scholarly journals Postmortem studies in schizophrenia

2000 ◽  
Vol 2 (4) ◽  
pp. 349-357 ◽  
Keyword(s):  
Brain Imaging ◽  
Aminobutyric Acid ◽  
Methodological Issues ◽  
Complementary Information ◽  
Research Designs ◽  
Postmortem Studies ◽  
Biochemical Pathology ◽  
The Brain

For over a century, postmortem studies have played a central part in the search for the structural and biochemical pathology of schizophrenia. However, for most of this time, little progress has been made. Recently, the situation has begun to change, helped by the emergence of more powerful methodologies and research designs, and by the availability of brain imaging to provide complementary information. As a result, it can now be clearly concluded that there are structural cerebral abnormalities in schizophrenia that are intrinsic to the disorder. The neuropathological process is not primarily degenerative, but involves a change in the normal cytoarchitecture of the brain, probably originating in development. Neurochemically, there is postmortem evidence for alterations in several transmitter systems including dopamine, glutamate, serotonin, and γ-aminobutyric acid (GABA). The cardinal findings are reviewed here, together with a consideration of the conceptual and methodological issues that face postmortem studies of schizophrenia.

Cerebrospinal fluid γ-aminobutyric acid levels in dogs with chronic portosystemic encephalopathy

1986 ◽  
Vol 71 (6) ◽  
pp. 749-753 ◽  
Author(s):  
J. E. Maddison ◽  
D. Yau ◽  
P. Stewart ◽  
G. C. Farrell
Keyword(s):  
Cerebrospinal Fluid ◽  
Aminobutyric Acid ◽  
Plasma Ammonia ◽  
Portosystemic Encephalopathy ◽  
Dog Model ◽  
Csf Levels ◽  
Neurological Features ◽  
The Brain ◽  
Biochemical Abnormalities

1. Cerebrospinal fluid (CSF) γ-aminobutyric acid (GABA) levels were measured in a dog model of spontaneous chronic portosystemic encephalopathy. 2. Dogs with congenital portacaval shunts (intra- or extra-hepatic) develop neurological features of abnormal psychomotor behaviour and depressed consciousness that are consistent with the symptoms of chronic portosystemic encephalopathy in humans. In the five dogs studied, plasma ammonia was elevated, as was CSF tryptophan, both usual biochemical abnormalities in portosystemic encephalopathy. 3. CSF levels of GABA in five dogs with portosystemic encephalopathy (100 ± 13 pmol/ml) were not significantly different from those in five control dogs (96 ± 14 pmol/ml). CSF levels of GABA were not altered after ammonia infusion. 4. If enhanced GABA-ergic neurotransmission, due to influx of gut-derived GABA into the brain, is responsible for the pathophysiology of chronic portosystemic encephalopathy in this model, it is not reflected by increased levels of GABA in CSF.

scholarly journals The brain timewise: how timing shapes and supports brain function

2015 ◽  
Vol 370 (1668) ◽  
pp. 20140170 ◽  
Author(s):  
Riitta Hari ◽  
Lauri Parkkonen
Keyword(s):  
Human Brain ◽  
Brain Imaging ◽  
Brain Function ◽  
Temporal Dynamics ◽  
Generative Models ◽  
Network Activity ◽  
Brain Diseases ◽  
Specific Information ◽  
Non Invasive ◽  
The Brain

We discuss the importance of timing in brain function: how temporal dynamics of the world has left its traces in the brain during evolution and how we can monitor the dynamics of the human brain with non-invasive measurements. Accurate timing is important for the interplay of neurons, neuronal circuitries, brain areas and human individuals. In the human brain, multiple temporal integration windows are hierarchically organized, with temporal scales ranging from microseconds to tens and hundreds of milliseconds for perceptual, motor and cognitive functions, and up to minutes, hours and even months for hormonal and mood changes. Accurate timing is impaired in several brain diseases. From the current repertoire of non-invasive brain imaging methods, only magnetoencephalography (MEG) and scalp electroencephalography (EEG) provide millisecond time-resolution; our focus in this paper is on MEG. Since the introduction of high-density whole-scalp MEG/EEG coverage in the 1990s, the instrumentation has not changed drastically; yet, novel data analyses are advancing the field rapidly by shifting the focus from the mere pinpointing of activity hotspots to seeking stimulus- or task-specific information and to characterizing functional networks. During the next decades, we can expect increased spatial resolution and accuracy of the time-resolved brain imaging and better understanding of brain function, especially its temporal constraints, with the development of novel instrumentation and finer-grained, physiologically inspired generative models of local and network activity. Merging both spatial and temporal information with increasing accuracy and carrying out recordings in naturalistic conditions, including social interaction, will bring much new information about human brain function.

Abstract TP147: Central Post Stroke Pain: A Systematic Review

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Jonathan Singer ◽  
Alyssa Conigliaro ◽  
Elizabeth Spina ◽  
Susan Law ◽  
Steven Levine
Keyword(s):  
Systematic Review ◽  
Brain Imaging ◽  
Pain Scale ◽  
Post Stroke ◽  
Underlying Causes ◽  
Single Question ◽  
Thalamic Region ◽  
The Brain ◽  
A Current

Background: Central Post Stroke Pain (CPSP) is reportedly due to strokes in the thalamic region (Dishinbition Theory); however, the Central Imbalance Theory states that CPSP is due to damage to the spinothalamic pathway (STP). Aims: 1) Clarify the role of thalamic strokes and STP damage in CPSP patients. 2) Gain a current understanding of anatomic substrates, brain imaging, and treatment of CPSP. Methods: Two independent reviewers systematically reviewed PUBMED, CINAHL and Web of Science for studies including original, clinical studies and randomized controlled trials (RCTs) using PRISMA guidelines. Studies had to assess CPSP, using a single question or pain scale. Results: Search from January – July 2016, identifying 731 publications. We extracted data from 23 studies and categorized the articles’ aims into 4 sections: somatosensory deficits (5 studies), STP (3 studies), brain imaging (7 studies), and RCTs (8 studies). Somatosensory studies showed high rates of CPSP; however, the underlying causes of these deficits were unclear. Most studies did not refer to stroke location as playing a role in CPSP, but that pathways may. STP studies displayed consistent evidence that the STP plays a major role in CPSP, delineating that CPSP can occur even when the stroke is not in the thalamic region but in other regions (e.g. cerebellum, basal ganglia, medulla). Four of the brain imaging studies found CPSP not related and 3 found it was related to thalamic strokes. All 7 studies had major limitations including sample size, no control groups, and selection bias. RCTs were mostly negative, but brain stem and motor cortex stimulation studies showed the most promise. Conclusions: While CPSP has been linked to the thalamic region since the early 1900’s, the peer-reviewed literature showed equivocal results when examining location of stroke. Our systematic review suggests damage to the STP is associated with CPSP and this could provide insights into mechanisms and treatment. Moreover, historical connection of strokes in the thalamic region and CPSP should be reevaluated as many studies noted that strokes in other regions of the brain also produce CPSP.

Krešimir Krnjević (1927–2021) and GABAergic inhibition: a lifetime dedication

2021 ◽  
pp. 1-4
Author(s):  
Yehezkel Ben-Ari ◽  
Enrico Cherubini ◽  
Massimo Avoli
Keyword(s):  
Canadian Journal ◽  
Chief Editor ◽  
Aminobutyric Acid ◽  
Gabaergic Inhibition ◽  
Inhibitory Neurotransmitter ◽  
Neuroscience Research ◽  
Personal Interactions ◽  
The Brain ◽  
Made In

After over seven decades of neuroscience research, it is now well established that γ-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the brain. In this paper dedicated to Krešimir Krnjević (1927–2021), a pioneer and leader in neuroscience, we briefly highlight the fundamental contributions he made in identifying GABA as an inhibitory neurotransmitter in the brain and our personal interactions with him. Of note, between 1972 and 1978 Dr. Krnjević was a highly reputed Chief Editor of the Canadian Journal of Physiology and Pharmacology.

scholarly journals Dietary γ-Aminobutyric Acid Affects the Brain Protein Synthesis Rate in Ovariectomized Female Rats

2009 ◽  
Vol 55 (1) ◽  
pp. 75-80 ◽  
Author(s):  
Kazuyo TUJIOKA ◽  
Miho OHSUMI ◽  
Kenji HORIE ◽  
Mujo KIM ◽  
Kazutoshi HAYASE ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Female Rats ◽  
Aminobutyric Acid ◽  
Synthesis Rate ◽  
Protein Synthesis Rate ◽  
Brain Protein ◽  
Brain Protein Synthesis ◽  
The Brain

Effect of adrenalectomy on convulsions induced by high-pressure oxygen

1979 ◽  
Vol 57 (7) ◽  
pp. 688-694 ◽  
Author(s):  
A. K. Singh ◽  
E. W. Banister
Keyword(s):  
High Pressure ◽  
Acid Level ◽  
Amino Acid Level ◽  
Aminobutyric Acid ◽  
Pressure Oxygen ◽  
Significant Difference ◽  
High Pressure Oxygen ◽  
Brain Gaba ◽  
The Brain ◽  
Adrenalectomized Rats

Adrenalectomized rats exposed to high pressure oxygen (OHP) until convulsion convulse much later than sham-operated or normal rats. No significant changes in the concentration of noradrenaline (NA) and total catecholamines (TC) in the brain were noted in sham-operated or adrenalectomized rats resulting from sham or real surgery and no change occurred in these variables in normal sham-operated or adrenalectomized animals after OHP leading to convulsion. Brain adrenaline (A) concentration, however, decreased significantly in all three groups following OHP-induced convulsions. Activity of catecholamine O-methyltransferase (COMT) decreased significantly only in adrenalectomized rats. Brain γ-aminobutyric acid (GABA), glutamate, and other amino acid level remained unchanged after adrenalectomy whereas the concentration of ammonia decreased significantly when normal rats were adrenalectomized. After OHP-induced convulsions, the concentrations of brain GABA and glutamate decreased and ammonia and glutamine plus asparagine increased significantly in normal, sham-operated, and adrenalectomized rats. In the blood no significant difference was noted in the concentration of the catecholamines, ammonia, and amino acids either in normal or sham-operated rats. In adrenalectomized rats, the blood A and NA concentrations decreased significantly and tyrosine increased significantly. The concentration of NA, ammonia, and glutamine plus asparagine in rats from all three groups increased after OHP-induced convulsions, whereas the concentration of glutamate decreased significantly. Since the concentration of A increased significantly after convulsions in normal and sham-operated rats but did not change in adrenalectomized rats, it might be proposed that adrenalectomy protects against OHP-induced convulsions by reducing the circulating concentration of A and ammonia.However, these are not the only factors involved in the protection since the sham-operated rats also convulsed much later than normal rats but had similar ammonia and A concentrations to normal animals.

scholarly journals Temporal Lobe Malformations in Achondroplasia: Expanding the Brain Imaging Phenotype Associated withFGFR3-Related Skeletal Dysplasias

2017 ◽  
Vol 39 (2) ◽  
pp. 380-384 ◽  
Author(s):  
S.A. Manikkam ◽  
K. Chetcuti ◽  
K.B. Howell ◽  
R. Savarirayan ◽  
A.M. Fink ◽  
...  
Keyword(s):  
Brain Imaging ◽  
Temporal Lobe ◽  
Skeletal Dysplasias ◽  
The Brain
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