Abstract
Sensory information is transferred to the cerebellar cortex via the mossy fiber–granule cell (MF–GC) pathway, which participates in motor coordination and motor learning. We previously reported that chronic ethanol exposure from adolescence facilitated the sensory-evoked molecular layer interneuron–Purkinje cell synaptic transmission in adult mice in vivo. Herein, we investigated the effect of chronic ethanol exposure from adolescence on facial stimulation-evoked MF–GC synaptic transmission in the adult mouse cerebellar cortex using electrophysiological recording techniques and pharmacological methods. Chronic ethanol exposure from adolescence induced an enhancement of facial stimulation-evoked MF–GC synaptic transmission in the cerebellar cortex of adult mice. The application of an N-methyl-D-aspartate receptor (NMDAR) antagonist, D-APV (250 μM), induced stronger depression of facial stimulation-evoked MF–GC synaptic transmission in chronic ethanol-exposed mice compared with that in control mice. Chronic ethanol exposure-induced facilitation of facial stimulation evoked by MF–GC synaptic transmission was abolished by a selective GluN2A antagonist, PEAQX (10 μM), but was unaffected by the application of a selective GluN2B antagonist, TCN-237 (10 μM), or a type 1 metabotropic glutamate receptor blocker, JNJ16259685 (10 μM). These results indicate that chronic ethanol exposure from adolescence enhances facial stimulation-evoked MF–GC synaptic transmission via GluN2A, which suggests that chronic ethanol exposure from adolescence impairs the high-fidelity transmission capability of sensory information in the cerebellar cortex by enhancing the NMDAR-mediated components of MF–GC synaptic transmission in adult mice in vivo.
Highlights
Ethanol is the most widely used and abused psychoactive substance and can cause damage to the central nervous system that leads to impairment of its function
The area under the curve (AUC) of the N2 in the ethanol-exposed group was 6.85 ± 0.52 mV/ms (n = 10 mice), which was significantly larger than that in the control group (4.56 ± 0.49 mV/ms; n = 10 mice; F = 4.41, P = 0.002; Figure 1E). These results indicate that the chronic ethanol exposure from adolescence induces a significant enhancement in the later components of facial stimulation-evoked mossy fiber– granule cell (MF–granule cells (GCs)) synaptic transmission in mice in vivo
We found that the chronic ethanol exposure from adolescence led to an enhancement in the facial stimulationevoked mossy fibers (MFs)–GC synaptic transmission, which was blocked by a selective N-methyl-D-aspartate receptor (NMDAR) antagonist
Summary
Ethanol is the most widely used and abused psychoactive substance and can cause damage to the central nervous system that leads to impairment of its function. Acute overdose ethanol exposure inhibited the facial stimulation-evoked outward current by activating cannabinoid receptor 1 via the protein kinase A signaling pathway in the mouse cerebellar cortex (Wu et al, 2016). Chronic ethanol exposure impairs neuronal function, reduces the number of neurons via activation of N-methyl-D-aspartate receptors (NMDARs) (Nagy, 2004), and significantly inhibits the simple spike and complex spike activities of PCs (Servais et al, 2005). Chronic ethanol exposure impairs sensory stimulation-induced molecular layer interneuron–PC long-term depression via the activation of the nitric oxide signaling pathway (Li et al, 2019) and significantly facilitates sensory stimulation-evoked molecular layer interneuron–PC synaptic transmission via the nitric oxide signaling pathway in the mouse cerebellar cortex (Sun et al, 2020)
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