1995 — 2006 |
Metzner, Walter |
R01Activity Code Description: To support a discrete, specified, circumscribed project to be performed by the named investigator(s) in an area representing his or her specific interest and competencies. R29Activity Code Description: Undocumented code - click on the grant title for more information. |
Neural Basis of Audio-Vocal Integration @ University of California Riverside
The long-term goal of these studies is to understand how sensory information about the environment is transformed into motor commands that guide adaptive behavior. In this context, the neural mechanisms underlying the control of vocalization in response to auditory feedback in the mammalian central nervous system will be investigated. Focus is on the significance of certain neurons (VOC-inhibition neurons) situated in the midbrain paralemniscal tegmentum for auditory feedback control of vocalizations in awake, behaving horseshoe bats. These bats accurately control the frequency of their echolocation calls through auditory feedback both when the bat is at rest (resting frequency) and when it is flying and compensating for frequency-shifted echo signals (Doppler-shift compensation behavior). Previous studies suggest that VOC-inhibition neurons in the paralemniscal tegmentum play an important role in the control of vocalization frequencies through an inhibitory auditory feedback mechanism. This hypothesis will be verified by employing an experimental approach that proved to be successful in previous studies on the sensory-motor control of another vertebrate behavior, the "Jamming Avoidance Response" in electric fish. Specifically: (1) It will be tested whether paralemniscal VOC-inhibition neurons are actively involved in the control of the resting frequency and of Doppler-shift compensation behavior. For that purpose, the region containing these neurons will be identified stereotaxically and electrophysiologically and then VOC- inhibition neurons will be reversibly inactivated with the GABA agonists Muscimol (GABA-A, R(+)Baclofen (GABA-B), and trans-4-aminocrotonic acid (GABAC), respectively, while the resting frequency and the Doppler-shift compensation behavior are monitored. (2) It will be determined whether VOC-inhibition neurons provide auditory feedback by means of an inhibitory or excitatory mechanism. This will be achieved by stimulating VOC- inhibition neurons with the Glutamate agonists NMDA, AMPA, and Kainic acid, respectively, while monitoring the effects of glutamate agonist injections on the vocalization frequency. If audio-vocal feedback is inhibitory, stimulation and thus increasing neuronal activity should decrease vocalization frequencies emitted at rest and during Doppler-shift compensation while they should increase if the feedback is excitatory. The results of these studies will provide new insights into the neural implementation of audio-vocal control mechanisms in awake, behaving animals and could also provide an approach to better understand various malfunctions of basic parameters of human voice, such as changes in the fundamental frequency that occur in speaking deaf humans.
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1 |
1998 — 2001 |
Metzner, Walter |
N/AActivity Code Description: No activity code was retrieved: click on the grant title for more information |
Stimulus Encoding and Feature Extraction in Neuronal Spike Trains @ University of California-Riverside
IBN 97-28731 METZNER and KOCH The long term goal of this project is to determine how higher order nerve cells ("neurons") within the central nervous system extract behaviorally relevant features from their sensory input, a task common to all sensory systems. To address this question, we will focus on the question of how information is encoded at the primary sensory neuron level and subsequently processed by higher order neurons in the electrosensory system of weakly electric fish. These weakly electric fish produce a sinusoidally varying weak electric field in their environments using a specialized "electric organ." Electrosensory receptor cells located along the body of the fish detect modulations in the amplitude of the electrical field produced by the presence of nearby objects. Primary sensory neurons ("P-receptor afferents") transmit this information to the next level of the sensory pathway, the electrosensory lateral line lobe (ELL). There, behaviorally relevant features are extracted and encoded in the spike trains of pyramidal cells, the output neurons of the ELL. The mechanisms underlying this feature extraction will be investigated by combining neurophysiological, neuroanatomical and computational data analysis techniques. Major aims are: First, to characterize the accuracy and robustness of P-receptor afferent responses (the "nerve impulses" or "spikes" electrical fields cause) to time- varying modulations of electric field amplitude and second to perform simultaneous recordings from several pyramidal cells during presentation of the same stimuli. Accuracy and robustness of the impulse firing of primary sensory neurons will be studied using recently developed measures of "distance" between spike trains and standard signal processing techniques. The responses of pyramidal cells will be analyzed using signal detection techniques adapted to multiple spike train data. The proposed project is designed as a group proposal: experiments will be conducted in the laboratory of Dr. Metzner (UCR) and the computational analysis in the laboratory of Dr. Koch with participation of Dr. Gabbiani (both Caltech). This combination of neuroethological and computational/information theoretical approaches will clarify the nature of early sensory processing in a model sensory system ideally suited for this kind of analysis. In particular, this work is expected to lead to a quantitative understanding of the code used to represent and transmit sensory information across multiple neurons.
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0.975 |