Detecting Activity in Olfactory Bulb Glomeruli with Astrocyte Recording

Abstract

In the olfactory bulb, axons of olfactory sensory neurons (OSNs) expressing the same olfactory receptor converge on specific glomeruli. These afferents form axodendritic synapses with mitral/tufted and periglomerular cell dendrites, whereas the dendrites of mitral/tufted cells and periglomerular interneurons form dendrodendritic synapses. The two types of intraglomerular synapses appear to be spatially isolated in subcompartments delineated by astrocyte processes. Because each astrocyte sends processes into a single glomerulus, we used astrocyte recording as an intraglomerular detector of neuronal activity. In glomerular astrocytes, a single shock in the olfactory nerve layer evoked a prolonged inward current, the major part of which was attributable to a barium-sensitive potassium current. The K

Plasticity of astroglial networks in olfactory glomeruli

“…In the GL, GJC between astrocytes is preferentially confined within OG and thus overlaps neuronal organization. This feature results from at least two astroglial properties: (i) the oriented morphology of glomerular astrocytes processes toward the OG center (7)(8)(9) where most of the GL neuronal transmission occurs, and (ii) the enriched expression of the two astroglial Cxs within functional units, as already reported in the somatosensory cortex (25). In addition, the physical barrier formed by the somata of the juxtaglomerular neurons can also contribute to the gap in Cx expression observed around glomeruli (Fig.…”

“…The goal of this study is to determine how Cx-mediated intercellular communication in astrocytes is organized and modulated in this brain structure characterized by functional units. Features of OG astrocytes studied so far include their morphology (7,8), membrane currents (9,10), and contribution to hemodynamic responses (11)(12)(13). Here, we report that in the glomerular layer (GL), astroglial morphologies and Cx expression patterns lead to a gap junctional communication (GJC) favored within individual OG.…”

Disynaptic Amplification of Metabotropic Glutamate Receptor 1 Responses in the Olfactory Bulb

“…Furthermore, as discussed above, the mitral cell response evoked by ON stimulation is usually completely blocked by NMDA and AMPA receptor antagonists (Chen and Shepherd, 1997;Carlson et al, 2000;Schoppa and Westbrook, 2001;De Saint Jan and Westbrook, 2005). However, a small mGluR1-mediated EPSP was occasionally observed in previous experiments in the presence of NBQX (20 M) and AP-5 (150 M), conditions that prevent release of glutamate from postsynaptic mitral/tufted cell dendrites (De Saint Jan and Westbrook, 2005). In our experiments, the size of this small mGluR1 response, evoked in the presence of NBQX and AP-5, increased in response to short 100 Hz stimulus trains (3-10 stimuli) (Fig.…”

“…Although the olfactory nerve (ON)-evoked mitral cell depolarization is usually abolished by AMPA and NMDA receptor antagonists (Chen and Shepherd, 1997;Carlson et al, 2000;Schoppa and Westbrook, 2001;De Saint Jan and Westbrook, 2005), the duration of the EPSP far exceeds even the slow NMDA receptor-mediated EPSP in most pathways, suggesting that another component is likely. The metabotropic glutamate receptor 1 (mGluR1) is expressed in mitral cell postsynaptic dendrites (van den Pol, 1995) and can affect mitral cell excitability (Schoppa and Westbrook, 2001;Heinbockel et al, 2004).…”

“…The metabotropic glutamate receptor 1 (mGluR1) is expressed in mitral cell postsynaptic dendrites (van den Pol, 1995) and can affect mitral cell excitability (Schoppa and Westbrook, 2001;Heinbockel et al, 2004). However, mGluR1-mediated EPSPs/EPSCs have only been reported after high-frequency stimulation of presynaptic neurons or when glutamate transporters are blocked (Batchelor and Garthwaite, 1997;Brasnjo and Otis, 2001;Dzubay and Otis, 2002;Huang et al, 2004;De Saint Jan and Westbrook, 2005;Ennis et al, 2006;Yuan and Knopfel, 2006). Such protocols presumably are required because they facilitate glutamate spillover onto perisynaptic loci where mGluRs are generally expressed (Baude et al, 1993).…”