It is important to understand the neurochemical aspects of sensory processing since it is conceivable that a number of neurologic abnormalities such as receptive aphasia, neural prebycusis, auditory perceptual dysfunction and sensory-induced seizures involve neurochemical fault(s). This study will continue the attempt to identify and characterize the neurotransmitters which mediate synaptic transmission at specific sites in the central auditory pathway. Microiontophoresis will be used to apply putative neurotransmitters and their respective antagonists in tests of mimicry (identity of action) and antagonism (pharmacologic identity) of the synaptically released compound. Alterations of threshold, spontaneous activity, response patterns, and rate-intensity functions will be examined for neurons in brainstem auditory structures. Putative neurotransmitters to be tested are selected based on morphologic, physiologic, neurochemical, and histochemical information. Binaural neurons in the superior olivary complex (SOC) provide an opportunity to selectively control synaptic excitation and inhibition to a given neuron by manipulation of the acoustic input to each ear. Our recent findings suggest that glycine may mediate binaural inhibition in certain SOC neurons. The action of a second inhibitory neurotransmitter, GABA, and the role of excitant amino aicds at SOC synapses will be examined using selected amino acid receptor antagonists. Baclofen, a proposed inhibitor of excitant amino aicd release, reduces the response of neurons in the cochlear nucleus (CN). The effect of this drug and recently available specific antagonists of excitant amino acids will be examined in the SOC and will be used to further test the hypothesis that an excitant amino acid is the transmitter at acoustic nerve synapses. Intracellular recordings will be used as a more rigorous test of identity of action in the CN. The combination of neurophysiologic and neuropharmacologic techniques proposed should aid in the identification of auditory neurotransmitters and an elucidation of their role in the coding process.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Research Project (R01)
Project #
5R01NS015640-06
Application #
3396382
Study Section
Hearing Research Study Section (HAR)
Project Start
1979-08-01
Project End
1986-06-30
Budget Start
1985-07-01
Budget End
1986-06-30
Support Year
6
Fiscal Year
1985
Total Cost
Indirect Cost
Name
Southern Illinois University School of Medicine
Department
Type
Schools of Medicine
DUNS #
City
Springfield
State
IL
Country
United States
Zip Code
62794
Caspary, D M; Faingold, C L (1989) Non-N-methyl-D-aspartate receptors may mediate ipsilateral excitation at lateral superior olivary synapses. Brain Res 503:83-90
Faingold, C L; Gehlbach, G; Caspary, D M (1989) On the role of GABA as an inhibitory neurotransmitter in inferior colliculus neurons: iontophoretic studies. Brain Res 500:302-12
Finlayson, P G; Caspary, D M (1989) Synaptic potentials of chinchilla lateral superior olivary neurons. Hear Res 38:221-8
Caspary, D M; Pazara, K E; Kossl, M et al. (1987) Strychnine alters the fusiform cell output from the dorsal cochlear nucleus. Brain Res 417:273-82
Faingold, C L; Gehlbach, G; Caspary, D M (1986) Decreased effectiveness of GABA-mediated inhibition in the inferior colliculus of the genetically epilepsy-prone rat. Exp Neurol 93:145-59