L. Reibring

Bio: L. Reibring is an academic researcher. The author has contributed to research in topics: Positron emission tomography & Serotonin. The author has an hindex of 5, co-authored 7 publications receiving 211 citations.

Low brain uptake of L-[11C]5-hydroxytryptophan in major depression: a positron emission tomography study on patients and healthy volunteers.

Abstract: The precursor of serotonin, L-5-hydroxytryptophan (L-5-HTP), was radiolabelled with 11C in the beta-position, yielding [beta-11C]serotonin after decarboxylation, allowing positron emission tomography studies of L-5-HTP uptake across the blood-brain barrier. We studied 8 healthy volunteers and 6 patients with histories of DSM-III major depression, 2 with repeated examinations after clinically successful treatment. We report a significantly lower uptake of [11C]5-HTP across the blood-brain barrier in depressed patients, irrespective of phase of illness. The findings emphasize that serotonin is involved in depressive pathophysiology and support earlier suggestions that the transport of 5-HTP across the blood-brain barrier is compromised in major depression.

Brain kinetics of L-[beta-11C]dopa in humans studied by positron emission tomography.

Abstract: The in vivo dopamine precursor L-3,4-dihydroxyphenylalanine (L-DOPA) labelled with 11C in the beta position has been used for positron emission tomography studies of L-DOPA utilization in the brain. The brain uptake and kinetics of L-[11C]DOPA-derived radioactivity were studied in healthy male volunteers, and the specific utilization, i.e. decarboxylation rate of L-[11C]DOPA in different brain areas, was quantified using a brain region devoid of specific L-[11C]DOPA utilization as reference. Total uptake of L-[11C]DOPA-derived radioactivity measured in the brain varied two- to three-fold between subjects, with highest radioactivity in the striatal region. Specific utilization of L-[11C]DOPA radioactivity in the striatal region and in the prefrontal cortex varied twofold between subjects. No specific utilization was observed in other regions of the brain. The uptake of radioactivity in the brain increased dose-dependently with the simultaneous administration of unlabelled L-DOPA up to 10 mg. On the other hand, a decrease in brain radioactivity uptake was measured after pretreatment with 1 mg/kg oral L-DOPA, indicating competition for transport across the blood-brain barrier. Benserazide 0.5 mg/kg orally increased somewhat the radioactivity uptake to the brain. None of these pharmacological perturbations demonstrated any clearcut effect on specific utilization of L-[11C]DOPA. Thus, 11C-labelled L-DOPA is introduced as an alternative to the well-established L-6-[18F]fluoro-DOPA methodology in clinical studies on brain L-DOPA uptake and dopamine synthesis.

Monoamine metabolism in human prefrontal cortex and basal ganglia. Pet studies using [β‐11C] l–5‐hydroxytryptophan and [β‐11C] L‐dopa in healthy volunteers and patients with unipolar major depression

Abstract: The 11C-labelled precursors for serotonin and dopamine synthesis, [β-11C] L-5-hydroxytryptophan (5-HTP) and [β-11C] L-DOPA, were employed as tracer ligands using positron emission tomography (PET) for the evaluation of their regional brain utilization. Study objects were fifteen healthy volunteers and eight patients suffering from, primary RDC unipolar major depression. Specific utilizations of [11C] 5-HTP and [11C] L-DOPA were detected in medial aspects of the prefrontal cortex (PFC) and in the basal ganglia. Utilization of[11C], but not [11C] L-DOPA, was significantly further increased in lower areas of the medial PFC in depressive illness. There were no differences between volunteers and patients with respect to specific utilization within basal ganglia. Alterations in utilization of [11C]5-HTP and [11C] L-DOPA in the medial PFC may reflect the degree of activation of serotonergic and dopaminergic cell bodies in the mesencephalic nuclei, suggesting mesencephalocortical regulation. Earlier, we have reported a decrease in the uptake of [11C] 5-HTP over the blood-brain barrier in depressed patients compared with healthy volunteers. A hypothetic activation of serotonin synthetic capacity, topographically limited to the medial PFC and relevant to depressive illness, might represent a pathophysiological compensation related to serotonin precursor deficiency. However, the sum of events may still result in a state that does not exclude a serotonergic hypofitnction in major depression. Depression 1:71–81 (1993). © 1993 Wiley-Liss, Inc.

A neuropsychological theory of multiple systems in category learning

Abstract: A neuropsychological theory is proposed that assumes category learning is a competition between separate verbal and implicit (i.e., procedural-learning-based) categorization systems. The theory assumes that the caudate nucleus is an important component of the implicit system and that the anterior cingulate and prefrontal cortices are critical to the verbal system. In addition to making predictions for normal human adults, the theory makes specific predictions for children, elderly people, and patients suffering from Parkinson's disease, Huntington's disease, major depression, amnesia, or lesions of the prefrontal cortex. Two separate formal descriptions of the theory are also provided. One describes trial-by-trial learning, and the other describes global dynamics. The theory is tested on published neuropsychological data and on category learning data with normal adults.

Interactions Between Monoamines, Glutamate, and GABA in Schizophrenia: New Evidence

Abstract: In spite of its proven heuristic value, the dopamine hypothesis of schizophrenia is now yielding to a multifactorial view, in which the other monoamines as well as glutamate and GABA are included, with a focus on neurotransmitter interactions in complex neurocircuits. The primary lesion(s) in schizophrenia does not necessarily involve any of these neurotransmitters directly but could deal with a more general defect, such as a faulty connectivity of developmental origin. Nevertheless, a precise identification of neurotransmitter aberrations in schizophrenia will probably provide clues for a better understanding of the disease and for the development of new treatment and prevention strategies.