Atypical longitudinal development of speech-evoked auditory brainstem response in preschool children with autism spectrum disorders.

Language impairment is common in children with autism spectrum disorders (ASDs). Previous research has shown that this disability may be, in part, due to atypical auditory processing of speech stimuli. However, how speech sounds are processed in children with ASD remains largely unknown.

Presynaptic inhibition by α2 receptor/adenylate cyclase/PDE4 complex at retinal rod bipolar synapse.

G-protein-coupled receptor (GPCR)-mediated presynaptic inhibition is a fundamental mechanism regulating synaptic transmission in the CNS. The classical GPCR-mediated presynaptic inhibition in the CNS is produced by direct interactions between the G(βγ) subunits of the G-protein and presynaptic Ca(2+) channels, K(+) channels, or synaptic proteins that affect transmitter release. This mode of action is shared by well known GPCRs such as the α2, GABA(B), and CB1 receptors.

Nimodipine enhancement of alpha2 adrenergic modulation of NMDA receptor via a mechanism independent of Ca2+ channel blocking.

Purpose: To further understand alpha2 receptor signaling in the retina and the mechanisms that mediate ocular beneficial effects of brimonidine (an alpha2 agonist) and nimodipine (an L-type Ca(2+) channel blocker).

Methods: The authors used in situ retinal ganglion cells (RGCs) in the isolated rat retina to characterize alpha2 modulation of NMDA receptor function and a rabbit retinal NMDA excitotoxicity model to verify in vitro findings under in vivo conditions. Electrophysiological (whole-cell patch clamp) recordings and Ca(2+) imaging were used to characterize NMDA receptor function and to verify the effect of various Ca(2+) channel blockers.

Alpha2 adrenergic modulation of NMDA receptor function as a major mechanism of RGC protection in experimental glaucoma and retinal excitotoxicity.

Purpose: alpha2 Agonists, such as brimonidine, have been shown to protect retinal ganglion cells (RGCs) in animal models of glaucoma and acute retinal ischemia. In this study, the authors investigated the neural mechanism that may underlie alpha2 neuroprotection of RGCs.

Methods: The authors used in situ RGCs in the isolated rat retina to investigate possible interactions between alpha2 and N-methyl-D-aspartate (NMDA) receptors and rat glaucoma or rabbit retinal NMDA excitotoxicity models to verify in vitro findings under in vivo conditions.

Alpha2 adrenergic receptor-mediated modulation of cytosolic Ca++ signals at the inner plexiform layer of the rat retina.

Purpose: Compelling evidence suggests that alpha2 agonists, such as brimonidine, protect retinal ganglion cells (RGCs) from injury in a wide range of animal models. However, the mechanism of action for this protection and the physiological role of the alpha2 adrenergic system in the retina is not well understood. A major goal of this work was to explore the role of the alpha2 adrenergic system in the modulation of cytosolic Ca(2+) signaling at retinal synaptic layers, particularly the inner plexiform layer (IPL), where communication between RGCs and their presynaptic cells takes place.

Contribution to ischemic injury of rat optic nerves by intracellular sodium overload.

Ischemic insult to axons of retinal ganglion cells (RGCs) is believed to contribute significantly to preferential loss of RGCs in glaucoma. In this study, we characterized the role of intracellular Na(+) overload in ischemic injury of acutely isolated rat optic nerves by evaluating electrically elicited compound action potentials (CAPs) from the optic nerves. Under control conditions, robust and stable CAPs can be recorded for more than 5 h.

An overview of drug development with special emphasis on the role of visual electrophysiological testing.

Visual electrophysiological techniques, such as electroretinography (ERG) and visual evoked potentials (VEP) can provide useful information on the safety, efficacy, and proper dosing of chemical entities under development as new drug therapies. During post-marketing safety surveillance, a variety of visual electrophysiological measures can be used to objectively assess and document individual patient response to ophthalmic drugs and ocular or visual system side effects of non-ophthalmic drugs. In this paper, the discovery, exploratory development, full-development and post-marketing stages of drug development are briefly outlined.

Origins of the electroretinogram oscillatory potentials in the rabbit retina.

The electroretinogram (ERG) oscillatory potential (OP) is a high-frequency, low-amplitude potential that is superimposed on the rising phase of the b-wave. It provides noninvasive evaluation of inner retina function in vivo and is a useful tool in basic research as well as in the clinic. While the OP is widely believed to be generated mainly by activity of the inner retina, the exact underlying neural mechanisms are not well understood.

Temporal modulation of scotopic visual signals by A17 amacrine cells in mammalian retina in vivo.

We examined function of the feedback pathway from A17 GABAergic amacrine cells to rod bipolar cells (A17 feedback), a critically located inhibitory circuit in the classic rod pathway of the mammalian retina whose role in processing of scotopic visual information is still poorly understood. We show evidence that this A17 feedback has a profound influence on the temporal properties of rod-driven postphotoreceptoral responses (assessed with the scotopic electroretinogram b-wave). Application of a GABA(c) antagonist prolonged preferentially the decay of the scotopic b-wave.

GABAc feedback pathway modulates the amplitude and kinetics of ERG b-wave in a mammalian retina in vivo.

The electroretinogram b-wave is generally believed to reflect mainly light-induced activity of ON-center bipolar cells and Muller cells. Recently, there is increasing evidence that third-order retinal neurons can also contribute significantly to the b-wave. In a previous study (Vis.