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Anthony Ricci

Publications and source records attributed to Anthony Ricci.

5 recordsLinked to original sources
PubMed2005

Homeostatic scaling of vesicular glutamate and GABA transporter expression in rat neocortical circuits.

Homeostatic control of pyramidal neuron firing rate involves a functional balance of feedforward excitation and feedback inhibition in neocortical circuits. Here, we reveal a dynamic scaling in vesicular excitatory (vesicular glutamate transporters VGLUT1 and VGLUT2) and inhibitory (vesicular inhibitory amino acid transporter VIAAT) transporter mRNA and synaptic protein expression in rat neocortical neuronal cultures, using a well established in vitro protocol to induce homeostatic plasticity. During the second and third week of synaptic differentiation, the predominant vesicular transporters expressed in neocortical neurons, VGLUT1 and VIAAT, are both dramatically upregulated. In mature cultures, VGLUT1 and VIAAT exhibit bidirectional and opposite regulation by prolonged activity changes. Endogenous coregulation during development and homeostatic scaling of the expression of the transporters in functionally differentiated cultures may serve to control vesicular glutamate and GABA filling and adjust functional presynaptic excitatory/inhibitory balance. Unexpectedly, hyperexcitation in differentiated cultures triggers a striking increase in VGLUT2 mRNA and synaptic protein, whereas decreased excitation reduces levels. VGLUT2 mRNA and protein are expressed in subsets of VGLUT1-encoded neocortical neurons that we identify in primary cultures and in neocortex in situ and in vivo. After prolonged hyperexcitation, downregulation of VGLUT1/synaptophysin intensity ratios at most synapses is observed, whereas a subset of VGLUT1-containing boutons selectively increase the expression of VGLUT2. Bidirectional and opposite regulation of VGLUT1 and VGLUT2 by activity may serve as positive or negative feedback regulators for cortical synaptic transmission. Intracortical VGLUT1/VGLUT2 coexpressing neurons have the capacity to independently modulate the level of expression of either transporter at discrete synapses and therefore may serve as a plastic interface between subcortical thalamic input (VGLUT2) and cortical output (VGLUT1) neurons.

Aging↗
PubMed2003

Active hair bundle movements and the cochlear amplifier.

The "active process" is a term used to describe amplification and filtering processes that are essential for obtaining the exquisite sensitivity of hearing organs. Understanding the components of the active process is important both for our understanding of the normal physiology of hearing and because perturbations of the cochlear amplifier may lead to such maladies as threshold shifts (both temporary and permanent), tinnitus, sensorineural hearing loss and presbicusis. To date the cochlear amplifier has largely been attributed to outer hair cell electromotility; however, recent evidence suggests, that active properties of the hair bundle may also be important. Most likely both somatic motility and active hair bundle movements contribute to establishing the cochlear active process. This paper reviews recent evidence regarding known active processes in the hair bundle gating compliance, and fast and slow adaptation.

Acoustic Stimulation↗
PubMed2002

Differences in mechano-transducer channel kinetics underlie tonotopic distribution of fast adaptation in auditory hair cells.

The first step in audition is a deflection of the sensory hair bundle that opens mechanically gated channels, depolarizing the sensory hair cells. Two mechanism of adaptation of mechano-electric transducer (MET) channels have been identified in turtle auditory hair cells. The rate of fast adaptation varies tonotopically and is postulated to underlie a mechanical tuning mechanism in turtle auditory hair cells. Fast adaptation is driven by a calcium-dependent feedback process associated with MET channels. The purpose of this paper is to test the hypothesis that fast adaptation contributes to MET channel kinetics and that variations in channel kinetics underlie the tonotopic distribution of fast adaptation. To test for kinetic differences, the open channel blocker dihydrostreptomycin (DHS) was used. DHS blocked MET currents from low-frequency cells (IC(50) = 14 +/- 2 microM) more effectively than high-frequency cells (IC(50) = 75 +/- 5 microM), suggesting differences in MET channel properties. DHS block showed similar calcium sensitivities at both papilla locations. No difference in calcium permeation or block of the transducer channels was observed, indicating that the DHS effect was not due to differences in the channel pore. Slowing adaptation increased DHS efficacy, and speeding adaptation decreased DHS efficacy, suggesting that adaptation was influencing DHS block. DHS block of MET channels slowed adaptation, most likely by reducing the peak intraciliary calcium concentration achieved, supporting the hypothesis that the rate of adaptation varies with the calcium load per stereocilia. Another channel blocker, amiloride showed similar efficacy for high- and low-frequency cells with an IC(50) of 24.2 +/- 0.5 microM and a Hill coefficient of 2 but appeared to block high-frequency channels faster than low-frequency channels. To further explore MET channel differences between papilla locations, stationary noise analysis was performed. Spectral analysis of the noise gave half power frequencies of 1,185 +/- 148 Hz (n = 6) and 551 +/- 145 Hz (n = 5) for high- and low-frequency cells in 2.8 mM external calcium. The half power frequency showed similar calcium sensitivity to that of adaptation shifting to 768 +/- 205 Hz (n = 4) and 289 +/- 63 Hz (n = 4) for high- and low-frequency cells in 0.25 mM external calcium. Both the pharmacological data and the noise analysis data are consistent with the hypothesis that the tonotopic distribution of fast adaptation is in part due to differences in MET channel kinetics. An increase in the number of MET channels per stereocilia (termed summation) and or intrinsic differences in MET channel kinetics may be the underlying mechanism involved in establishing the gradient.

Adaptation, Physiological↗