Publications by authors named "Alejandro Alcaino"

Background: Serotonin (5-HT) is known to be synthesized and accumulated in the vertebrate retina through the 5-HT transporter, SERT. While manipulation of the serotonergic system has been shown to impact visual processing, the role of 5-HT and SERT as modulators of retinal synaptic function remains poorly understood.

Results: Using mouse retinal slices, we show that acute application of 5-HT produces a cell-type specific reduction in light-evoked excitatory responses (L-EPSC) in ON-OFF retinal ganglion cells (RGCs), but not in ON RGCs.

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BK channels can control neuronal function, but their functional relevance in activity-dependent changes of synaptic function remains elusive. Here, we report that repetitive low-frequency stimulation activates BK channels through 12(S)HPETE, an arachidonic acid metabolite, produced downstream of postsynaptic metabotropic glutamate receptors (mGluRs) to trigger long-term depression (LTD) at CA3-CA1 synapses in hippocampal slices from P7-P10 mice. Activation of BK channels is subunit specific, as paxilline but not iberiotoxin blocked mGluR-LTD.

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Article Synopsis
  • Depression is a common mental illness linked to glutamate system dysfunction, with a specific focus on the neuronal glutamate transporter EAAT3 as a potential contributor to depressive-like behaviors.
  • Research involving mice showed that those with increased EAAT3 expression in the forebrain were more resilient to developing depressive-like behaviors after undergoing chronic mild stress.
  • Results indicated that EAAT3 overexpression not only protected these mice from depressive symptoms but also preserved their memory and normal synaptic activity, suggesting EAAT3's crucial role in mitigating the effects of chronic stress on mental health.
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Purpose: In the mammalian retina, cannabinoid type 1 receptors (CB1Rs) are well-positioned to alter inhibitory synaptic function from amacrine cells and, thus, might influence visual signal processing in the inner retina. However, it is not known if CB1R modulates amacrine cells feedback inhibition at retinal bipolar cell (BC) terminals.

Methods: Using whole-cell voltage-clamp recordings, we examined the pharmacological effect of CB1R activation and inhibition on spontaneous inhibitory postsynaptic currents (sIPSCs) and glutamate-evoked IPSCs (gIPSCs) from identified OFF BCs in light-adapted rat retinal slices.

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