scholarly journals Presynaptic Glycine Receptors Increase GABAergic Neurotransmission in Rat Periaqueductal Gray Neurons

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Kwi-Hyung Choi ◽  
Michiko Nakamura ◽  
Il-Sung Jang
Keyword(s):  
Glutamate Release ◽  
Glycine Receptor ◽  
Periaqueductal Gray ◽  
Nerve Terminals ◽  
Channel Blockers ◽  
Glycine Receptors ◽  
Glutamatergic Transmission ◽  
Gabaergic Neurotransmission ◽  
Nociceptive Transmission ◽  
Descending Inhibitory Pathway

The periaqueductal gray (PAG) is involved in the central regulation of nociceptive transmission by affecting the descending inhibitory pathway. In the present study, we have addressed the functional role of presynaptic glycine receptors in spontaneous glutamatergic transmission. Spontaneous EPSCs (sEPSCs) were recorded in mechanically dissociated rat PAG neurons using a conventional whole-cell patch recording technique under voltage-clamp conditions. The application of glycine (100 µM) significantly increased the frequency of sEPSCs, without affecting the amplitude of sEPSCs. The glycine-induced increase in sEPSC frequency was blocked by 1 µM strychnine, a specific glycine receptor antagonist. The results suggest that glycine acts on presynaptic glycine receptors to increase the probability of glutamate release from excitatory nerve terminals. The glycine-induced increase in sEPSC frequency completely disappeared either in the presence of tetrodotoxin or Cd2+, voltage-gated Na+, or Ca2+channel blockers, suggesting that the activation of presynaptic glycine receptors might depolarize excitatory nerve terminals. The present results suggest that presynaptic glycine receptors can regulate the excitability of PAG neurons by enhancing glutamatergic transmission and therefore play an important role in the regulation of various physiological functions mediated by the PAG.

NMDA-coupled periaqueductal gray glycine receptors modulate anxioselective drug effects on plus-maze performance

1998 ◽  
Vol 90 (2) ◽  
pp. 157-165 ◽  
Author(s):  
Márcia Maria De Souza ◽  
Luiz Carlos Schenberg ◽  
Antonio de Pádua Carobrez
Keyword(s):  
Drug Effects ◽  
Periaqueductal Gray ◽  
Maze Performance ◽  
Glycine Receptors ◽  
Plus Maze

scholarly journals GLYCINE RECEPTOR ANTIBODY—A MARKER FOR NMO/ NON-MS DEMYELINATION?

2015 ◽  
Vol 86 (11) ◽  
pp. e4.36-e4
Author(s):  
Shahd Hamid ◽  
Liene Elsone ◽  
Patrick Waters ◽  
Mark Woodhall Woodhall ◽  
Kerry Mutch ◽  
...  
Keyword(s):  
Optic Neuritis ◽  
Neurological Disorders ◽  
Glycine Receptor ◽  
Prognostic Significance ◽  
Transverse Myelitis ◽  
Functional Disorders ◽  
Glycine Receptors ◽  
Cns Diseases ◽  
Receptor Antibody

BackgroundAntibodies against glycine receptors (GlyR Ab) have been strongly linked to progressive encephalomyelitis with rigidity and myoclonus (PERM). Their association with other neurological disorders is poorly understood.MethodsWe looked retrospectively at all patients who were tested for (GlyR Abs) in the Walton Centre between 2010–2014.Results138 patients were tested. The pre-test diagnoses (n) were transverse myelitis (34), NMO (22, (7 AQP4 IgG+ve and 15 AQP4 IgG-ve), optic neuritis (17), MS (22), ADEM (4), other atypical demyelination (4), encephalitis (11), epilepsy (4), dementia (4), parkinsonism (3), functional disorders (3) and others (10). 53.6% (74) had a relapsing course6/138 (4%) were positive for GlyR Ab. The diagnoses (n) were optic neuritis (2) one of which was AQP4 IgG+ve, NMO-AQP4-IgG negative (1), transverse myelitis (1), tumefactive demyelination (1) and undiagnosed spastic ataxic syndrome with normal imaging (1). 5/6 had a relapsing course and are on immunosuppressants.ConclusionAntibodies against GlyR are not common and seem to be associated with some non-PERM inflammatory CNS diseases, with a relapsing course. Larger studies are required to understand the clinical and prognostic significance of these early findings.

scholarly journals PICALM rescues glutamatergic neurotransmission, behavioural function and survival in a Drosophila model of Aβ42 toxicity

2020 ◽  
Vol 29 (14) ◽  
pp. 2420-2434
Author(s):  
Yifan Yu ◽  
Teresa Niccoli ◽  
Ziyu Ren ◽  
Nathaniel S Woodling ◽  
Benjamin Aleyakpo ◽  
...  
Keyword(s):  
Association Studies ◽  
Glutamate Release ◽  
Glutamate Transporter ◽  
Genome Wide Association Studies ◽  
Glutamatergic System ◽  
Glutamatergic Transmission ◽  
Direct Role ◽  
Genome Wide ◽  
Drosophila Model ◽  
Behavioural Function

Abstract Alzheimer’s disease (AD) is the most common form of dementia and the most prevalent neurodegenerative disease. Genome-wide association studies have linked PICALM to AD risk. PICALM has been implicated in Aβ42 production and turnover, but whether it plays a direct role in modulating Aβ42 toxicity remains unclear. We found that increased expression of the Drosophila PICALM orthologue lap could rescue Aβ42 toxicity in an adult-onset model of AD, without affecting Aβ42 level. Imbalances in the glutamatergic system, leading to excessive, toxic stimulation, have been associated with AD. We found that Aβ42 caused the accumulation of presynaptic vesicular glutamate transporter (VGlut) and increased spontaneous glutamate release. Increased lap expression reversed these phenotypes back to control levels, suggesting that lap may modulate glutamatergic transmission. We also found that lap modulated the localization of amphiphysin (Amph), the homologue of another AD risk factor BIN1, and that Amph itself modulated postsynaptic glutamate receptor (GluRII) localization. We propose a model where PICALM modulates glutamatergic transmission, together with BIN1, to ameliorate synaptic dysfunction and disease progression.

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