Unique Distribution of Benzodiazepine Receptors in the Brain during the First Two Years of Life

2016 ◽  
Vol 51 (5) ◽  
pp. 244-248
Author(s):  
Sadahiro Nomura ◽  
Hiroyasu Koizumi ◽  
Eiichi Suehiro ◽  
Hidekatsu Kiya ◽  
Michiyasu Suzuki
Keyword(s):  
Benzodiazepine Receptors ◽  
Unique Distribution ◽  
The Brain

Different effects of long-term haloperidol administration on GABAA and benzodiazepine receptors in various parts of the brain

1986 ◽  
Vol 101 (4) ◽  
pp. 460-463 ◽  
Author(s):  
�. �. Vasar ◽  
A. M. Nurk ◽  
M. O. Maimets ◽  
A. H. Soosaar ◽  
L. H. Allikmets
Keyword(s):  
Benzodiazepine Receptors ◽  
The Brain

scholarly journals What Are the Molecular Mechanisms by Which Functional Bacterial Amyloids Influence Amyloid Beta Deposition and Neuroinflammation in Neurodegenerative Disorders?

2020 ◽  
Vol 21 (5) ◽  
pp. 1652 ◽  
Author(s):  
Robert P. Friedland ◽  
Joseph D. McMillan ◽  
Zimple Kurlawala
Keyword(s):  
Amyloid Beta ◽  
Neurodegenerative Disorders ◽  
Innate Immune System ◽  
Molecular Mechanisms ◽  
Innate Immune ◽  
Know How ◽  
Unique Distribution ◽  
The Brain

Despite the enormous literature documenting the importance of amyloid beta (Ab) protein in Alzheimer's disease, we do not know how Ab aggregation is initiated and why it has its unique distribution in the brain. In vivo and in vitro evidence has been developed to suggest that functional microbial amyloid proteins produced in the gut may cross-seed Ab aggregation and prime the innate immune system to have an enhanced and pathogenic response to neuronal amyloids. In this commentary, we summarize the molecular mechanisms by which the microbiota may initiate and sustain the pathogenic processes of neurodegeneration in aging.

Benzodiazepine Receptors in the Periphery

2020 ◽  
pp. 81-96
Author(s):  
Robert B. Raffa
Keyword(s):  
Immune Function ◽  
Cholesterol Metabolism ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Peripheral Benzodiazepine Receptor ◽  
Pharmacologic Effect ◽  
Ion Influx ◽  
Transmembrane Potential Difference ◽  
The Brain

The benzodiazepines are almost universally thought to produce one and only one pharmacologic effect: positive allosteric modulation of GABAA receptors located in the brain. This results in an increased Cl−ion influx, greater negative transmembrane potential difference, and neurons that are less likely to fire in response to anxiety-producing stimulation. Unfortunately, the simplicity and success of this mono-target belief has distracted researchers and clinicians from studying and appreciating their other pharmacology. A glaring example is the general lack of awareness of the peripheral benzodiazepine receptor. The peripheral benzodiazepine receptor alters mitochondrial function (energy supply), cholesterol transport, and immune function. A patient who is on long-term benzodiazepine therapy (or withdrawing from them) will have these sites affected, just as are the sites located in the brain. One can easily imagine that the adverse effects associated with the peripheral sites would be fundamental, varied, and potentially profound—involving lack of energy, altered cholesterol metabolism, and aberrant immune function.

The Benzodiazepine Receptor in Normal and Pathological Human Brain

1978 ◽  
Vol 133 (3) ◽  
pp. 261-268 ◽  
Author(s):  
H. Möhler ◽  
T. Okada
Keyword(s):  
Central Nervous System ◽  
Membrane Fraction ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Synaptic Membrane ◽  
Huntington's Chorea ◽  
High Affinity ◽  
Cortical Areas ◽  
The Central Nervous System ◽  
The Brain

SummaryBenzodiazepines bind with high affinity to a specific benzodiazepine receptor, which occurs exclusively in the central nervous system. The affinity of various benzodiazepines to the receptor closely parallels their pharmacological and therapeutic potency. Binding to the receptor is stereospecific. The receptor is mainly localized in the synaptic membrane fraction and has its highest density in cortical areas of the brain. In Huntington's chorea a decrease in benzodiazepine receptor binding is found in caudate nucleus and putamen, which, at least in putamen, is due to a loss of benzodiazepine receptors apparently located on GABA neurones, which degenerate in Huntington's chorea. The loss of benzodiazepine receptors might explain why the ameliorative effects of benzodiazepines in the early stages of the disease are not sustained in the later stages.

Benzodiazepine receptors in the brain as affected by different experimental stresses: The changes are small and not undirectional

1979 ◽  
Vol 65 (3) ◽  
pp. 273-277 ◽  
Author(s):  
C. Braestrup ◽  
M. Nielsen ◽  
E. B. Nielsen ◽  
M. Lyon
Keyword(s):  
Benzodiazepine Receptors ◽  
The Brain

Stress-induced norepinephrine release in the rat prefrontal cortex measured by microdialysis

1994 ◽  
Vol 267 (6) ◽  
pp. R1559-R1566 ◽  
Author(s):  
H. Nakane ◽  
N. Shimizu ◽  
T. Hori
Keyword(s):  
Prefrontal Cortex ◽  
Benzodiazepine Receptors ◽  
Benzodiazepine Receptor ◽  
Intracerebral Microdialysis ◽  
Fg 7142 ◽  
Basal Release ◽  
Benzodiazepine Receptor Agonist ◽  
Series Of Experiments ◽  
Medial Pfc ◽  
The Brain

Norepinephrine (NE) release in the medial prefrontal cortex (PFC) of rats was studied during immobilization using an intracerebral microdialysis technique. A series of experiments using pharmacological and physiological manipulations indicated that the NE recovered in the medial PFC dialysate was mainly derived from nerve terminals and that the dorsal noradrenergic bundle was a major source of NE in the medial PFC. Immobilization stress immediately elevated NE levels to 176.0 +/- 9.0% of basal release, and this increase continued for the entire period of stress and 20 min after termination of the stress. Preinjection of a benzodiazepine receptor agonist, diazepam (5 mg/kg ip), significantly attenuated immobilization-induced NE release, while injection of an anxiogenic compound, FG-7142 (20 mg/kg ip), facilitated NE release in an obviously nonstressed condition. These results therefore suggest that stressful stimuli activate the NE system in the medial PFC, which may be modulated by an activation of benzodiazepine receptors in the brain.

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