| Type of Document |
Dissertation |
| Author |
Davila III, Nestor Gabriel
|
| URN |
etd-11172003-231726 |
| Title |
Characterization of Dopamine and Kainate Receptors in Olfactory Bulb Neurons and Their Effects on Glutamatergic Transmission |
| Degree |
Doctor of Philosophy |
| Department |
Biological Science, Department of |
| Advisory Committee |
| Advisor Name |
Title |
| Paul Trombley |
Committee Chair |
| Betty Gaffney |
Committee Member |
| Charles Ouimet |
Committee Member |
| Marc Freeman |
Committee Member |
| Michael Meredith |
Committee Member |
|
| Keywords |
|
| Date of Defense |
2003-11-05 |
| Availability |
unrestricted |
Abstract
The main olfactory bulb (OB) receives odorant information from the nasal epithelium, interprets much of that information, and transmits the results to higher cortical regions. The predominant excitatory neurotransmitter in the OB and throughout the brain is glutamate. Modulators of glutamatergic activity influence synaptic transmission of intrabulbar circuits profoundly; therefore, the effects of neuromodulators must be thoroughly characterized in order to understand fully how OB circuits function. Investigations performed here address the capacity of dopamine receptor (DAR) and kainate receptor (KAR) activation to modulate glutamate transmission from principal cells to interneurons in OB primary cultures. Initially, I obtained immunocytochemical evidence for DARs expressed in principal cells. Subsequent electrophysiological analyses revealed that the D2-like receptor subtype (D2Rs) attenuated both spontaneous and evoked glutamatergic transmission. Information gleaned from studies of input resistances and calcium currents allowed me to determine that the site of modulation is located on the presynaptic cell. My research into KARs demonstrated the existence of functional KARs in OB neurons and began to elucidate their physiological roles in OB neurotransmission. First, I gathered immunocytochemical evidence to visualize KARs expressed both at and near synapses. In situ hybridization (ISH) was employed to map which OB neurons express mRNA for each KAR subunit. Expression levels for each subunit were quantified in parallel studies using the reverse transcriptase-polymerase chain reaction (RT-PCR). Electrophysiological approaches were used to determine whether or not KARs participate in synaptic transmission between OB neurons in primary cultures. I provide evidence for KAR-mediated modulation of both spontaneous and evoked glutamatergic transmission between OB neurons. Taken together, this work supports the notion that synaptic transmission of OB neurons can be modulated by either metabotropic or ionotropic ligand-gated ion channels. In addition, this is the first thorough characterization of KAR expression and physiology in OB neurons.
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| Files |
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56K Modem |
ISDN (64 Kb) |
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NGD-Diss+Revzns-1.pdf |
19.17 Mb |
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