Previous studies, using electrophysiological and fluorimetric analysis with a calcium sensitive dye, have shown that 5-7 DIV developing spinal cord neurons displayed high levels of glycinergic transmission. GABAergic and AMPAergic neurotransmission contributed much less to the overall transmission. Here, we show that culturing neurons in absence of a glia cell monolayer reduced the frequency of glycinergic spontaneous IPSCs (0.1 +/- 0.01 Hz), without altering the level of overall transmission (3 +/- 1.1 Hz). The predominant transmission was mediated by GABA(A) receptors (72% of total synaptic events). In addition, combination of bicuculline and CNQX blocked synaptically mediated calcium transients recorded with fluo-3. Furthermore, application of glycine revealed the presence of extrasynaptic receptors in these neurons (25 +/- 6 pA/pF). Culturing neurons on a glial cell monolayer increased the frequency of glycinergic currents (0.4 +/- 0.02 Hz), without changing the amplitude of the current (20 +/- 4 pA). The use of a glia-conditioned media reversed the effect of growing the neurons in a glia-deprived condition. These results indicate that the establishment of glycinergic transmission is dependent on the presence of a glia derived soluble factor. However, functional GlyRs were still able to insert in the neuronal membrane in a glia-independent manner.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.mcn.2005.01.001DOI Listing

Publication Analysis

Top Keywords

presence glia
8
spinal cord
8
cord neurons
8
glycinergic transmission
8
culturing neurons
8
cell monolayer
8
frequency glycinergic
8
transmission
6
neurons
6
glycinergic
5

Similar Publications

Background: Down syndrome (DS) is associated with mitochondrial dysfunction leading to higher levels of oxidative stress and cell degeneration. This fact, together with the overexpression of AD-related genes in trisomy 21, increases the risk of developing Alzheimer's disease (AD). Thus, it is important to look for interventions that could prevent mitochondrial damage before symptoms occur.

View Article and Find Full Text PDF

Biomarkers.

Alzheimers Dement

December 2024

Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.

Background: Glial reactivity is a key phenomenon in Alzheimer's disease (AD) and is closely associated with amyloid-β (Aβ) pathology. Although compelling experimental data suggest that microglial activation modulates reactive astrogliosis, it remains to be elucidated whether microglial activation influences the association of Aβ pathology with reactive astrogliosis in the living AD human brain. Here, we tested the association of microglial activation and Aβ pathology with reactive astrogliosis in individuals across the aging and AD clinical spectrum.

View Article and Find Full Text PDF

Background: Microglia are the brain resident immune cells that function as immune surveillance and engulf and clear damage-associated molecular patterns (DAMPs), such as misfolded and oligomeric tau (TO) relevant Alzheimer's disease (AD) and prevent nuclear factor-kB (NF-kB) mediated immune-activation. IκBα is an endogenous inhibitor of the NF-kB subunit p50-p65/c-Rel protein complex. IkBα's association is precisely regulated in microglia to prevent excessive NF-kB activation and neuroinflammation, which is one of the hallmarks of AD.

View Article and Find Full Text PDF

Background: We hypothesized that TSPO PET, which measures microglia density, would be elevated in the presence of amyloid and impairment across different clinical variants in a pattern that follows their characteristic tau distribution.

Method: Participants (n = 17 amyloid-negative control, 3 amyloid-positive AD, 2 amyloid-positive PCA, 6 amyloid-negative with impairment (1 aMCI, 1 MCI, 3 AD, 1 LATE); age = 69±7, 43% women) from the Longitudinal Imaging of Microglial Activation in Different Clinical Variants of Alzheimer's Disease study underwent amyloid PET (Florbetaben), tau PET (MK6240), and TSPO PET (ER176). Amyloid positivity was determined by visual read.

View Article and Find Full Text PDF

Background: Microglial reactivity and neuroinflammation are crucial pathological processes in Alzheimer's Disease (AD). Several attempts to develop a treatment by supressing the immune response in AD have been made, yet these yielded very limited results. Recent studies suggest contrasting effects of microglial reactivity, indicating a biphasic response with both beneficial and deleterious effects at distinct stages of AD.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!