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Raquel Riquelme

Publications and source records attributed to Raquel Riquelme.

4 recordsLinked to original sources
PubMed2006

Optimizing the stimuli to evoke the amplitude modulation following response (AMFR) in neonates.

OBJECTIVE: The goal was to identify stimulus features that enhance the detection of the amplitude modulation following response (AMFR) in neonates. The features explored were (1) envelope type, sinusoidal versus a half-wave rectified sinusoid (transposed); (2) best modulation frequency; and (3) spectral content, i.e., tone versus band-pass noise. DESIGN: Results are based on recordings from 149 babies (80 babies in the neonatal intensive care unit and 69 newborn infants). All had passed hearing screening based on the click-evoked ABR. Babies were not sedated. We used carrier frequencies of approximately 500, 1000, 2000, and 4000 Hz and modulation frequencies between approximately 25 and 98 Hz. For the noise stimuli, we used band-pass noise at center frequencies of 500, 1000, 2000, and 4000 Hz. All stimuli were presented through insert earphones delivered simultaneously to both ears, at intensities ranging from 20 to 70 dB SPL. Magnitude squared coherence, phase coherence, and spectral criteria were used to detect criterion AMFRs. We analyzed four measures: (1) percent of satisfied runs; (2) the amplitude of criterion AMFR; (3) time to detect a criterion AMFR; and (4) response strength (e.g., the value of the magnitude squared coherence when it reached criterion minus the critical value it had to exceed for that number of averages all divided by the critical value). RESULTS: (1) The AMFRs evoked by transposed tones were larger and detected faster than those to sinusoidal amplitude modulated tones. Consequently, remaining protocols all used the transposed envelopes. (2) The range of effective modulation frequencies was broad (41 to 88 Hz) across carrier frequencies. (3) The AMFRs evoked by transposed noise were faster and more efficient than those to transposed tones. CONCLUSIONS: In neonates, transposed tones are more effective than sinusoidal amplitude modulated tones in evoking the AMFR, modulation frequencies between 41 to 88 Hz are almost equally effective in evoking the AMFR, and band-pass noises are more effective in evoking the AMFR than tones. These three stimulus factors all add incrementally to the efficiency of evoking the AMFR. The short detection times indicate that the AMFR could be an effective tool for hearing screening.

Acoustic Stimulation↗
PubMed2005

GRIP1 in GABAergic synapses.

The glutamate receptor-interacting protein GRIP1 is present in glutamatergic synapses and interacts with the GluR2/3/4c subunits of the AMPA receptors. This interaction plays important roles in trafficking, synaptic targeting, and recycling of AMPA receptors as well as in the plasticity of glutamatergic synapses. Although GRIP1 has been shown to be present at GABAergic synapses in cultured neurons, the use of EM (electron microscopy) immunocytochemistry in the intact brain has failed to convincingly reveal the presence of GRIP1 in GABAergic synapses. Therefore, most studies on GRIP1 have focused on glutamatergic synapses. By using mild tissue fixation and embedding in EM, we show that in the intact brain the 7-PDZ domain GRIP1a/b is present not only in glutamatergic synapses but also in GABAergic synapses. In GABAergic synapses GRIP1a/b localizes both at the presynaptic terminals and postsynaptically, being frequently localized on the synaptic membranes or the synaptic junctional complex. Considerably higher density of GRIP1a/b is found in the presynaptic GABAergic terminals than in the glutamatergic terminals, while the density of GRIP1a/b in the postsynaptic complex is similar in both types of synapses. The results also show that the 7-PDZ and the shorter 4-PDZ domain splice forms of GRIP1 (GRIP1c 4-7) frequently colocalize with each other in individual GABAergic and glutamatergic synapses. The results suggest that GRIP1 splice forms might play important roles in brain GABAergic synapses.

Animals↗
PubMed2002

Bergmann glia GABA(A) receptors concentrate on the glial processes that wrap inhibitory synapses.

We studied the cellular and subcellular distribution of GABA(A) receptors in the Bergmann glia and Purkinje cells in the molecular layer of the cerebellum by using electron microscopy postembedding immunogold techniques. Gold particles corresponding to alpha2 and gamma1 immunoreactivity were localized in Bergmann glia processes that wrapped Purkinje cell somata, dendritic shafts, and some dendritic spines. The gold particles were mainly located on the glial plasma membrane or intracellularly but near the plasma membrane. The density of gold particles corresponding to alpha2 and gamma1 GABA(A) receptor subunits was 4.3-fold higher in the glial processes wrapping Purkinje cell somata than in the glial processes wrapping Purkinje cell dendritic spines. Moreover, the Bergmann glia GABA(A) receptors were often located in close proximity to the type II GABAergic synapses made by the basket cell axons on Purkinje cell somata. These GABAergic synapses were enriched in neuronal GABA(A) receptors containing alpha1 and beta2/3 subunits. Unexpectedly, 2.8% of the Purkinje cell dendritic spines also showed immunoreactivity for the neuronal alpha1 or beta2/3 subunits, which were located on the spine in type I synapses or extrasynaptically. Double-labeling immunogold experiments showed that approximately 50% of the dendritic spines that were immunolabeled with the neuronal GABA(A) receptors were wrapped by Bergmann glia processes containing glial GABA(A) receptors. These results are consistent with a role of the Bergmann glial GABA(A) receptors in sensing GABAergic synaptic function.

Animals↗