Intrinsic bulbar theta oscillations: a precise clockwork that synchronizes spontaneous mitral cell activity even in the absence of respiration.
Fri-S5-001
Presented by: Veronica Egger
Both spontaneous and odor-evoked network activity in rodent olfactory bulbs (OB) are patterned by respiration, resulting in oscillations within the θ regime. Previously, we observed θ rhythms in local field potential recordings (LFP) in semi-intact nose-brain preparations (NBP) of rats that were uncoupled from respiration (Perez et al. 2015). Thus, we hypothesized that the respiratory θ rhythm taps into an intrinsic θ resonance of the bulbar network.
Here we investigate the properties of these intrinsic θ rhythms via LFP recordings at the mitral cell layer within NBPs. Oscillations occurred within a range of 2.5 – 4 Hz and frequently displayed harmonics. All the respective spectral peaks were highly stable with regard to power and frequency and surprisingly narrow, with a bandwidth below 0.01 Hz. θ frequency and power did not change across a set of different recording locations, suggesting that the oscillation is a global feature of the OB network. θ oscillations disappeared upon degradation of the overall network activity, proving their neuronal origin.
The substantial spontaneous spiking activity recorded at the mitral cell layer was found to be correlated with the ongoing θ rhythm, replicating previous in vivo observations, also with regard to the preferred phase of spiking.
Possible mechanisms for intrinsic θ generation might involve globally synchronized bursting of external tufted cells in the glomerular layer. These bursts are known to rely on low-voltage Ca2+ channel activation. Local injections of the Na+ channel blocker lidocaine reduced mitral cell spiking and local network activity but did not interfere with θ. In contrast, global perfusion with the Ca2+ channel blocker NiCl2 resulted in decreasing θ power - but also reduced mitral cell spiking. These findings are coherent with an essential role for external tufted cells in intrinsic θ and a concomitant modulation of mitral cell activity, which itself does not contribute to intrinsic θ generation.
Here we investigate the properties of these intrinsic θ rhythms via LFP recordings at the mitral cell layer within NBPs. Oscillations occurred within a range of 2.5 – 4 Hz and frequently displayed harmonics. All the respective spectral peaks were highly stable with regard to power and frequency and surprisingly narrow, with a bandwidth below 0.01 Hz. θ frequency and power did not change across a set of different recording locations, suggesting that the oscillation is a global feature of the OB network. θ oscillations disappeared upon degradation of the overall network activity, proving their neuronal origin.
The substantial spontaneous spiking activity recorded at the mitral cell layer was found to be correlated with the ongoing θ rhythm, replicating previous in vivo observations, also with regard to the preferred phase of spiking.
Possible mechanisms for intrinsic θ generation might involve globally synchronized bursting of external tufted cells in the glomerular layer. These bursts are known to rely on low-voltage Ca2+ channel activation. Local injections of the Na+ channel blocker lidocaine reduced mitral cell spiking and local network activity but did not interfere with θ. In contrast, global perfusion with the Ca2+ channel blocker NiCl2 resulted in decreasing θ power - but also reduced mitral cell spiking. These findings are coherent with an essential role for external tufted cells in intrinsic θ and a concomitant modulation of mitral cell activity, which itself does not contribute to intrinsic θ generation.