3-Methoxy-4-hydroxyphenylglycol sulfate in brain and cerebrospinal fluid
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Cited by (180)
The role of dopamine in the expression of morphine withdrawal
1998, General Pharmacology- 1.
Both L-dopa and low doses of apomorphine potentiated withdrawal symptoms such as jumping,“wet dog” shakes and burrows. L-dopa reduced hypothermia and potentiated body weight loss, whereas apomorphine produced opposite effects.
- 2.
Higher doses of apomorphine attenuated jumping and burrows but had no effect on “wet dog” shakes. On the other hand, and with the exception of sulpiride, all other dopamine (DA) antagonists produced effects opposite those of the agonists with regard to jumping, “wet dog” shakes and burrows.
- 3.
In addition, DA antagonists reduced hypothermia and body weight loss. The effects of DA agonists and antagonists were investigated in mice injected with 6-hydroxydopamine (6-OHDA) intracerebrally to examine whether DA-mediated effects are somehow linked to noradrenergic pathways.
- 4.
Mice pretreated with 6-OHDA developed a higher degree of naloxone-induced withdrawal jumping than did untreated mice. 6-OHDA reversed the effects of apomorphine on “wet dog” shakes and burrows while abolishing those of L-dopa on all withdrawal symptoms, the only exception being jumping, which remained unchanged.
- 5.
6-OHDA also reversed the effects of sulpiride on all withdrawal symptoms while reversing the effects of pimozide on jumping, and it abolished its effect on hypothermia.
- 6.
These findings provide evidence suggesting that the effects of DA agonists and antagonists are dependent at least partly on intact noradrenergic pathways.
- 1.
Stress-induced norepinephrine release in the hypothalamic paraventricular nucleus and pituitary-adrenocortical and sympathoadrenal activity: In vivo microdialysis studies
1995, Frontiers in NeuroendocrinologyThe hypothalamic-pituitary-adrenocortical (HPA) axis and the autonomic nervous system are major effector systems that serve to maintain homeostasis during exposure to stressors. In the past decade, interest in neurochemical regulation and in pathways controlling activation of the HPA axis has focused on catecholamines, which are present in high concentrations in specific brain areas—specially in the hypothalamus. The work described in this review has concentrated on the application of in vivo microdialysis in rat brain regions such as the paraventricular nucleus (PVN) of the hypothalamus, the central nucleus of the amygdala (ACE) the bed nucleus of the stria terminalis (BNST), and the posterolateral hypothalamus in order to examine aspects of catecholaminergic function and relationships between altered catecholaminergic function and the HPA axis and sympathoadrenal system activation in stress. Exposure of animals to immobilization (IMMO) markedly and rapidly increases rates of synthesis, release, and metabolism of norepinephrine (NE) in all the brain areas mentioned above and supports previous suggestions that in the PVN NE stimulates release of corticotropin-releasing hormone (CRH). The role of NE in the ACE and the BNST and most other areas possessing noradrenergic innervation remains unclear. Studies involving lower brainstem hemisections show that noradrenergic terminals in the PVN are derived mainly from medullary catecholaminergic groups rather than from the locus ceruleus, which is the main source of NE in the brain. Moreover, the medullary catecholaminergic groups contribute substantially to IMMO-induced noradrenergic activation in the PVN. Data obtained from adrenalectomized rats, with or without glucocorticoid replacement, and from hypercortisolemic rats suggest that glucocorticoids feedback to inhibit CRH release in the PVN, via attenuation of noradrenergic activation. Results from rats exposed to different stressors have indicated substantial differences among stressors in eliciting PVN noradrenergic responses as well as of responses of the HPA, sympathoneural, and adrenomedullary systems. Finally, involvement of other areas that participate in the regulation of the HPA axis such as the ACE, the BNST, and the hippocampus and the importance of stress-induced changes in expression of immediate early genes such as c-fos are discussed.
Plasma-free and sulfoconjugated MHPG in major depressive disorders: Differences between responders to treatment and nonresponders
1993, Biological PsychiatryThe plasma levels of free and sulfoconjugated forms of 3-methoxy-4-hydroxyphenylglycol (MHPG) were examined before and after treatment in 16 patients with unipolar major depressive disorders without melancholia. The patients were treated with intravenous administration of clomipramine for 4 weeks. Seven depressive disorder patients who showed marked improvement (the improvement group) revealed significant reduction in their plasma sulfoconjugated MHPG levels. In 6 depressive disorder patients who showed no improvement (the no-improvement group), the plasma sulfoconjugated MHPG levels showed no significant change after treatment. The remaining 3 patients, who showed ambiguous change after treatment, were excluded from the analysis. Levels of plasma-free MHPG showed significant change after treatment in neither the improvement group nor in the no-improvement group. It is suggested that levels of plasma sulfoconjugated MHPG may serve as an indicator of brain noradrenergic activity.
3-Methoxy-4-hydroxyphenylethyleneglycol concentrations in discrete hypothalamic nuclei reflect the activity of noradrenergic neurons
1991, Brain ResearchAn analytical technique is described which permits the quantitation of picogram concentration of 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) in acid hydrolyzed extracts of microdissected regions of the rat brain, and this procedure is used to determine if alterations in the activity of noradrenergic neurons are reflected by changes in the concentrations of MHPG in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the rat hypothalamus. MHPG was not detected in non-hydrolyzed samples of either the PVN or SON, but following acid hydrolysis (heating of samples at 94°C for 5 min in 0.16 M perchloric acid) MHPG was detected in both of these regions. These results indicate that MHPG exists primarily as a conjugate in the PVN and SON. Neurotoxin-induced lesions of the ventral noradrenergic bundle decreased norepinephrine (NE) and MHPG concentrations in the PVN and SON, demonstrating that tissue levels of MHPG in these brain regions are dependent upon the presence of noradrenergic neurons. Electrical stimulation of the locus coeruleus increased MHPG concentrations in the PVN, but not in the SON, whereas electrical stimulation of the medial forebrain bundle increased MHPG concentrations in both of these regions. The α2-adrenergic receptor antagonist idazoxan incrased, while the α2-adrenergic receptor agonist clonidine decreased MHPG concentrations in both the PVN and SON, but neither idazoxan nor clonidine altered NE concentrations in these regions. Immobilization of rats in the supine position increased MHPG concentrations in the PVN and SON, and this was accompanied by a decrease in NE concentrations in the SON. The results of the present study reveal that experimental procedures that increase or decrease the activity of noradrenergic neurons terminating in the PVN and SON produce corresponding changes in the concentrations of MHPG in these nuclei, and suggest that MHPG concentrations (and the ratio of MHPG to NE) can be used as indices of the activity of noradrenergic neurons terminating in these hypothalamic regions.
The current concept of pseudo-dementia
1990, La Revue de medecine interneLa pseudodémence est un concept créé à la fin du siècle dernier pour qualifier un tableau clinique qui imite celui de la démence, mais réversible et sans processus neuropathologique sous-jacent. L'étiologie de loin la plus fréquente est représentée par la maladie dépressive, dont le retentissement sur les capacités cognitives peut prendre schématiquement deux formes : les « troubles cognitifs de la dépressionet le tableau plus spectaculaire de la « pseudodémence de Wernicke . Le problème principal est lié à la difficulté du diagnostic avec les démences organiques, en particulier les dégénérescences corticales de type Alzheimer. La reconnaissance de ces tableaux constitue une alternative importante au diagnostic de démence organique dans la mesure où elle permet l'instauration d'un traitement antidépressif efficace conditionnant l'éventuelle réversibilité des symptômes. Plusieurs travaux ont été récemment consacrés à l'individualisation de critères diagnostiques cliniques, biochimiques et électroencéphalographiques. Les critères de Wells considérés comme un élément classique du diagnostic ne présentent d'intérêt que dans leur partie anamnéstique. Enfin, sur le plan théorique, une approche critique de cette notion peut servir de base à une nouvelle conception neurologique de la dépression ainsi qu'à certaines hypothèses actuelles sur les relations de cette dernière à la démence.
The concept of pseudodementia was coined in the late XIXth century to refer to a syndrome mimicking dementia, but without underlying neurological lesions. Depressive disorders represent the main etiological factor and may present under two different forms, either « depressive cognitive disorders , or the more severe feature of « Wernicke's pseudodementia . The main issue remains diagnosing pseudodementia form organic dementia, especially from cortical degenerations of the Alzheimer type. Thus, the recognition of this clinical syndrome represents an alternative to the diagnosis of dementia which may lead to earlier and more effective psychiatric treatment. Recently, diagnostic criteria have been proposed to facilitate this distinction. Such criteria include clinical history, neuropsychological features, biological findings (dexamethasone suppression test and plasma MHPG) and electroencephalographic sleep studies. Finally, from a theorical point of neurological conception of depression as well as for current hypotheses on the relationship of this last one with dementia.
Cerebrospinal fluid constituents of cat vary with susceptibility to motion sickness
1989, Life SciencesSix female cats, varying in susceptibility to motion sickness, were implanted with chronic cannulae in the rostral portion of the fourth ventricle. The cats were then challenged with a motion sickness-inducing stimulus. Samples of cerebrospinal fluid were withdrawn before and after emesis or 30 min of motion if emesis did not occur and again on control (no motion) days. The samples were analyzed by HPLC with an array of 16 coulometric detectors. Thirty-six compounds were identified in the samples. Baseline levels of DOPAC, MHPGSO4, uric acid, DA, 5-HIAA and HVA were lower on motion and control days in cats which became motion sick when compared with cats which did not become motion sick. None of the identified compounds varied as a function of either exposure to motion or provocation of emesis. It is concluded that susceptibility to motion sickness is a manifestation of individual differences related to fundamental neurochemical composition.
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Present address: Department of Clinicial Pharmacology and Neurology, Duke University Medical Center, Durham, N.C.
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Present address: Department of Psychiatry, Harvard Medical School, Massachusetts Mental Health Center, Boston, Mass.