CSF-endorphines in acute and chronic brain lesions

Hamel, E.

doi:10.1007/bf01794687

Cited by 5 publications

(4 citation statements)

References 24 publications

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“…These variations appeared to be due to the diversity of methods and experimental conditions involving stress, pain-related manipulations, and infections [111,113,116-118,120,129-133] . Another complicating factor is that β-END levels show diurnal fluctuations in plasma as well as in the CSF [134,135]. The conclusion is that CSF β-END concentration mostly exceeds peripheral β-END, which excludes the possibility that central levels are a passive reflection of peripheral levels.…”

Section: Central and Peripheral β-End Are Regulated Differentiallymentioning

confidence: 99%

Volume transmission of beta-endorphin via the cerebrospinal fluid; a review

Veening

Gerrits

Barendregt

2012

Fluids Barriers CNS

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There is increasing evidence that non-synaptic communication by volume transmission in the flowing CSF plays an important role in neural mechanisms, especially for extending the duration of behavioral effects. In the present review, we explore the mechanisms involved in the behavioral and physiological effects of β-endorphin (β-END), especially those involving the cerebrospinal fluid (CSF), as a message transport system to reach distant brain areas. The major source of β-END are the pro-opio-melano-cortin (POMC) neurons, located in the arcuate hypothalamic nucleus (ARH), bordering the 3rd ventricle. In addition, numerous varicose β-END-immunoreactive fibers are situated close to the ventricular surfaces. In the present paper we surveyed the evidence that volume transmission via the CSF can be considered as an option for messages to reach remote brain areas. Some of the points discussed in the present review are: release mechanisms of β-END, independence of peripheral versus central levels, central β-END migration over considerable distances, behavioral effects of β-END depend on location of ventricular administration, and abundance of mu and delta opioid receptors in the periventricular regions of the brain.

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Section: Central and Peripheral β-End Are Regulated Differentiallymentioning

confidence: 99%

Volume transmission of beta-endorphin via the cerebrospinal fluid; a review

Veening

Gerrits

Barendregt

2012

Fluids Barriers CNS

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“…According to the literature, CSF-BE levels are highest early in the morning, between 6 and 9 a.m. [13,103]. In the present thesis, all lumbar puncture on patients were done between 8 and 9 a.m., whereas the timing of lumbar puncture in healthy controls ranged from early morning to very early afternoon.…”

Section: Circadian Variationsmentioning

confidence: 82%

The Cerebrospinal Fluid in Severe Pain Conditions : Clinical, Pharmacological and Proteomic Aspects

Bäckryd¹

2015

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The treatment of both cancer pain and non-cancer chronic pain is still suboptimal. The overall aim of this PhD thesis was to conduct translational pain research at the interface between clinical pain medicine and the field of human proteomics, using the practice of intrathecal analgesia at our institution as a starting point. Hence, the cerebrospinal fluid (CSF) is at the centre of the present dissertation, both as a target for infusing analgesics (Papers I and II – clinical and pharmacological aspects) and as an important biofluid for human biomarker studies (Papers III and IV – proteomic aspects). In Paper I, 28 cases of intrathecal analgesia in cancer patients were prospectively followed. Movement-evoked breakthrough pain remained a major clinical problem throughout the study month despite otherwise successful intrathecal analgesia (defined as good control of spontaneous resting pain paralleled by a marked decrease of concomitant systemic opioid doses). This study therefore illustrates the importance of considering not only spontaneous resting pain but also movement-evoked breakthrough pain. In Paper II, an expert-based algorithm for trialing the intrathecal analgesic ziconotide by bolus injections was evaluated in an open-label study of 23 patients with chronic neuropathic pain. We found few responders (13%) according to the strict criteria of the algorithm, but ziconotide bolus injection trialing seems feasible. The predictive power of ziconotide bolus trialing remains unclear, and the pharmacological profile of ziconotide (with very slow tissue penetration due to high hydrophilicity) calls the rationale for ziconotide bolus trialing into question. In Paper III, we found low levels of beta-endorphin in the CSF of chronic neuropathic pain patients (n=15) compared to healthy controls (n=19). We speculate that this might indicate dysfunctional top-down control of nociception. Substance P levels in the CSF did not differ by univariate statistics. In Paper IV, the CSF proteome of 11 patients with chronic neuropathic pain and 11 healthy controls was exploratively studied, combining gel-based proteomics with multivariate data analysis. After eliminating four proteins associated with age, 32 proteins were found to highly discriminate between groups. Among these, the seven proteins having the highest discriminatory power between patients and controls were: one isoform of angiotensinogen, two isoforms of alpha-1-antitrypsin, three isoforms of haptoglobin, and one isoform of pigment epithelium-derived factor. In conclusion, this PhD thesis demonstrates the fruitfulness of studying the CSF, both as a target for infusing analgesics and as a potential mirror of the neurobiological processes involved in pathological pain conditions. The thesis points to the need for more research into the mechanisms of different pain conditions, in order to hopefully achieve the vision of mechanism-based pain diagnoses

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“…These destructive sites may also explain why the p-endorphin concentration in CSF was lower than in the plasma of control guinea pigs. Hamel (25) found that CSF p-endorphin concentrations in man were significantly lower than in plasma. These results support our findings of a lower 0-endorphin concentration in CSF as compared with plasma of guinea pigs.…”

Section: Discussionmentioning

confidence: 97%

Possible Involvement of Endogenous -Endorphin in the Pathophysiological Mechanisms of Pichinde Virus-Infected Guinea Pigs

Guo

Liu

Peters

1992

Experimental Biology and Medicine

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Previously, we demonstrated that naloxone, an opiate antagonist, prolonged survival of strain 13 guinea pigs infected with Pichinde virus. Thus, endogenous opiates may be involved in the pathogenesis of this viral disease. To determine whether endogenous opiate levels were affected by Pichinde viral infection, beta-endorphin concentrations in plasma and cerebrospinal fluid (CSF) of normal and infected strain 13 guinea pigs were measured by radioimmunoassay. Cerebrospinal fluid beta-endorphin concentrations were 78.0 +/- 13.2 pg/ml on postinoculation day (PID) 7, 59.0 +/- 5.6 pg/ml on PID 12, and 58.8 +/- 5.4 pg/ml on PID 14. These values were significantly higher than baseline levels of CSF beta-endorphin: 30.8 +/- 1.9 pg/ml. Plasma beta-endorphin concentrations of infected animals increased significantly to 202.1 +/- 17.9 pg/ml on PID 7 and to 154.2 +/- 21.4 pg/ml on PID 12 from a mean baseline value of 84.2 +/- 13.1 pg/ml. After a primer intravenous injection of beta-endorphin (10, 15, or 30 micrograms/kg), followed by constant infusion of beta-endorphin (15, 45, or 90 micrograms/kg.hr) to control noninfected guinea pigs, heart rate (except with the lowest dose) and mean blood pressure decreased markedly. Under these experimental conditions, concentrations of plasma and CSF beta-endorphin increased simultaneously with different magnitude. Because both Pichinde viral infection and beta-endorphin administration produced a similar trend of cardiovascular disturbances, leading to hypotension and bradycardia, increased concentrations of plasma and CSF beta-endorphin may play a partial role in the pathophysiological mechanisms of Pichinde virus infection.

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CSF-endorphines in acute and chronic brain lesions

Cited by 5 publications

References 24 publications

Volume transmission of beta-endorphin via the cerebrospinal fluid; a review

Volume transmission of beta-endorphin via the cerebrospinal fluid; a review

The Cerebrospinal Fluid in Severe Pain Conditions : Clinical, Pharmacological and Proteomic Aspects

Possible Involvement of Endogenous -Endorphin in the Pathophysiological Mechanisms of Pichinde Virus-Infected Guinea Pigs

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