thus fostering neuromodulation of long-term synaptic plasticity and memory. Noradrenaline is an inductor of epigenetic modifications regulating transcriptional control of synaptic long-term plasticity to gate the endurance of memory storage. In conclusion, locus coeruleus activation primes the persistence of hippocampus-based long-term memory.
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7

Maeda, Toshihiro. "The locus coeruleus: history." Journal of Chemical Neuroanatomy 18, no. 1-2 (February 2000): 57–64. http://dx.doi.org/10.1016/s0891-0618(99)00051-4.

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8

Halliday, Glenda, and Kerry Baker. "NORADRENERGIC LOCUS COERULEUS NEURONS." Alcoholism: Clinical and Experimental Research 20, no. 1 (February 1996): 191–92. http://dx.doi.org/10.1111/j.1530-0277.1996.tb01064.x.

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9

Pohl, Robert, John M. Rainey, Aurelio Ortiz, Vikram K. Yeragani, and Kenneth I. Kaitin. "Locus coeruleus and anxiety." Biological Psychiatry 22, no. 1 (January 1987): 116–17. http://dx.doi.org/10.1016/0006-3223(87)90141-7.

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10

Bulhões, Margarida, Maria Margarida Ribeiro, and Luísa Veiga. "Ressonância Magnética no estudo do Locus Coeruleus e a relação com o processo cognitivo de atenção: revisão sistemática." ROENTGEN-Revista Científica das Técnicas Radiológicas 3, no. 2 (July 20, 2022): 40–51. http://dx.doi.org/10.46885/roentgen.v3i2.86.

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Introdução: A degeneração progressiva dos neurónios do Locus Coeruleus associada à diminuição de recetores adrenérgicos, alvos da Noradrenalina, conduz a uma diminuição da função cerebral, provocando uma baixa resposta hemodinâmica e atividade neuronal. A disfunção noradrenérgica pode, ainda, interromper a capacidade de monitorizar estímulos externos e alterar o processo cognitivo da atenção, como acontece na Doença de Alzheimer e na Doença de Parkinson. Objetivos: A investigação procurou unir estudos estruturais e funcionais do Locus Coeruleus, incluindo estudos pupilométricos na avaliação da atenção seletiva visual, que atendessem à resposta cerebral bem como à progressão da doença, com a finalidade de correlacionar o processo cognitivo de atenção com a imagem obtida por Ressonância Magnética do Locus Coeruleus. Materiais e Métodos: A estratégia de pesquisa foi desenvolvida para encontrar todos os potenciais artigos relevantes num conjunto de fontes, como: as bases de dados bibliográficas de biomedicina; bases de registos de ensaios clínicos randomizados e quase randomizados; repositórios científicos e sites agregadores de bases bibliográficas. Resultados: Estudos que avaliaram o Locus Coeruleus por Ressonância Magnética demonstram variações morfológicas dependentes da idade e estudos funcionais, juntamente com testes pupilométricos, apresentaram alterações na neuromodulação percutindo-se na seletividade da atenção. Conclusão: A compilação da análise dos estudos forneceu dados para o estudo do Locus Coeruleus e a relação com o processo cognitivo de atenção. Cientificamente, todos os aspetos morfológicos e funcionais sugerem possibilitar a análise da disfunção noradrenérgica sob o campo da imagem de Ressonância Magnética para compreender a incapacidade do Locus Coeruleus em monitorizar estímulos externos e alterar o processo cognitivo da atenção.
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11

Hwang, Kristy S., Jason Langley, Richa Tripathi, Xiaoping P. Hu, and Daniel E. Huddleston. "In vivo detection of substantia nigra and locus coeruleus volume loss in Parkinson’s disease using neuromelanin-sensitive MRI: Replication in two cohorts." PLOS ONE 18, no. 4 (April 13, 2023): e0282684. http://dx.doi.org/10.1371/journal.pone.0282684.

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Patients with Parkinson’s disease undergo a loss of melanized neurons in substantia nigra pars compacta and locus coeruleus. Very few studies have assessed substantia nigra pars compacta and locus coeruleus pathology in Parkinson’s disease simultaneously with magnetic resonance imaging (MRI). Neuromelanin-sensitive MRI measures of substantia nigra pars compacta and locus coeruleus volume based on explicit magnetization transfer contrast have been shown to have high scan-rescan reproducibility in controls, but no study has replicated detection of Parkinson’s disease-associated volume loss in substantia nigra pars compacta and locus coeruleus in multiple cohorts with the same methodology. Two separate cohorts of Parkinson’s disease patients and controls were recruited from the Emory Movement Disorders Clinic and scanned on two different MRI scanners. In cohort 1, imaging data from 19 controls and 22 Parkinson’s disease patients were acquired with a Siemens Trio 3 Tesla scanner using a 2D gradient echo sequence with magnetization transfer preparation pulse. Cohort 2 consisted of 33 controls and 39 Parkinson’s disease patients who were scanned on a Siemens Prisma 3 Tesla scanner with a similar imaging protocol. Locus coeruleus and substantia nigra pars compacta volumes were segmented in both cohorts. Substantia nigra pars compacta volume (Cohort 1: p = 0.0148; Cohort 2: p = 0.0011) and locus coeruleus volume (Cohort 1: p = 0.0412; Cohort 2: p = 0.0056) were significantly reduced in the Parkinson’s disease group as compared to controls in both cohorts. This imaging approach robustly detects Parkinson’s disease effects on these structures, indicating that it is a promising marker for neurodegenerative neuromelanin loss.
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12

Tomycz, Nestor D., and Robert M. Friedlander. "Neuromodulation of the Locus Coeruleus." Neurosurgery 68, no. 2 (February 1, 2011): N14—N15. http://dx.doi.org/10.1227/01.neu.0000393589.31014.61.

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13

Saper, Clifford B. "Function of the locus coeruleus." Trends in Neurosciences 10, no. 9 (January 1987): 343–44. http://dx.doi.org/10.1016/0166-2236(87)90063-4.

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14

Travagli, R. Alberto, Thomas V. Dunwiddie, and John T. Williams. "Opioid Inhibition in Locus Coeruleus." Journal of Neurophysiology 74, no. 2 (August 1, 1995): 519–28. http://dx.doi.org/10.1152/jn.1995.74.2.519.

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15

Kawauchi, Hiroki Watanabe, Akihiro. "Locus Coeruleus Function in Enuresis." Scandinavian Journal of Urology and Nephrology 33, no. 202 (January 1999): 14–17. http://dx.doi.org/10.1080/00365599950510111.

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16

Mather, M. "The locus coeruleus in aging." International Journal of Psychophysiology 188 (June 2023): 4. http://dx.doi.org/10.1016/j.ijpsycho.2023.05.007.

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17

Kourosh-Arami, M., and S. Hajizadeh. "Maturation of NMDA receptor-mediated spontaneous postsynaptic currents in the rat locus coeruleus neurons." Physiology International 107, no. 1 (March 2020): 18–29. http://dx.doi.org/10.1556/2060.2020.00010.

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AbstractIntroductionDuring mammalian brain development, neural activity leads to maturation of glutamatergic innervations to locus coeruleus. In this study, fast excitatory postsynaptic currents mediated by N-methyl-d-aspartate (NMDA) receptors were evaluated to investigate the maturation of excitatory postsynaptic currents in locus coeruleus (LC) neurons.MethodsNMDA receptor-mediated synaptic currents in LC neurons were evaluated using whole-cell voltage-clamp recording during the primary postnatal weeks. This technique was used to calculate the optimum holding potential for NMDA receptor-mediated currents and the best frequency for detecting spontaneous excitatory postsynaptic currents (sEPSC).ResultsThe optimum holding potential for detecting NMDA receptor-mediated currents was + 40 to + 50 mV in LC neurons. The frequency, amplitude, rise time, and decay time constant of synaptic responses depended on the age of the animal and increased during postnatal maturation.ConclusionThese findings suggest that most nascent glutamatergic synapses express functional NMDA receptors in the postnatal coerulear neurons, and that the activities of the neurons in this region demonstrate an age-dependent variation.
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18

Gool, Dominique Van. "Different modes of action of alprazolam in the treatment of panic attacks." Acta Neuropsychiatrica 12, no. 2 (June 2000): 41–45. http://dx.doi.org/10.1017/s0924270800035687.

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SUMMARYAlprazolam (a benzodiazepine in the group of the triazolo-benzodiazepines) is a potent drug for the treatment of panic disorder. This is possible due to four different interactions with neurotransmitter systems. First, it facilitates, as all diazepines, the inhibitory acitivity of gamma-amino-butyricacid (GABA). The chemical structure differs from the benzodiazepines by incorporation of the triazoloring. Due to this triazoloring, the drug has three additional modes of action. These modes of action inhibit the locus coeruleus which plays a role in the origin of panic disorder. A first specific action is a stimulation of the serotonergic system. Triazolobenzodiazepines are also α2-adrenoreceptor agonists. Both mechanisms are responsible for inhibition of the locus coeruleus. Triazolo-benzodiazepines inhibit the platelet-activating-factor (PAF). PAF stimulates the corticotropin-releasing-hormone (CRH). This hormone stimulates the locus coeruleus. CRH in patients with panic attacks is elevated. This could be a result of hyperactive metabolism of the right parahippocampal area, which is observed in patients with panic attacks. Triazolo-benzodiazepines decrease the activity of the locus coeruleus because of a low CRH-level due to inhibited PAF.
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19

O’Callaghan, Claire, Frank H. Hezemans, Rong Ye, Catarina Rua, P. Simon Jones, Alexander G. Murley, Negin Holland, et al. "Locus coeruleus integrity and the effect of atomoxetine on response inhibition in Parkinson’s disease." Brain 144, no. 8 (March 30, 2021): 2513–26. http://dx.doi.org/10.1093/brain/awab142.

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Abstract Cognitive decline is a common feature of Parkinson’s disease, and many of these cognitive deficits fail to respond to dopaminergic therapy. Therefore, targeting other neuromodulatory systems represents an important therapeutic strategy. Among these, the locus coeruleus-noradrenaline system has been extensively implicated in response inhibition deficits. Restoring noradrenaline levels using the noradrenergic reuptake inhibitor atomoxetine can improve response inhibition in some patients with Parkinson’s disease, but there is considerable heterogeneity in treatment response. Accurately predicting the patients who would benefit from therapies targeting this neurotransmitter system remains a critical goal, in order to design the necessary clinical trials with stratified patient selection to establish the therapeutic potential of atomoxetine. Here, we test the hypothesis that integrity of the noradrenergic locus coeruleus explains the variation in improvement of response inhibition following atomoxetine. In a double-blind placebo-controlled randomized crossover design, 19 patients with Parkinson’s disease completed an acute psychopharmacological challenge with 40 mg of oral atomoxetine or placebo. A stop-signal task was used to measure response inhibition, with stop-signal reaction times obtained through hierarchical Bayesian estimation of an ex-Gaussian race model. Twenty-six control subjects completed the same task without undergoing the drug manipulation. In a separate session, patients and controls underwent ultra-high field 7 T imaging of the locus coeruleus using a neuromelanin-sensitive magnetization transfer sequence. The principal result was that atomoxetine improved stop-signal reaction times in those patients with lower locus coeruleus integrity. This was in the context of a general impairment in response inhibition, as patients on placebo had longer stop-signal reaction times compared to controls. We also found that the caudal portion of the locus coeruleus showed the largest neuromelanin signal decrease in the patients compared to controls. Our results highlight a link between the integrity of the noradrenergic locus coeruleus and response inhibition in patients with Parkinson’s disease. Furthermore, they demonstrate the importance of baseline noradrenergic state in determining the response to atomoxetine. We suggest that locus coeruleus neuromelanin imaging offers a marker of noradrenergic capacity that could be used to stratify patients in trials of noradrenergic therapy and to ultimately inform personalized treatment approaches.
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20

Hezemans, Frank H., Noham Wolpe, Claire O’Callaghan, Rong Ye, Catarina Rua, P. Simon Jones, Alexander G. Murley, et al. "Noradrenergic deficits contribute to apathy in Parkinson’s disease through the precision of expected outcomes." PLOS Computational Biology 18, no. 5 (May 9, 2022): e1010079. http://dx.doi.org/10.1371/journal.pcbi.1010079.

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Apathy is a debilitating feature of many neuropsychiatric diseases, that is typically described as a reduction of goal-directed behaviour. Despite its prevalence and prognostic importance, the mechanisms underlying apathy remain controversial. Degeneration of the locus coeruleus-noradrenaline system is known to contribute to motivational deficits, including apathy. In healthy people, noradrenaline has been implicated in signalling the uncertainty of expectations about the environment. We proposed that noradrenergic deficits contribute to apathy by modulating the relative weighting of prior beliefs about action outcomes. We tested this hypothesis in the clinical context of Parkinson’s disease, given its associations with apathy and noradrenergic dysfunction. Participants with mild-to-moderate Parkinson’s disease (N = 17) completed a randomised double-blind, placebo-controlled, crossover study with 40 mg of the noradrenaline reuptake inhibitor atomoxetine. Prior weighting was inferred from psychophysical analysis of performance in an effort-based visuomotor task, and was confirmed as negatively correlated with apathy. Locus coeruleus integrity was assessed in vivo using magnetisation transfer imaging at ultra-high field 7T. The effect of atomoxetine depended on locus coeruleus integrity: participants with a more degenerate locus coeruleus showed a greater increase in prior weighting on atomoxetine versus placebo. The results indicate a contribution of the noradrenergic system to apathy and potential benefit from noradrenergic treatment of people with Parkinson’s disease, subject to stratification according to locus coeruleus integrity. More broadly, these results reconcile emerging predictive processing accounts of the role of noradrenaline in goal-directed behaviour with the clinical symptom of apathy and its potential pharmacological treatment.
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21

Pisani, Flavio, Valerio Pisani, Francesca Arcangeli, Alice Harding, and Sim K. Singhrao. "Locus Coeruleus Dysfunction and Trigeminal Mesencephalic Nucleus Degeneration: A Cue for Periodontal Infection Mediated Damage in Alzheimer’s Disease?" International Journal of Environmental Research and Public Health 20, no. 2 (January 5, 2023): 1007. http://dx.doi.org/10.3390/ijerph20021007.

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Alzheimer’s disease (AD) is a leading neurodegenerative disease with deteriorating cognition as its main clinical sign. In addition to the clinical history, it is characterized by the presence of two neuropathological hallmark lesions; amyloid-beta (Aβ) and neurofibrillary tangles (NFTs), identified in the brain at post-mortem in specific anatomical areas. Recently, it was discovered that NFTs occur initially in the subcortical nuclei, such as the locus coeruleus in the pons, and are said to spread from there to the cerebral cortices and the hippocampus. This contrasts with the prior acceptance of their neuropathology in the enthorinal cortex and the hippocampus. The Braak staging system places the accumulation of phosphorylated tau (p-tau) binding to NFTs in the locus coeruleus and other subcortical nuclei to precede stages I-IV. The locus coeruleus plays diverse psychological and physiological roles within the human body including rapid eye movement sleep disorder, schizophrenia, anxiety, and depression, regulation of sleep-wake cycles, attention, memory, mood, and behavior, which correlates with AD clinical behavior. In addition, the locus coeruleus regulates cardiovascular, respiratory, and gastrointestinal activities, which have only recently been associated with AD by modern day research enabling the wider understanding of AD development via comorbidities and microbial dysbiosis. The focus of this narrative review is to explore the modes of neurodegeneration taking place in the locus coeruleus during the natural aging process of the trigeminal nerve connections from the teeth and microbial dysbiosis, and to postulate a pathogenetic mechanism due to periodontal damage and/or infection focused on Treponema denticola.
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22

Hall, Sean R., Brian Milne, and Christopher Loomis. "Spinal Action of Ketorolac, S(+)- and R(-)-ibuprofen on Non-noxious Activation of the Cathechol Oxidation in the Rat Locus Coeruleus." Anesthesiology 90, no. 1 (January 1, 1999): 165–73. http://dx.doi.org/10.1097/00000542-199901000-00022.

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Background Blockade of spinal glycine receptors with intrathecal strychnine produces an allodynia-like state in the anesthetized rat. Innocuous hair deflection in the presence of intrathecal strychnine induces a nociceptive-like activation of catechol oxidation in the locus coeruleus and enhances cardiovascular responses. Because prostaglandins play a central role in augmenting pain, this study evaluated the effect of intrathecal nonsteroidal antiinflammatory drugs in strychnine-induced allodynia. Methods In urethane-anesthetized rats, changes in catechol oxidation in the locus coeruleus, measured using in vivo voltammetry, and cardiovascular parameters evoked by hair deflection of caudal dermatomes were determined after strychnine (40 microg) or saline were administered intrathecally. Subsequently, the effects of 30 microg ketorolac, 10 microg S(+)-ibuprofen, and 10 microg R(-)-ibuprofen administered intrathecally were evaluated. Results After strychnine was administered intrathecally, hair deflection evoked an increase in the locus coeruleus catechol oxidation (peak, 149.7+/-7.2% of baseline) and mean arterial blood pressure (peak, 127.5+/-3.8% of baseline). These responses were not observed after saline was administered intrathecally. All hair deflection-evoked, strychnine-dependent peak responses were attenuated significantly with intrathecally administered ketorolac and S(+)-ibuprofen but not with R(-)-ibuprofen. Conclusions Locus coeruleus catechol oxidation is a sensitive biochemical index of strychnine-induced allodynia and is correlated temporally with the cardiovascular responses evoked by hair deflection during spinal glycinergic inhibition. The ability of intrathecally administered ketorolac and S(+)-ibuprofen, but not R(-)-ibuprofen, to suppress the locus coeruleus catechol oxidation and cardiovascular peak responses evoked during strychnine-induced allodynia provide evidence that central prostaglandins play an important role in the abnormal sensory processing of strychnine-induced allodynia.
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Wang, Sijia, Zhirong Wang, and Yu Mu. "Locus Coeruleus in Non-Mammalian Vertebrates." Brain Sciences 12, no. 2 (January 20, 2022): 134. http://dx.doi.org/10.3390/brainsci12020134.

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The locus coeruleus (LC) is a vertebrate-specific nucleus and the primary source of norepinephrine (NE) in the brain. This nucleus has conserved properties across species: highly homogeneous cell types, a small number of cells but extensive axonal projections, and potent influence on brain states. Comparative studies on LC benefit greatly from its homogeneity in cell types and modularity in projection patterns, and thoroughly understanding the LC-NE system could shed new light on the organization principles of other more complex modulatory systems. Although studies on LC are mainly focused on mammals, many of the fundamental properties and functions of LC are readily observable in other vertebrate models and could inform mammalian studies. Here, we summarize anatomical and functional studies of LC in non-mammalian vertebrate classes, fish, amphibians, reptiles, and birds, on topics including axonal projections, gene expressions, homeostatic control, and modulation of sensorimotor transformation. Thus, this review complements mammalian studies on the role of LC in the brain.
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24

Seo, Dong-oh, and Michael R. Bruchas. "Polymorphic computation in locus coeruleus networks." Nature Neuroscience 20, no. 11 (November 2017): 1517–19. http://dx.doi.org/10.1038/nn.4663.

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25

Feinstein, Bertram, Curtis A. Gleason, and Benjamin Libet. "Stimulation of Locus Coeruleus in Man." Stereotactic and Functional Neurosurgery 52, no. 1 (1989): 26–41. http://dx.doi.org/10.1159/000099484.

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26

Gargaglioni, Luciane H., Lynn K. Hartzler, and Robert W. Putnam. "The locus coeruleus and central chemosensitivity." Respiratory Physiology & Neurobiology 173, no. 3 (October 2010): 264–73. http://dx.doi.org/10.1016/j.resp.2010.04.024.

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27

Barnes, Charles D. "Locus coeruleus in development and dysfunction." Brain Research Bulletin 35, no. 5-6 (January 1994): 395. http://dx.doi.org/10.1016/0361-9230(94)90149-x.

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28

Page, Michelle E., and Rita J. Valentino. "Locus coeruleus activation by physiological challenges." Brain Research Bulletin 35, no. 5-6 (January 1994): 557–60. http://dx.doi.org/10.1016/0361-9230(94)90169-4.

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29

Nestler, Eric J., Meenakshi Alreja, and George K. Aghajanian. "Molecular control of locus coeruleus neurotransmission." Biological Psychiatry 46, no. 9 (November 1999): 1131–39. http://dx.doi.org/10.1016/s0006-3223(99)00158-4.

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30

Glennon, Erin, Ioana Carcea, Ana Raquel O. Martins, Jasmin Multani, Ina Shehu, Mario A. Svirsky, and Robert C. Froemke. "Locus coeruleus activation accelerates perceptual learning." Brain Research 1709 (April 2019): 39–49. http://dx.doi.org/10.1016/j.brainres.2018.05.048.

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31

Pompeiano, O., D. Manzoni, C. D. Barnes, G. Stampacchia, and P. D'ascanio. "Labyrinthine Influences on Locus Coeruleus Neurons." Acta Oto-Laryngologica 105, no. 5-6 (January 1988): 576–81. http://dx.doi.org/10.3109/00016488809119523.

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32

Forno, L. S. "THE LOCUS COERULEUS IN PICKʼS DISEASE." Journal of Neuropathology and Experimental Neurology 46, no. 3 (May 1987): 374. http://dx.doi.org/10.1097/00005072-198705000-00134.

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33

McBurney-Lin, Jim, Greta Vargova, Machhindra Garad, Edward Zagha, and Hongdian Yang. "The locus coeruleus mediates behavioral flexibility." Cell Reports 41, no. 4 (October 2022): 111534. http://dx.doi.org/10.1016/j.celrep.2022.111534.

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34

Libet, Benjamin, and Curtis A. Gleason. "The human locus coeruleus and anxiogenesis." Brain Research 634, no. 1 (January 1994): 178–80. http://dx.doi.org/10.1016/0006-8993(94)90274-7.

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35

Zweig, R. M., C. A. Ross, J. C. Hedreen, C. Peyser, J. E. Cardillo, S. E. Folstein, and D. L. Price. "Locus Coeruleus Involvement in Huntington's Disease." Archives of Neurology 49, no. 2 (February 1, 1992): 152–56. http://dx.doi.org/10.1001/archneur.1992.00530260052019.

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36

Drolet, Guy, and Pierre Gauthier. "Similar poststimulatory pressor responses with different mechanisms in response to excitation of the locus coeruleus before and after acute adrenalectomy." Canadian Journal of Physiology and Pharmacology 65, no. 6 (June 1, 1987): 1136–41. http://dx.doi.org/10.1139/y87-179.

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Electrical stimulation of the locus coeruleus in anesthetized rats evoked a biphasic pressor response consisting of an initial sharp rise in blood pressure at the onset of stimulation, followed by a second elevation after cessation of the stimulus. This response, which was accompanied by an increase in plasma noradrenaline and adrenaline levels, was stable and could be easily reproduced over time. Sympathectomy by administration of guanethidine selectively abolished the primary pressor response. β-Adrenergic blockade by intravenous administration of sotalol enhanced the secondary pressor response without affecting the primary component. Adrenal demedullation performed 24–48 h before the experiments selectively prevented the secondary pressor component. In contrast, acute adrenalectomy carried out during the experiment to impair the adrenomedullary secretions eliminated the secondary pressor response to stimulation of the locus coeruleus only in sympathectomized or in sotalol-treated rats but not in intact rats in which the response persisted. The latter, however, could be abolished by the administration of either guanethidine or sotalol, and it disappeared following repeated stimulation of the locus coeruleus. The study demonstrates that similar poststimulatory pressor responses with different underlying mechanisms can be elicited on excitation of the locus coeruleus before and after acute adrenalectomy in the rat. The results also suggest that intraneuronal adrenaline may be involved in the response evoked in acutely adrenalectomized animals.
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37

Finlayson, Paul G., and Kenneth C. Marshall. "Characterization of a developmentally transient adrenergic depolarizing response in cultured locus coeruleus neurons." Canadian Journal of Physiology and Pharmacology 66, no. 12 (December 1, 1988): 1547–54. http://dx.doi.org/10.1139/y88-253.

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The effects of iontophoretically applied noradrenaline have been tested on intracellularly recorded locus coeruleus neurons grown in explant cultures from neonatal mice. In addition to hyperpolarizing responses mediated by α2-adrenergic receptors, as observed in locus coeruleus neurons in vivo and in brain slices from adult animals, α1-mediated depolarizations were observed to succeed the initial hyperpolarizations in some cultures. It was shown that the depolarizing responses were only present in younger cultures, i.e., less than 26 days in vitro. In cultures less than 20 days old, all cells displayed the biphasic hyperpolarizing-depolarizing responses. Both components of the response appear to be direct, since they were present when synaptic transmission was blocked by including tetrodotoxin or by altering divalent cations in the perfusate. The depolarizing responses were frequently reduced in solutions with altered divalent cation content, and this might reflect a calcium dependency of this response. The hyperpolarizing and depolarizing components of the responses to noradrenaline were progressively blocked by increasing concentrations of the selective antagonists yohimbine and prazosin, respectively, in the dose ranges of 100 nM – 1 μM (yohimbine) and 20–200 nM (prazosin). Recent results from electrophysiological studies of locus coeruleus neurons in brain slices suggest that similar changes occur in the animal as well as in culture. It is possible that the transient depolarizing responses reflect a developmentally important enhanced responsiveness of locus coeruleus neurons during the early postnatal period.
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38

Holland, Negin, Trevor W. Robbins, and James B. Rowe. "The role of noradrenaline in cognition and cognitive disorders." Brain 144, no. 8 (March 16, 2021): 2243–56. http://dx.doi.org/10.1093/brain/awab111.

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Abstract Many aspects of cognition and behaviour are regulated by noradrenergic projections to the forebrain originating from the locus coeruleus, acting through alpha and beta adrenoreceptors. Loss of these projections is common in neurodegenerative diseases and contributes to their cognitive and behavioural deficits. We review the evidence for a noradrenergic modulation of cognition in its contribution to Alzheimer’s disease, Parkinson’s disease and other cognitive disorders. We discuss the advances in human imaging and computational methods that quantify the locus coeruleus and its function in humans, and highlight the potential for new noradrenergic treatment strategies.
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39

Landa, Adriana I., and Alfredo O. Donoso. "Blockade of pro-oestrus LH surge and ovulation by GABA increase in the rat locus coeruleus." Acta Endocrinologica 115, no. 4 (August 1987): 490–96. http://dx.doi.org/10.1530/acta.0.1150490.

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Abstract. The effects of gamma-aminobutyric acid (GABA) increase at the nucleus locus coeruleus (LC) on pro-oestrus LH release and ovulation were evaluated in rats. Local microinjection of the GABA-transaminase inhibitor gamma-vinyl-GABA (GVG) produced 6 h later a marked increase in GABA in the LC. Such action caused a significant decrease of plasma LH levels and prevented the pro-oestrus LH surge. In some animals, plasma prolactin levels were also lowered, but in others its plasma concentrations were high and similar to that in controls. Ovulation did not occur in the rats treated with GVG. In additional experiments, the periventricular gray substance (PGS) close to the locus coeruleus was injected with GVG. Results obtained show a LH surge blockade and failure of ovulation in most of these rats. These findings may be interpreted on the basis of GABA action on rostral LC cells that project to the PGS. The results altogether suggest that through neurons of the locus coeruleus, GABA may exert an inhibitory role in the regulation of LH secretion.
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Milne, Brian, Luc Quintin, Jean Yves Gillon, and Jean-François Pujol. "Fentanyl decreases catecholamine metabolism measured by in vivo voltammetry in the rat locus coeruleus." Canadian Journal of Physiology and Pharmacology 67, no. 5 (May 1, 1989): 532–36. http://dx.doi.org/10.1139/y89-085.

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The objective of this study was to investigate under controlled conditions the effects of fentanyl on the rat locus coeruleus catechol oxidation current. Using differential normal pulse voltammetry combined with electrochemically treated carbon fiber electrodes to measure the catechol oxidation current, catecholamine metabolism can be reliably monitored. Male Sprague–Dawley rats weighing 500–600 g had carbon fiber electrodes implanted into the locus coeruleus under halothane – O2 – air anesthesia with controlled ventilation and muscle relaxation. Experiments consisted of four groups of rats given the following treatments: (A) saline (n = 6); (B) fentanyl, 10 μg∙kg−1 i.v. (n = 6); (C) naloxone, 800 μg∙kg−1 i.v. followed 2 min later by fentanyl, 10 μg∙kg−1 (n = 5); (D) clonidine, 200 μg∙kg−1 i.p. (n = 6). There was no significant change in the catechol oxidation current following saline. Fentanyl produced a significant (ANOVA, p < 0.05) decrease in the catechol oxidation current (maximum 32 min postinjection was 75.8 ± 4.6% of baseline). This decrease was prevented by a prior injection of naloxone. Clonidine produced a significant decrease in catechol oxidation current (maximum 40 min postinjection was 54.1 ± 7.0% of baseline). Systolic blood pressure was significantly decreased following clonidine and there were no significant changes in arterial blood gases throughout the experiments. The α2-adrenergic agonist clonidine and the opioid fentanyl produced a decrease in locus coeruleus catechol oxidation current measured by in vivo voltammetry, which monitors catecholamine turnover.Key words: catecholamine, clonidine, fentanyl, opiates, locus coeruleus, in vivo voltammetry.
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41

Chan-Palay, Victoria. "Locus Coeruleus and Norepinephrine in Parkinson's Disease." Psychiatry and Clinical Neurosciences 45, no. 2 (June 1991): 519–21. http://dx.doi.org/10.1111/j.1440-1819.1991.tb02540.x.

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42

Yamasaki, Miwako, and Tomonori Takeuchi. "Locus Coeruleus and Dopamine-Dependent Memory Consolidation." Neural Plasticity 2017 (2017): 1–15. http://dx.doi.org/10.1155/2017/8602690.

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Most everyday memories including many episodic-like memories that we may form automatically in the hippocampus (HPC) are forgotten, while some of them are retained for a long time by a memory stabilization process, called initial memory consolidation. Specifically, the retention of everyday memory is enhanced, in humans and animals, when something novel happens shortly before or after the time of encoding. Converging evidence has indicated that dopamine (DA) signaling via D1/D5receptors in HPC is required for persistence of synaptic plasticity and memory, thereby playing an important role in the novelty-associated memory enhancement. In this review paper, we aim to provide an overview of the key findings related to D1/D5receptor-dependent persistence of synaptic plasticity and memory in HPC, especially focusing on the emerging evidence for a role of the locus coeruleus (LC) in DA-dependent memory consolidation. We then refer to candidate brain areas and circuits that might be responsible for detection and transmission of the environmental novelty signal and molecular and anatomical evidence for the LC-DA system. We also discuss molecular mechanisms that might mediate the environmental novelty-associated memory enhancement, including plasticity-related proteins that are involved in initial memory consolidation processes in HPC.
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43

Cherubini, E., R. A. North, and J. T. Williams. "Synaptic potentials in rat locus coeruleus neurones." Journal of Physiology 406, no. 1 (December 1, 1988): 431–42. http://dx.doi.org/10.1113/jphysiol.1988.sp017389.

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44

HAJÓS, M., G. JANCSÓ, and G. ENGBERG. "Capsaicin-induced excitation of locus coeruleus neurons." Acta Physiologica Scandinavica 129, no. 3 (March 1987): 415–20. http://dx.doi.org/10.1111/j.1748-1716.1987.tb08086.x.

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45

Marín, O., W. J. A. J. Smeets, and A. González. "Do amphibians have a true locus coeruleus?" NeuroReport 7, no. 8 (May 1996): 1447. http://dx.doi.org/10.1097/00001756-199605310-00025.

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46

Nunes, Ana Rita, Emilia Monteiro, and Estelle Gauda. "Soluble adenylyl cyclase in the locus coeruleus." Respiratory Physiology & Neurobiology 201 (September 2014): 34–37. http://dx.doi.org/10.1016/j.resp.2014.05.011.

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47

Singewald, N. "Release of neurotransmitters in the locus coeruleus." Progress in Neurobiology 56, no. 2 (October 1998): 237–67. http://dx.doi.org/10.1016/s0301-0082(98)00039-2.

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48

ORDWAY, GREGORY A. "Pathophysiology of the Locus Coeruleus in Suicide." Annals of the New York Academy of Sciences 836, no. 1 Neurobiology (December 1997): 233–52. http://dx.doi.org/10.1111/j.1749-6632.1997.tb52363.x.

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49

Ammar, Ahmed A., Per Södersten, and Allan E. Johnson. "Locus coeruleus noradrenergic lesions attenuate intraoral intake." Neuroreport 12, no. 14 (October 2001): 3095–99. http://dx.doi.org/10.1097/00001756-200110080-00023.

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50

Llorca-Torralba, Meritxell, Gisela Borges, Fani Neto, Juan Antonio Mico, and Esther Berrocoso. "Noradrenergic Locus Coeruleus pathways in pain modulation." Neuroscience 338 (December 2016): 93–113. http://dx.doi.org/10.1016/j.neuroscience.2016.05.057.

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