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David De Wied - One of the best experts on this subject based on the ideXlab platform.

  • Chapter 29 – Endorphins and schizophrenia
    Progress in Brain Research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Endorphins are produced in brain neurons, and as neuropeptides, they play a role as neuromessengers in the regulation of endocrine, autonomic, and behavioral functions. This chapter describes three hypotheses concerning a role of Endorphins in schizophrenia: the endorphin-excess hypothesis, the γ-type endorphin hypotheses focus, and the fundamental and clinical research induced by these hypotheses. Because the Endorphins have been implicated, particularly in brain functions that are of importance for adaptation to environmental challenges, it is feasible therefore that the malfunctions of endorphin systems can lead to diseases of adaptation that involve inadequate behavior as is seen for instance in schizophrenia. The antipsychotic actions of γ-type Endorphins in schizophrenic patients may relate to the deficiency in γ-E-type activity that has been postulated as an ethiological factor in schizophrenia. Animal experiments have indicated that γ-type Endorphins interfere with brain dopamine activity. Understanding of the actions of γ-type Endorphins in the brain and of the possible role of these peptides in schizophrenia is only beginning to emerge. Yet, the data that are now available provide a basis for further fundamental and clinical research that may eventually lead to the development of more causal therapies for such devastating diseases as schizophrenia based on peptide- or peptidomimetic drugs.

  • Endorphins and schizophrenia.
    Progress in brain research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Clinical endorphin research in schizophrenia has so far fanned out in the following directions: (a) studies of endorphin concentration in body fluids, and (b) studies of the effects in schizophrenic patients of opiate (endorphin) antagonists, and of Endorphins and endorphin derivatives. The main results are reviewed in this paper. The conclusions drawn are: (1) Body fluid research has so far yielded no conclusive evidence of disrupted endorphin metabolism in schizophrenia. Technology for the measurement of small quantities of Endorphins is, however, still deficient. (2) The opiate antagonist issue is controversial. One of the major problems is that the studies undertaken differ considerably from each other in patient selection, dose and route of administration, making comparisons difficult. Furthermore, only single dose studies have been reported; the results of repeated administrations may be different. (3) To date only β-endorphin, DTγE (a fragment of γ-endorphin) and FK33-824 (a synthetic met-enkephalin derivative) have been studied therapeutically. Of these, DTγE is the most interesting in scientific terms, firstly because, pharmacologically, it seems to be related to the ‘true’ neuroleptics, and secondly because its lacks morphinomimetic properties. The therapeutic potential of this substance, if confirmed, would therefore not be related to morphine-like activity but to a ‘genuine’ opiate-receptor-independent anti-psychotic action.

Victor M. Wiegant - One of the best experts on this subject based on the ideXlab platform.

  • Chapter 29 – Endorphins and schizophrenia
    Progress in Brain Research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Endorphins are produced in brain neurons, and as neuropeptides, they play a role as neuromessengers in the regulation of endocrine, autonomic, and behavioral functions. This chapter describes three hypotheses concerning a role of Endorphins in schizophrenia: the endorphin-excess hypothesis, the γ-type endorphin hypotheses focus, and the fundamental and clinical research induced by these hypotheses. Because the Endorphins have been implicated, particularly in brain functions that are of importance for adaptation to environmental challenges, it is feasible therefore that the malfunctions of endorphin systems can lead to diseases of adaptation that involve inadequate behavior as is seen for instance in schizophrenia. The antipsychotic actions of γ-type Endorphins in schizophrenic patients may relate to the deficiency in γ-E-type activity that has been postulated as an ethiological factor in schizophrenia. Animal experiments have indicated that γ-type Endorphins interfere with brain dopamine activity. Understanding of the actions of γ-type Endorphins in the brain and of the possible role of these peptides in schizophrenia is only beginning to emerge. Yet, the data that are now available provide a basis for further fundamental and clinical research that may eventually lead to the development of more causal therapies for such devastating diseases as schizophrenia based on peptide- or peptidomimetic drugs.

  • Endorphins and schizophrenia.
    Progress in brain research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Clinical endorphin research in schizophrenia has so far fanned out in the following directions: (a) studies of endorphin concentration in body fluids, and (b) studies of the effects in schizophrenic patients of opiate (endorphin) antagonists, and of Endorphins and endorphin derivatives. The main results are reviewed in this paper. The conclusions drawn are: (1) Body fluid research has so far yielded no conclusive evidence of disrupted endorphin metabolism in schizophrenia. Technology for the measurement of small quantities of Endorphins is, however, still deficient. (2) The opiate antagonist issue is controversial. One of the major problems is that the studies undertaken differ considerably from each other in patient selection, dose and route of administration, making comparisons difficult. Furthermore, only single dose studies have been reported; the results of repeated administrations may be different. (3) To date only β-endorphin, DTγE (a fragment of γ-endorphin) and FK33-824 (a synthetic met-enkephalin derivative) have been studied therapeutically. Of these, DTγE is the most interesting in scientific terms, firstly because, pharmacologically, it seems to be related to the ‘true’ neuroleptics, and secondly because its lacks morphinomimetic properties. The therapeutic potential of this substance, if confirmed, would therefore not be related to morphine-like activity but to a ‘genuine’ opiate-receptor-independent anti-psychotic action.

Chhabil Dass - One of the best experts on this subject based on the ideXlab platform.

  • quantification of endogenous α and γ Endorphins in rat brain by liquid chromatography tandem mass spectrometry
    Analytical Biochemistry, 2009
    Co-Authors: Hari Kosanam, Suma Ramagiri, Chhabil Dass
    Abstract:

    Abstract Quantification of α- and γ-Endorphins in rat brain using liquid chromatography–electrospray ionization–tandem mass spectrometry is described. [D-Ala2]-γ-endorphin is used as an internal standard. The precursor-to-product ion MRM transitions for α-endorphin, γ-endorphin, and [D-Ala2]-γ-endorphin were m/z 873.6 → 429.6; 929.6 → 542.3; 936.6 → 542.3, respectively. The method was validated in terms of linearity, specificity, sensitivity, recovery, precision, and accuracy. The assay was linear over a concentration range of 0.1–200 ng/mL with the limit-of-detection of 0.03 ng/mL and limit-of-quantification of 0.1 ng/mL. The endogenous concentrations of α- and γ-Endorphins in rat brains were 13.8 ± 0.57 (mean ± SD; n = 5) and 2.5 ± 0.43 ng/g of wet tissue weight, respectively.

Eric Ronken - One of the best experts on this subject based on the ideXlab platform.

  • Chapter 29 – Endorphins and schizophrenia
    Progress in Brain Research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Endorphins are produced in brain neurons, and as neuropeptides, they play a role as neuromessengers in the regulation of endocrine, autonomic, and behavioral functions. This chapter describes three hypotheses concerning a role of Endorphins in schizophrenia: the endorphin-excess hypothesis, the γ-type endorphin hypotheses focus, and the fundamental and clinical research induced by these hypotheses. Because the Endorphins have been implicated, particularly in brain functions that are of importance for adaptation to environmental challenges, it is feasible therefore that the malfunctions of endorphin systems can lead to diseases of adaptation that involve inadequate behavior as is seen for instance in schizophrenia. The antipsychotic actions of γ-type Endorphins in schizophrenic patients may relate to the deficiency in γ-E-type activity that has been postulated as an ethiological factor in schizophrenia. Animal experiments have indicated that γ-type Endorphins interfere with brain dopamine activity. Understanding of the actions of γ-type Endorphins in the brain and of the possible role of these peptides in schizophrenia is only beginning to emerge. Yet, the data that are now available provide a basis for further fundamental and clinical research that may eventually lead to the development of more causal therapies for such devastating diseases as schizophrenia based on peptide- or peptidomimetic drugs.

  • Endorphins and schizophrenia.
    Progress in brain research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Clinical endorphin research in schizophrenia has so far fanned out in the following directions: (a) studies of endorphin concentration in body fluids, and (b) studies of the effects in schizophrenic patients of opiate (endorphin) antagonists, and of Endorphins and endorphin derivatives. The main results are reviewed in this paper. The conclusions drawn are: (1) Body fluid research has so far yielded no conclusive evidence of disrupted endorphin metabolism in schizophrenia. Technology for the measurement of small quantities of Endorphins is, however, still deficient. (2) The opiate antagonist issue is controversial. One of the major problems is that the studies undertaken differ considerably from each other in patient selection, dose and route of administration, making comparisons difficult. Furthermore, only single dose studies have been reported; the results of repeated administrations may be different. (3) To date only β-endorphin, DTγE (a fragment of γ-endorphin) and FK33-824 (a synthetic met-enkephalin derivative) have been studied therapeutically. Of these, DTγE is the most interesting in scientific terms, firstly because, pharmacologically, it seems to be related to the ‘true’ neuroleptics, and secondly because its lacks morphinomimetic properties. The therapeutic potential of this substance, if confirmed, would therefore not be related to morphine-like activity but to a ‘genuine’ opiate-receptor-independent anti-psychotic action.

Gábor L. Kovács - One of the best experts on this subject based on the ideXlab platform.

  • Chapter 29 – Endorphins and schizophrenia
    Progress in Brain Research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Endorphins are produced in brain neurons, and as neuropeptides, they play a role as neuromessengers in the regulation of endocrine, autonomic, and behavioral functions. This chapter describes three hypotheses concerning a role of Endorphins in schizophrenia: the endorphin-excess hypothesis, the γ-type endorphin hypotheses focus, and the fundamental and clinical research induced by these hypotheses. Because the Endorphins have been implicated, particularly in brain functions that are of importance for adaptation to environmental challenges, it is feasible therefore that the malfunctions of endorphin systems can lead to diseases of adaptation that involve inadequate behavior as is seen for instance in schizophrenia. The antipsychotic actions of γ-type Endorphins in schizophrenic patients may relate to the deficiency in γ-E-type activity that has been postulated as an ethiological factor in schizophrenia. Animal experiments have indicated that γ-type Endorphins interfere with brain dopamine activity. Understanding of the actions of γ-type Endorphins in the brain and of the possible role of these peptides in schizophrenia is only beginning to emerge. Yet, the data that are now available provide a basis for further fundamental and clinical research that may eventually lead to the development of more causal therapies for such devastating diseases as schizophrenia based on peptide- or peptidomimetic drugs.

  • Endorphins and schizophrenia.
    Progress in brain research, 1992
    Co-Authors: Victor M. Wiegant, Gábor L. Kovács, Eric Ronken, David De Wied
    Abstract:

    Clinical endorphin research in schizophrenia has so far fanned out in the following directions: (a) studies of endorphin concentration in body fluids, and (b) studies of the effects in schizophrenic patients of opiate (endorphin) antagonists, and of Endorphins and endorphin derivatives. The main results are reviewed in this paper. The conclusions drawn are: (1) Body fluid research has so far yielded no conclusive evidence of disrupted endorphin metabolism in schizophrenia. Technology for the measurement of small quantities of Endorphins is, however, still deficient. (2) The opiate antagonist issue is controversial. One of the major problems is that the studies undertaken differ considerably from each other in patient selection, dose and route of administration, making comparisons difficult. Furthermore, only single dose studies have been reported; the results of repeated administrations may be different. (3) To date only β-endorphin, DTγE (a fragment of γ-endorphin) and FK33-824 (a synthetic met-enkephalin derivative) have been studied therapeutically. Of these, DTγE is the most interesting in scientific terms, firstly because, pharmacologically, it seems to be related to the ‘true’ neuroleptics, and secondly because its lacks morphinomimetic properties. The therapeutic potential of this substance, if confirmed, would therefore not be related to morphine-like activity but to a ‘genuine’ opiate-receptor-independent anti-psychotic action.