Effect of the Depletion of Brain Noradrenaline on the Plasma FSH and Growth Hormone Levels in Ovariectomized Rats

Endröczi, E; Marton, I; Radnai, Z; Biro, J

doi:10.1530/acta.0.0870055

Cited by 4 publications

(3 citation statements)

References 9 publications

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“…Conversely, several pieces of evidence suggest that LC may directly participate to gonadotropin secretion and thus its impairment might significantly affect the ovarian cycle. Endroczi and colleagues found that follicle-stimulating hormone plasma levels were reduced after LC lesion (Endroczi et al 1978 ); furthermore, LC lesion affects luteinizing hormone secretion both in basal conditions and during ovulation (Dotti and Taleisnik 1982 , 1984 ; Franci and Antunes-Rodrigues 1985 ; Anselmo-Franci et al 1997 ; Martins-Afférri et al 2003 ).…”

Section: Connections Between the Lc And The Hypothalamus: Potential Functional Effects Of Lc Lossmentioning

confidence: 99%

The connections of Locus Coeruleus with hypothalamus: potential involvement in Alzheimer’s disease

Giorgi

Galgani²,

Puglisi-Allegra

et al. 2021

J Neural Transm

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The hypothalamus and Locus Coeruleus (LC) share a variety of functions, as both of them take part in the regulation of the sleep/wake cycle and in the modulation of autonomic and homeostatic activities. Such a functional interplay takes place due to the dense and complex anatomical connections linking the two brain structures. In Alzheimer’s disease (AD), the occurrence of endocrine, autonomic and sleep disturbances have been associated with the disruption of the hypothalamic network; at the same time, in this disease, the occurrence of LC degeneration is receiving growing attention for the potential roles it may have both from a pathophysiological and pathogenetic point of view. In this review, we summarize the current knowledge on the anatomical and functional connections between the LC and hypothalamus, to better understand whether the impairment of the former may be responsible for the pathological involvement of the latter, and whether the disruption of their interplay may concur to the pathophysiology of AD. Although only a few papers specifically explored this topic, intriguingly, some pre-clinical and post-mortem human studies showed that aberrant protein spreading and neuroinflammation may cause hypothalamus degeneration and that these pathological features may be linked to LC impairment. Moreover, experimental studies in rodents showed that LC plays a relevant role in modulating the hypothalamic sleep/wake cycle regulation or neuroendocrine and systemic hormones; in line with this, the degeneration of LC itself may partly explain the occurrence of hypothalamic-related symptoms in AD.

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Section: Connections Between the Lc And The Hypothalamus: Potential Functional Effects Of Lc Lossmentioning

confidence: 99%

The connections of Locus Coeruleus with hypothalamus: potential involvement in Alzheimer’s disease

Giorgi

Galgani²,

Puglisi-Allegra

et al. 2021

J Neural Transm

View full text Add to dashboard Cite

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“…In Alzheimer Type Dementia (ATD), both the concentration of noradrenaline and the noradrenaline transporters sites are significantly decreased in a number of brain regions including the Locus coeruleus, cingulate gyrus, putamen, hypothalamus, medial thalamic nucleus, and raphe area (Arai et al, 1984;Tejani et al, 1993). Evidence has accumulated suggesting that noradrenaline is also involved in controlling body temperature (Lin et al, 1981, Sallinen et al, 1997, endocrine secretion (Endroczi et al, 1978;Valet et al, 1989;Ruffolo et al, 1991), and sexual behaviour (Morales et al, 1987;Guiliano & Rampin, 1997).…”

Section: Noradrenaline Functionsmentioning

confidence: 99%

Mechanisms of Parkinson's Disease

Hewitt

Whitworth

2017

Current Topics in Developmental Biology

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The power of Drosophila genetics has attracted attention in tackling important biomedical challenges such as the understanding and prevention of neurodegenerative diseases. Parkinson's disease (PD) is the most common neurodegenerative movement disorder which results from the relentless degeneration of midbrain dopaminergic neurons. Over the past two decades tremendous advances have been made in identifying genes responsible for inherited forms of PD. The ease of genetic manipulation in Drosophila has spurred the development of numerous models of PD, including expression of human genes carrying pathogenic mutations or the targeted mutation of conserved orthologs. The genetic and cellular analysis of these models is beginning to reveal fundamental insights into the pathogenic mechanisms. Numerous pathways and processes are disrupted in these models but some common themes are emerging. These often implicate aberrant synaptic function, protein aggregation, autophagy, oxidative stress, and mitochondrial dysfunction. Moreover, an impressive list of small molecule compounds have been identified as effective in reversing pathogenic phenotypes, paving the way to explore these for therapeutic interventions.

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Section: Noradrenaline Functionsmentioning

confidence: 99%

Noradrenergic Mechanisms in Parkinson’s Disease and L-DOPA-Induced Dyskinesia: Hypothesis and Evidences from Behavioural and Biochemical Studies

Alachkar¹

2012

Mechanisms in Parkinson's Disease - Models and Treatments

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Although the predominant pathology of PD is the loss of dopaminergic cells in the substantia nigra, however, there is also degeneration of other neurotransmission systems, such as cholinergic, noradrenergic, serotoninergic and peptidergic brainstem nuclei (Jellinger, 1991). Some of these alterations in neurotransmitters occur before the appearance of parkinsonian symptoms (Bezard et al, 2001). Noradrenaline (NA) is particularly implicated in certain symptoms of Parkinson's disease. Biochemical analysis revealed that 40-80% of the brain's content of NA is depleted in PD (Agid, et al., 1987; Gerlach et al, 1994). Current strategies for the treatment of PD still depend largely on the replacement of lost dopamine. Levodopa, a precursor of dopamine, has proved very successful as an antiparkinsonian agent (Cotzias et al 1967). L-DOPA can cross the blood-brain barrier and is converted to dopamine by aromatic amino acid decarboxylase, presumably in the striatum at the synaptic sites of surviving nigrostriatal cells (Melamed et al 1984). However, due to the massive degeneration of nigrostriatal terminals, it is unlikely that the majority of dopamine synthesis occurs in nigrostriatal terminals (Snyder & Zigmond, 1990). Within the striatum, 5-HT terminals, striatal interneurons and glial cells also contain aromatic amino acid decarboxylase, and these sites may play a role in the conversion of L-DOPA to dopamine in the degenerated striatum (Opacka-Juffry, 1995; Mura et al, 1995). Initially, L-DOPA is successful in reversing parkinsonian symptoms, akinesia, rigidity and tremor. However, as treatment progresses, the effectiveness of L-DOPA treatment decreases and dyskinesia, fluctuations in mobility and freezing episodes, occur (Marsden & Parkes, 1976; Mouradian et al, 1991). With the progress of treatment, the dose of L-DOPA required to induce dyskinesia gradually decreases and the dose of L-DOPA required to alleviate parkinsonian symptoms is increased, thereby, resulting in the development of a narrow therapeutic window (Mouradian et al, 1988). The mechanism, underlying L-DOPA-induced dyskinesia, is still far from being fully understood. The fact, that dyskinesia results from prolonged replacement of dopamine, suggests that it arises through the overactivity of dopaminergic mechanisms. Similarities in the choreic dyskinesia seen among various brain disorders, i.e. L-DOPA-induced dyskinesia, tardive dyskinesia and hemiballism, has led to the suggestion of a common mechanism for all dyskinesia (Crossman (review) 1990). According to the most acceptable model, L-DOPA-induced dyskinesia is associated with an imbalance of basal ganglia circuitry in favour of the direct pathway. Data obtained from animal models of PD have implicated a relative underactivity of the indirect pathway, and overactivity of the direct pathway. The net effect of the overactive GABAergic projection in the direct and indirect pathways and the underactive glutamatergic projection of the STN, will lead to the cumulative inhibitory effects on the output nuclei...

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Effect of the Depletion of Brain Noradrenaline on the Plasma FSH and Growth Hormone Levels in Ovariectomized Rats

Cited by 4 publications

References 9 publications

The connections of Locus Coeruleus with hypothalamus: potential involvement in Alzheimer’s disease

The connections of Locus Coeruleus with hypothalamus: potential involvement in Alzheimer’s disease

Mechanisms of Parkinson's Disease

Noradrenergic Mechanisms in Parkinson’s Disease and L-DOPA-Induced Dyskinesia: Hypothesis and Evidences from Behavioural and Biochemical Studies

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