Date on Master's Thesis/Doctoral Dissertation

8-2010

Document Type

Doctoral Dissertation

Degree Name

Ph. D.

Department

Anatomical Sciences and Neurobiology

Committee Chair

Bickford, Martha E.

Author's Keywords

Substance P; Superior colliculus; Thalamus; Lateral posterior nucleus

Subject

Substance P; Thalamus

Abstract

Cortical and tectal inputs to the caudal LPN in the rat were examined using anatomical and physiological techniques. Pyramidal cells in layer 6 of the visual cortex and wide-field vertical cells in the stratum opticum of the superior colliculus (SC) project to the caudal LPN. Ultrastructural examination revealed that cortical terminals within the caudal LPN were small, contacted small dendrites, and could be identified through vGLUT1 immunohistochemistry. In contrast, tectal terminals were much larger, contacted large dendrites, and could be identified through vGLUT2 immunohistochemistry. In whole cell current clamp recording, stimulation of corticothalmic fibers elicited EPSPs that showed a frequency dependent facilitation and stimulation of the tectothalmic fibers elicited stable EPSPs. The neuropeptide Substance P (SP) and the receptor to which it binds, neurokinin-1 (NK-1), can both be found within the LPN of the rat. We examined the origin of the SP-positive terminals, their anatomical relationship to the NK-1 receptor, and the physiological effects of SP within the LPN. Light and confocal microscopy revealed that NK-1 positive cells were localized in the caudal LPN and were embedded within aSP positive terminal field. At the ultrastructural level, SP terminals were the same size as tecto-LPN terminals and terminals that contain vGLUT2 and they synapsed with large NK-1 positive dendrites. Lesions of the superior colliculus (SC) with ibotenic acid reduced the level of SP and vGLUT2 immunoreactivity in the caudal LPN. Bath application of SP depolarized the neurons, increased their membrane resistance, and produced long-term potentiation (LTP) of the EPSPs. These effects were blocked by simultaneous application of the NK-1 antagonist L-703,606. Considering that high frequency firing is often necessary for the release of neuropeptides, both the corticothalamic and tectothalamic fibers were stimulated at 100Hz. Stimulation of the corticothalmic fibers had no effect on the membrane resistance or on EPSP amplitudes. In contrast, stimulation of the tectothalmic fibers depolarized the neurons, increased their membrane resistance, and produced LTP. These results suggest that wide-field vertical cells in the stratum opticum of the SC project to the caudal LPN and when activated at high frequency produce LTP through the activation of NK-1 receptors.

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