Threshold modulation and homeostatic control of spike timing via circuit plasticity
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1
University of Pittsburgh, Department of Mathematics, United States
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2
University of Pittsburgh, Department of Otolaryngology, United States
Activity-dependent plasticity enables neuronal circuits to encode the large dynamic range of sensory stimuli. However, the known mechanisms underlying plasticity of firing rates also affect spike timing neural codes. Therefore these rate adaptation mechanisms may not be applicable to many sensory systems encoding temporally precise inputs. The auditory system is an ideal site for studying the cellular mechanisms underlying coordinated spike rate modulation and preservation of spike timing. In auditory circuits, activity-dependent spike rate adaptation is common, yet faithful encoding of the fine temporal structure of auditory inputs via an invariant temporal code is necessary for accurate stimulus identification and discrimination. We present in vitro characterization of disynaptic parallel fiber (PF) synapses in dorsal cochlear nucleus, an auditory brainstem structure. The direct PF excitation onto principal DCN neurons has a Hebbian spike timing dependent plasticity (STDP) rule, whereas excitation onto DCN interneurons has an anti-Hebbian STDP rule [1,2]. The coordinated recruitment of long-term potentiation (LTP) and long-term depression (LTD) in the PF feedforward, inhibitory circuit increases the duration of the principal cell integration window to PF-PF and PF-auditory nerve inputs. We use a simple computational model of DCN integration and spike dynamics to show that plasticity induced increase in fusiform cell integration window modulates the spike response threshold to auditory nerve inputs, while preserving a spike latency code. This latency code invariance to threshold changes permits any latency decoder to be well tuned for a broad distribution of stimulus intensities, offering a simple solution to parcel rate and temporal decoding schemes. Previous studies have established that neural circuits use homeostatic plasticity to maintain stable firing rate [3]. Nevertheless, neurons also perform time sensitive tasks and we propose that homeostatic control of temporal coding, similar to that outlined in our study, is a general feature of neural circuit design.
References
1. Tzounopoulos, T., Kim, Y., Oertel, D., and Trussell, L.O. (2004). Cellspecific, spike timing-dependent plasticities in the dorsal cochlear nucleus. Nat. Neurosci. 7, 719-725.
2. Tzounopoulos, T., Rubio, M.E., Keen, J.E. & Trussell, L.O. Coactivation of pre- and postsynaptic signaling mechanisms determines cell-specific spiketiming- dependent plasticity. Neuron 54, 291-301 (2007).
3. Turrigiano, G.G. The self-tuning neuron: synaptic scaling of excitatory synapses. Cell 135, 422-435 (2008).
Conference:
Computational and Systems Neuroscience 2010, Salt Lake City, UT, United States, 25 Feb - 2 Mar, 2010.
Presentation Type:
Oral Presentation
Topic:
Oral presentations
Citation:
Doiron
B,
Zhao
Y and
Tzounopoulos
T
(2010). Threshold modulation and homeostatic control of spike timing via circuit plasticity.
Front. Neurosci.
Conference Abstract:
Computational and Systems Neuroscience 2010.
doi: 10.3389/conf.fnins.2010.03.00010
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Received:
17 Feb 2010;
Published Online:
17 Feb 2010.
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Correspondence:
Brent Doiron, University of Pittsburgh, Department of Mathematics, Pittsburgh, United States, bdoiron@pitt.edu