scholarly journals Characterization of the phenotype and birthdates of pyknotic dead cells in the nervous system by a combination of DNA staining and immunohistochemistry for 5'-bromodeoxyuridine and neural antigens.

1993 ◽  
Vol 41 (6) ◽  
pp. 819-827 ◽  
Author(s):  
E Soriano ◽  
J A Del Río ◽  
C Auladell
Keyword(s):  
Nervous System ◽  
Normal Development ◽  
Temporal Distribution ◽  
Neural Tissue ◽  
Aminobutyric Acid ◽  
Phenotypic Characterization ◽  
Gamma Aminobutyric Acid ◽  
Pregnant Mice ◽  
The Times

Cells displaying highly condensed pyknotic nuclei, the most characteristic feature of apoptosis, are considered as dead cells in neural tissue. The present study aimed to devise methods that could allow the neurogenetic and phenotypic characterization of dying pyknotic cells. In the first set of experiments, pregnant mice were labeled at embryonic days E10-E16 with pulses of 5'-bromodeoxyuridine visualization of BrdU after an immunoperoxidase reaction. In addition to normal, healthy immunopositive nuclei, these preparations displayed a number of pyknotic nuclei that were immunoreactive for BrdU. Both the regional and the temporal distribution of BrdU-positive pyknotic cells were coincidental with the peaks of dead cells in neural tissue. For example, pulses of BrdU at E10-E11 resulted in the visualization of immunoreactive pyknotic cells in the subplate and white matter of the cerebral cortex in early postnatal (P) animals. Thus, the times of generation (birthdates) of cells subjected to degenerative processes can be unequivocally identified. In the second set of experiments, brain sections from unlabeled littermates were immunostained for a variety of neural and glial markers and counterstained with bisbenzimide, to find antigens which, by being present in degenerate pyknotic cells, could indicate the phenotype of such cells. Although no pyknotic cells were positively immunostained for neurofilaments, neuropeptide Y, somatostatin, vasoactive intestinal polypeptide, or vimentin, a number of pyknotic cells were found to be immunoreactive for microtubule-associated protein 2, gamma-aminobutyric acid, calbindin 28KD, and glial fibrillary acidic protein. The percentage of pyknotic cells labeled with neural antigens accounted for more than 20% of the total number of pyknotic cells in a given brain region. In contrast, GFAP-positive pyknotic cells represented up to 50% of the total pyknotic cell population. The method shown here has enabled us to determine that both neurons and glial cells undergo degeneration during normal development.

scholarly journals The effect of baclofen on spontaneous and evoked behavioural expression of experimental neuropathic chronic pain

1999 ◽  
Vol 57 (3B) ◽  
pp. 753-760 ◽  
Author(s):  
TEREZINHA DE JESUS T. SANTOS ◽  
CARLOS M. DE CASTRO-COSTA ◽  
SÍLVIO D. A. GIFFONI ◽  
FRANKLIN J. C. SANTOS ◽  
RODRIGO S. N. RAMOS ◽  
...  
Keyword(s):  
Chronic Pain ◽  
Nervous System ◽  
Neuropathic Pain ◽  
Aminobutyric Acid ◽  
Thermal Stimulus ◽  
Dependent Manner ◽  
Gamma Aminobutyric Acid ◽  
Analgesic Effects ◽  
Nociceptive Stimulus ◽  
Dose Dependent

Baclofen (beta-p-chlorophenyl-GABA) has been used in humans to treat spasticity, as well as trigeminal neuralgia. Since GABA (gamma-aminobutyric acid) has been implicated in inhibitory and analgesic effects in the nervous system, it was of interest to study the effect of baclofen in experimental neuropathic pain. With this purpose, experiments were carried out in 17 neuropathic rats with constrictive sciatic injury, as described by Bennet and Xie (1988), taking as pain parameters scratching behaviour and the latency to the thermal nociceptive stimulus. The results showed that baclofen induces, in a dose-dependent manner, significant decrease (p < 0.05) of scratching behaviour and significant increase (p < 0.05) of the latency to the nociceptive thermal stimulus. The absence of antagonism of naloxone suggested a non-participation of an opioid-mediated mechanism in this analgesic effect of baclofen on experimental neuropathic pain.

Abstract 12631: Peripheral Gamma-aminobutyric Acid(gaba) Signaling in Brown Adipose Tissue Induces Metabolic Dysfunction in Obesity

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Ryutaro Ikegami ◽  
Ippei Shimizu ◽  
Takeshi Sato ◽  
Shuang Jiao ◽  
Yohko Yoshida ◽  
...  
Keyword(s):  
Nervous System ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Mitochondrial Function ◽  
Aminobutyric Acid ◽  
Mitochondrial Calcium ◽  
Metabolic Dysfunction ◽  
Gamma Aminobutyric Acid ◽  
Brown Adipose ◽  
Gaba Signaling

Accumulating evidence suggests that adult humans possess active brown adipose tissue (BAT) that may contribute significantly to systemic metabolism because of its high energy consumption capacity. Recently, we demonstrated that metabolic stress induced BAT hypoxia and impaired mitochondrial function, leading to the development of BAT “whitening” and systemic metabolic dysfunction in murine obese models. Various neurotransmitters are known to be involved in the maintenance of BAT homeostasis. Among them, the gamma-aminobutyric acid (GABA) signaling in the central nervous system is well accepted to have anti-obesity effects through the activation of the sympathetic nervous system. Here we show the previously unknown role of peripheral GABA signaling in the development of systemic metabolic dysfunction in obesity. We generated an obese model by imposing a high fat/high sucrose (HFHS) diet on C57BL/6NCr mice. Mass spectrometry analysis demonstrated a significant increase in GABA level in BAT of the dietary obese model. Addition of GABA into drinking water induced BAT whitening, reduced the thermogenic response upon cold tolerance test, and promoted systemic metabolic dysfunction in the obese mice. Mitochondrial calcium is important for the maintenance of mitochondrial homeostasis, whereas calcium overload is reported to inhibit mitochondrial function. Treatment of BAT cells with GABA markedly increased mitochondrial calcium level, promoted the production of reactive oxygen species (ROS), and inhibited mitochondrial respiration. These results indicate that peripheral GABA contributes to the development of systemic metabolic dysfunction by inhibiting BAT function in obesity. The inhibition of peripheral GABA signaling would become a new therapeutic target for obesity and diabetes.

Distribution of gamma-aminobutyric acid (GABA) in the central nervous system of the male mud crab, Scylla olivacea

Crustaceana ◽  
2020 ◽  
Vol 93 (9-10) ◽  
pp. 1123-1134
Author(s):  
Kanjana Khornchatri ◽  
Jirawat Saetan ◽  
Sirirak Mukem ◽  
Prasert Sobhon ◽  
Tipsuda Thongbuakaew
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Distribution Pattern ◽  
Nerve Cord ◽  
Ventral Nerve Cord ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Mud Crab ◽  
Decapod Crustaceans ◽  
The Central Nervous System

Abstract Gamma-aminobutyric acid (GABA) is a neurotransmitter that is widely spread in vertebrate and invertebrate nervous systems and modulates essential physiological roles. Previous studies have reported the distribution of several neurotransmitters throughout the central nervous system (CNS) of decapod crustaceans. However, the existence and distribution of GABA in the mud crab’s, Scylla olivacea, CNS has still not been reported. In this study, we investigated the distribution of GABA using immunohistochemistry. The result revealed that GABA immunoreactivity (-ir) was observed in neurons and fibres throughout the CNS, including the eyestalk, brain, and ventral nerve cord of S. olivacea. Therefore, the existence and extensive distribution pattern of GABA in the CNS of the male mud crab suggest its possible roles in feeding, locomotion, and also reproduction.

Extrasynaptic receptors on cell bodies of neurons in central nervous system of the leech

1977 ◽  
Vol 40 (2) ◽  
pp. 446-452 ◽  
Author(s):  
P. B. Sargent ◽  
K. W. Yau ◽  
J. G. Nicholls
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glutamic Acid ◽  
Systematic Study ◽  
Receptive Fields ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Light Touch ◽  
Nociceptive Neurons ◽  
Extrasynaptic Receptors

1. A systematic study has been made of the sensitivity of identified sensory and motoneurons in the leech central nervous system to chemical transmitter substances. 2. The following substances elicited responses from the cell bodies of individual neurons: acetylcholine, 5-hydroxytryptamine, gamma-aminobutyric acid, glutamic acid, glycine, dopamine, and norepinephrine. Since the cell bodies of leech neurons are free of synapses, the receptors that give rise to these responses are extrasynaptic. 3. Sensory and motoneurons of different function had characteristic complements of extrasynaptic receptors. For example, mechanosensory cells responding to light touch, to pressure, and to noxious stimuli could be distinguished by their responses to iontophoretically applied compounds. For one of these modalities (nociceptive), neurons with different receptive fields but otherwise similar properties had markedly distinct extrasynaptic receptors. The possible significance of extrasynaptic receptors is discussed.

GAMMA-AMINOBUTYRIC ACID AND OTHER BLOCKING COMPOUNDS IN CRUSTACEA: I. CENTRAL NERVOUS SYSTEM

1963 ◽  
Vol 26 (5) ◽  
pp. 721-728 ◽  
Author(s):  
J. Dudel ◽  
R. Gryder ◽  
A. Kaji ◽  
S. W. Kuffler ◽  
D. D. Potter
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid

scholarly journals Antisera to gamma-aminobutyric acid. II. Immunocytochemical application to the central nervous system.

1985 ◽  
Vol 33 (3) ◽  
pp. 240-248 ◽  
Author(s):  
P Somogyi ◽  
A J Hodgson ◽  
I W Chubb ◽  
B Penke ◽  
A Erdei
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Solid Phase ◽  
Colchicine Treatment ◽  
Aminobutyric Acid ◽  
Gamma Aminobutyric Acid ◽  
Beta Alanine ◽  
The Central Nervous System ◽  
Solid Phase Adsorption ◽  
Gaba Immunostaining

An antiserum to gamma-aminobutyric acid (GABA) was tested for the localization of GABAergic neurons in the central nervous system using the unlabeled antibody enzyme method under pre- and postembedding conditions. GABA immunostaining was compared with glutamate decarboxylase (GAD) immunoreactivity in the cerebellar cortex and in normal and colchicine-injected neocortex and hippocampus of cat. The types, distribution, and proportion of neurons and nerve terminals stained with either sera showed good agreement in all areas. Colchicine treatment had little effect on the density of GABA-immunoreactive cells but increased the number of GAD-positive cells to the level of GABA-positive neurons in normal tissue. GABA immunoreactivity was abolished by solid phase adsorption to GABA and it was attenuated by adsorption to beta-alanine or gamma-amino-beta-hydroxybutyric acid, but without selective loss of immunostaining. Reactivity was not affected by adsorption to glutamate, aspartate, taurine, glycine, cholecystokinin, or bovine serum albumin. The concentration (0.05-2.5%) of glutaraldehyde in the fixative was not critical. The antiserum allows the demonstration of immunoreactive GABA in neurons containing other neuroactive substances; cholecystokinin and GABA immunoreactivities have been shown in the same neurons of the hippocampus. In conclusion, antisera to GABA are good markers for the localization of GABAergic neuronal circuits.

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