Gill Seminar. Michael Beierlein, University of Texas Medical School. "Cholinergic Synaptic Signaling in the Thalamus"
Abstract: Cholinergic neurons in the basal forebrain and the brain stem form extensive projections to a number of thalamic nuclei. Activation of cholinergic afferents during distinct behavioral states can regulate neuronal firing, transmitter release at glutamatergic and GABAergic synapses, and synchrony in thalamic networks, thereby controlling the flow of sensory information. These effects are thought to be mediated by slow and persistent increases in extracellular acetylcholine (ACh) levels, resulting in the modulation of populations of thalamic neurons over large temporal and spatial scales. However, the synaptic mechanisms underlying cholinergic signaling in the thalamus are not well understood. Our studies demonstrate highly reliable cholinergic transmission in the mouse thalamic reticular nucleus (TRN), a brain structure essential for sensory processing, arousal, and attention. We find that the synaptic release of ACh release leads to biphasic excitatory-inhibitory (E-I) postsynaptic responses, mediated by the activation of postsynaptic α4β2 nicotinic (nAChRs) and M2 muscarinic ACh receptors (mAChRs), respectively. ACh can also bind to mAChRs expressed near cholinergic release sites, resulting in autoinhibition of release. We show that the activation of postsynaptic nAChRs by transmitter release from only a small number of individual axons is sufficient to trigger action potentials in TRN neurons. Furthermore, brief trains of cholinergic synaptic inputs can powerfully entrain ongoing TRN neuronal activity. Our work highlights the presence of fast and precise cholinergic synaptic signaling, suggesting novel computational mechanisms for the control of neuronal activity in thalamic circuits.
- Wednesday March 06, 2013 04:00 PM
- Wednesday March 06, 2013 05:00 PM
- Multidisciplinary Science Building Phase II, Gill Conference Rm. 102
- The Linda and Jack Gill Center for Biomolecular Science
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