Parvalbumin (PV) and cholecystokinin (CCK) proteins are found in the basolateral amygdala nuclei, particularly in gamma-aminobutyric acid (GABA) interneurons. PV+ neurons were localized to the basolateral amygdala and they expressed the GABA neuron marker glutamic acid decarboxylase (GAD). Here, we used Cre recombinase mouse lines to induce expression of mutant muscarinic inhibitory (hM4D) and excitatory (hM3D) receptors on PV+ or CCK+ neurons. Activation of the mutant receptors with clozapine-n-oxide (CNO) was used to measure how amygdala neural changes affect the acoustic startle reflex (ASR). Excitation of amygdala PV+ neurons potentiated the ASR. Activation of basolateral amygdalar CCK+ neurons potentiated the ASR and caused seizures, possibly by activating glutamate CCK+ neurons. The CCK+ subset of GAD neurons were targeted with a new triple transgenic mouse line (Dlx5-flpe/CCK-Cre/FrePe) to show that most CCK+ neurons were GAD negative. These findings are compared with optogenetic approaches to target specific neuronal populations.
| Identifer | oai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/42763 |
| Date | 21 November 2013 |
| Creators | Curry, Thomas |
| Contributors | Yeomans, John S. |
| Source Sets | University of Toronto |
| Language | en_ca |
| Detected Language | English |
| Type | Thesis |
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