A multidimensional approach to analysis of cerebrospinal fluid biogenic amines in schizophrenia: I. Comparisons with healthy control subjects and neuroleptic-treated/ unmedicated pairs analyses

Issa, Fuad; Gerhardt, Greg A.; Bartko, John J.; Suddath, Robert; Lynch, Michael; Gamache, Paul H.; Freedman, Robert; Wyatt, Richard Jed; Kirch, Darell G.

doi:10.1016/0165-1781(94)90069-8

Cited by 25 publications

(8 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The separations and quantitations of HVA and MHPG in the samples were carried out using a gradient HPLC coupled to coulometric electrochemical detectors arranged in series set at increasing potentials (CEAS; ESA, Chelmsford, Mass.) as described by Issa et al [48].…”

Section: Catecholamine Metabolite Measurementmentioning

confidence: 99%

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

et al. 1999

View full text Add to dashboard Cite

Schizophrenic patients have decreased inhibition of the P50 auditory evoked potential response to the second of two paired click stimuli delivered 500 ms apart. This deficit in inhibitory gating does not change during treatment with typical neuroleptics. We recently reported that neuroleptic-resistant schizophrenics had enhanced P50 gating after 1 month of clozapine treatment, if they responded with decreased clinical symptoms. This study reports the outcome of more prolonged treatment. Ten treatment-refractory schizophrenic patients were studied at baseline, after 1 month on clozapine, and again after 15 ± 6.1 (SD) months of clozapine treatment. Eight subjects reached a clinically stable improved state, at which time they had significantly improved P50 auditory gating. One patient had a return of impaired gating after stopping clozapine, as did another during a clinical relapse. Decreasing plasma 3-methoxy-4-hydroxyphenylglycol levels with clozapine treatment were correlated with improved P50 gating and improved Brief Bsychiatric Rating Scale-positive scores. This study provides further evidence that improved P50 gating in schizophrenic patients treated with clozapine coincides with clinical improvement and that this improvement can be sustained for at least 1 year.

show abstract

Section: Catecholamine Metabolite Measurementmentioning

confidence: 99%

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

et al. 1999

View full text Add to dashboard Cite

show abstract

“…Moreover, schizophrenia patients also presented with increased levels of tryptophan in the CSF and plasma, which was independent of antipsychotic treatment. 113,114 The above mentioned evidence could point towards a decrease in 5-HT synthesis, but with concomitantly increased neurotoxic metabolites synthesised from tryptophan ( fig. 3), ultimately leading to deregulated neuro-circuitries and neuro-degeneration, observed in schizophrenia.…”

Section: Immune-inflammatory Pathwaysmentioning

confidence: 93%

Neurodevelopmental Animal Models Reveal the Convergent Role of Neurotransmitter Systems, Inflammation, and Oxidative Stress as Biomarkers of Schizophrenia: Implications for Novel Drug Development

Möller

Swanepoel

Harvey

2015

ACS Chem. Neurosci.

View full text Add to dashboard Cite

Schizophrenia is a life altering disease with a complex etiology and pathophysiology, and although antipsychotics are valuable in treating the disorder, certain symptoms and/or sufferers remain resistant to treatment. Our poor understanding of the underlying neuropathological mechanisms of schizophrenia hinders the discovery and development of improved pharmacological treatment, so that filling these gaps is of utmost importance for an improved outcome. A vast amount of clinical data has strongly implicated the role of inflammation and oxidative insults in the pathophysiology of schizophrenia. Preclinical studies using animal models are fundamental in our understanding of disease development and pathology as well as the discovery and development of novel treatment options. In particular, social isolation rearing (SIR) and pre- or postnatal inflammation (PPNI) have shown great promise in mimicking the biobehavioral manifestations of schizophrenia. Furthermore, the "dual-hit" hypothesis of schizophrenia states that a first adverse event such as genetic predisposition or a prenatal insult renders an individual susceptible to develop the disease, while a second insult (e.g., postnatal inflammation, environmental adversity, or drug abuse) may be necessary to precipitate the full-blown syndrome. Animal models that emphasize the "dual-hit" hypothesis therefore provide valuable insight into understanding disease progression. In this Review, we will discuss SIR, PPNI, as well as possible "dual-hit" animal models within the context of the redox-immune-inflammatory hypothesis of schizophrenia, correlating such changes with the recognized monoamine and behavioral alterations of schizophrenia. Finally, based on these models, we will review new therapeutic options, especially those targeting immune-inflammatory and redox pathways.

show abstract

“…small amounts of EPI are stored in the brain, its extracellular level in the hypothalamus and LC as measured by microdialysis and push-pull cannula is nearly as high as that of NE [37][38][39], and its metabolite, metanephrine (MN), is present at high concentration in the CSF [40] suggesting that it is a major brain neurotransmitter.…”

Section: Brain Localization Of Behaviorally-activating α 1 -Receptorsmentioning

confidence: 99%

The Brain Epinephrine-α1-Adrenoceptor System in Behavioral Activation and Depression

Quartermain¹

2005

CPSR

View full text Add to dashboard Cite

Disabling behavioral inactivity is a prominent symptom of a number of psychiatric disorders, most notably, major depressive illness. The neurobiology of these inactive states is currently believed to involve alterations in central serotonergic, noradrenergic or dopaminergic neurotransmission as affected by various etiological and predisposing factors. Recent evidence suggests that there is another system that consists of a subset of brain α 1 -adrenoceptors stimulated primarily by brain epinephrine (EPI) that potentially modulates the above three monoamine systems and plays a critical role in behavioral activation and depression. The present review covers the evidence for this system and includes findings that brain α 1 -adrenoceptors are instrumental in behavioral activation, are located near the major monoamine cell groups or target areas, receive EPI as their neurotransmitter, are impaired or inhibited in depressed patients or after stress in animal models, and are restored by a number of antidepressants. This "EPI-α 1 system" may therefore represent a new target system for disabling inactivity.

show abstract

A multidimensional approach to analysis of cerebrospinal fluid biogenic amines in schizophrenia: I. Comparisons with healthy control subjects and neuroleptic-treated/ unmedicated pairs analyses

Cited by 25 publications

References 32 publications

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

Neurodevelopmental Animal Models Reveal the Convergent Role of Neurotransmitter Systems, Inflammation, and Oxidative Stress as Biomarkers of Schizophrenia: Implications for Novel Drug Development

The Brain Epinephrine-α1-Adrenoceptor System in Behavioral Activation and Depression

Contact Info

Product

Resources

About

A multidimensional approach to analysis of cerebrospinal fluid biogenic amines in schizophrenia: I. Comparisons with healthy control subjects and neuroleptic-treated/ unmedicated pairs analyses

Cited by 25 publications

References 32 publications

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

Auditory P50 in Schizophrenics on Clozapine: Improved Gating Parallels Clinical Improvement and Changes in Plasma 3-Methoxy-4-Hydroxyphenylglycol

Neurodevelopmental Animal Models Reveal the Convergent Role of Neurotransmitter Systems, Inflammation, and Oxidative Stress as Biomarkers of Schizophrenia: Implications for Novel Drug Development

The Brain Epinephrine-&#945;1-Adrenoceptor System in Behavioral Activation and Depression

Contact Info

Product

Resources

About

The Brain Epinephrine-α1-Adrenoceptor System in Behavioral Activation and Depression