230 research outputs found
GABA(A) and strychnine-sensitive glycine receptors modulate N-methyl-d-aspartate-evoked acetylcholine release from rat spinal motoneurons: A possible role in neuroprotection
No full textIncreasing experimental and clinical evidence suggests
that abnormal glutamate transmission might play a
major role in a vast number of neurological disorders.
As a measure of glutamatergic excitation, we have studied
the acetylcholine (ACh) release induced by N-methyl-D-aspartate
(NMDA) receptor stimulation in primary cultured rat
ventral horn spinal neurons and we have evaluated the possibility
to limit the consequences of the hyperactivation of
glutamatergic receptors, by recruiting the inhibitory transmission
mediated by GABA and glycine. For this purpose, we have
exposed cell cultures, previously loaded with [3H]choline, to
NMDA, which increased the spontaneous tritium efflux in a
concentration-dependent manner. Tritium release is dependent
upon external Ca2+, tetrodotoxin, Cd2+ ions and w-conotoxin
GVIA, but not on w-conotoxin MVIIC nor nifedipine, suggesting
the involvement of N-type voltage-sensitive calcium channels.
NMDA-mediated [3H]ACh release was completely prevented by
MK-801, 5,7-diclorokynurenic acid and ifenprodil, while it was
strongly inhibited by a lower external pH, suggesting that the
involved NMDA receptors contain NR1 and NR2B subunits.
Muscimol inhibited NMDA-evoked [3H]ACh release and its effect
was antagonized by SR95531 and potentiated by diazepam,
indicating the involvement of benzodiazepine-sensitive GABAA
receptors. Also glycine, via strychnine-sensitive receptors, inhibited
the effect of NMDA.
It is concluded that glutamate acts on the NMDA receptors
situated on spinal motoneurons to evoke ACh release, which
can be inhibited through the activation of GABAA and glycine
receptors present on the same neurons. These data suggest
that glutamatergic overload of receptors located onto spinal
cord motoneurons might be decreased by activating GABAA and glycine receptors
Gender-dependent effect of P2X7 antagonism on motor neuron dysfunction in a mouse model of ALS
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GABAA and glycine strychnine-sensitive receptor modulate NMDA-evoked acetylcholine release from rat spinal motor neurons: A possible role in neuroprotection
No full textExtracellular cGMP control of kainate receptor activation in rat cerebellar astrocyte processes
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The impact of organic inhibitors of the hyperpolarization activated current (Ih) on the electroretinogram (ERG) of rodents
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NdCoO3 perovskite as possible candidate for CO sensors: thin films synthesis and sensing properties
No full textIn this paper the preparation of neodymium cobaltite (NdCoO3) thin films by means of rf-magnetron sputtering is presented. The sensing
properties towards the CO were analyzed by following the resistivity response when changing the gas composition from air to air with
CO. Measurements have shown a good response in the temperature range between 250 and 400 ◦C for CO concentration until 1000 ppm.
Measurable resistance changes are accomplished within few minutes after gas switch. The optimal working temperature was found to be
around 300 ◦C by taking into account the amount of resistance variation and the time required to achieve an easily measurable response for
different temperatures and CO concentrations. In order to explain the results obtained, a possible model for the NCO response mechanism
towards CO is presented
Carbenoxolone inhibits volume-regulated anion conductance in cultured rat cortical astroglia
No full textAccumulating evidence indicate that the gap-junction inhibitor carbenoxolone (CBX) regulates neuronal synchronization, depresses epileptiform activity and has a neuroprotective action. These CBX effects do not depend solely on its ability to inhibit gap junction channels formed by connexins (Cx), but the underlying mechanisms remain to be elucidated. Here we addressed the questions whether CBX modulates volume-regulated anion channels (VRAC) involved in the regulatory volume decrease and regulates the associated release of excitatory amino acids in cultured rat cortical astrocytes. We found that CBX inhibits VRAC conductance with potency comparable to that able to depress the activity of the most abundant astroglial gap junction protein connexin43 (Cx43). However, the knock down of Cx43 with small interfering RNA (siRNA) oligonucleotides and the use of various pharmacological tools revealed that VRAC inhibition was not mediated by interaction of CBX with astroglial Cx proteins. Comparative experiments in HEK293 cells stably expressing another putative target of CBX, the purinergic ionotropic receptor P2X7, indicate that the presence of this receptor was not necessary for CBX-mediated depression of VRAC. Finally, we show that in COS-7 cells, which are not endowed with pannexin-1 protein, another astroglial plasma membrane interactor of CBX, VRAC current retained its sensitivity to CBX. Complementary analyses indicate that the VRAC-mediated release of excitatory amino acid aspartate was decreased by CBX. Collectively, these findings support the notion that CBX could affect astroglial ability to modulate neuronal activity by suppressing excitatory amino acid release through VRAC, thereby providing a possible mechanistic clue for the neuroprotective effect of CBX in vivo
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