C. Fernando Valenzuela

Genetic ablation of the t-SNARE SNAP-25 distinguishes mechanisms of neuroexocytosis.

Neurosteroids enhance spontaneous glutamate release in hippocampal neurons. Possible role of metabotropic sigma1-like receptors.

Neurosteroids enhance bandpass filter characteristics of the rat Schaffer collateral-to-CA1 synapse.

Ethanol withdrawal upregulates kainate receptors in cultured rat hippocampal neurons.

Cocaine inhibits 5-HT3 receptor function in neurons from transgenic mice overexpressing the receptor.

Chronic prenatal ethanol exposure alters ionotropic glutamate receptor subunit protein levels in the adult guinea pig cerebral cortex.

Alcohol potently inhibits the kainate receptor-dependent excitatory drive of hippocampal interneurons.

Evidence that nitric oxide regulates the acute effects of ethanol on rat N-methyl-D-aspartate receptors in vitro.

Neurosteroid modulation of glutamate release in hippocampal neurons: lack of an effect of a chronic prenatal ethanol exposure paradigm.

Treatment of rats with antipsychotic drugs: lack of an effect on brain N-acetyl aspartate levels.

Alcohol enhances GABAergic transmission to cerebellar granule cells via an increase in Golgi cell excitability.

Fetal alcohol exposure alters neurosteroid levels in the developing rat brain.

Neurosteroid-induced plasticity of immature synapses via retrograde modulation of presynaptic NMDA receptors.

Neurosteroid paradoxical enhancement of paired-pulse inhibition through paired-pulse facilitation of inhibitory circuits in dentate granule cells.

Differential expression of NMDA receptor subunits and splice variants among the CA1, CA3 and dentate gyrus of the adult rat.

Alcohol is a potent stimulant of immature neuronal networks: implications for fetal alcohol spectrum disorder.

Single-amino-acid difference in the sequence of alpha6 subunit dramatically increases the ethanol sensitivity of recombinant GABAA receptors.

Neuroactive steroids and ethanol.

Developmentally regulated actions of alcohol on hippocampal glutamatergic transmission.

Synchronized network activity in developing rat hippocampus involves regional hyperpolarization-activated cyclic nucleotide-gated (HCN) channel function.

Alcohol potently modulates climbing fiber-->Purkinje neuron synapses: role of metabotropic glutamate receptors.

Alcohol increases efficacy of immature synapses in a neurosteroid-dependent manner.

Connexin-36 gap junctions mediate electrical coupling between ventral tegmental area GABA neurons.

Expression and function of SNAP-25 as a universal SNARE component in GABAergic neurons.

Immature hippocampal neuronal networks do not develop tolerance to the excitatory actions of ethanol.

Modulation of GABAA receptors in cerebellar granule neurons by ethanol: a review of genetic and electrophysiological studies.

Brain stimulation reward is integrated by a network of electrically coupled GABA neurons.

Modulation of glutamatergic transmission by sulfated steroids: role in fetal alcohol spectrum disorder.

Ethanol sensitivity of GABAergic currents in cerebellar granule neurons is not increased by a single amino acid change (R100Q) in the alpha6 GABAA receptor subunit.

Ethanol decreases Purkinje neuron excitability by increasing GABA release in rat cerebellar slices.

Alcohol impairs long-term depression at the cerebellar parallel fiber-Purkinje cell synapse.

Modulation of GABAergic and glutamatergic transmission by ethanol in the developing neocortex: an in vitro test of the excessive inhibition hypothesis of fetal alcohol spectrum disorder.

Schizophrenia-like GABAergic gene expression deficits in cerebellar Golgi cells from rats chronically exposed to low-dose phencyclidine.

Prenatal exposure to moderate levels of ethanol alters social behavior in adult rats: relationship to structural plasticity and immediate early gene expression in frontal cortex.

Ethanol acutely inhibits ionotropic glutamate receptor-mediated responses and long-term potentiation in the developing CA1 hippocampus.

Low concentrations of alcohol inhibit BDNF-dependent GABAergic plasticity via L-type Ca2+ channel inhibition in developing CA3 hippocampal pyramidal neurons.

Repeated third trimester-equivalent ethanol exposure inhibits long-term potentiation in the hippocampal CA1 region of neonatal rats.

Alcohol excites cerebellar Golgi cells by inhibiting the Na+/K+ ATPase.

Patterns of social-experience-related c-fos and Arc expression in the frontal cortices of rats exposed to saccharin or moderate levels of ethanol during prenatal brain development.

A review of synaptic plasticity at Purkinje neurons with a focus on ethanol-induced cerebellar dysfunction.

Behavioral effects of ethanol in cerebellum are age dependent: potential system and molecular mechanisms.

Alcohol exposure decreases CREB binding protein expression and histone acetylation in the developing cerebellum.

Activation of steroid-sensitive TRPM3 channels potentiates glutamatergic transmission at cerebellar Purkinje neurons from developing rats.

Excitation of rat cerebellar Golgi cells by ethanol: further characterization of the mechanism.

Ethanol increases GABAergic transmission and excitability in cerebellar molecular layer interneurons from GAD67-GFP knock-in mice.

Bestrophin1 Channels are Insensitive to Ethanol and Do not Mediate Tonic GABAergic Currents in Cerebellar Granule Cells.

Does moderate drinking harm the fetal brain? Insights from animal models.

Effects of third trimester-equivalent ethanol exposure on Cl(-) co-transporter expression, network activity, and GABAergic transmission in the CA3 hippocampal region of neonatal rats.

Moderate Prenatal Alcohol Exposure Reduces Plasticity and Alters NMDA Receptor Subunit Composition in the Dentate Gyrus.

Na+/K+-ATPase inhibition partially mimics the ethanol-induced increase of the Golgi cell-dependent component of the tonic GABAergic current in rat cerebellar granule cells.

Focus on: neurotransmitter systems.

A report on the Fetal Alcohol Spectrum Disorders Study Group meeting of 2012, theme title, "Biomarkers for FASD".

Repeated intermittent alcohol exposure during the third trimester-equivalent increases expression of the GABA(A) receptor δ subunit in cerebellar granule neurons and delays motor development in rats.

Acute ethanol exposure inhibits silencing of cerebellar Golgi cell firing induced by granule cell axon input.

Third trimester-equivalent ethanol exposure does not alter complex spikes and climbing fiber long-term depression in cerebellar Purkinje neurons from juvenile rats.