Comment in Sensory systems: the hungry sense. [Nat Rev Neurosci. 2014] Inhaling: endocannabinoids and food intake. [Nat Neurosci. 2014]International audienceHunger arouses sensory perception, eventually leading to an increase in food intake, but the underlying mechanisms remain poorly understood. We found that cannabinoid type-1 (CB1) receptors promote food intake in fasted mice by increasing odor detection. CB1 receptors were abundantly expressed on axon terminals of centrifugal cortical glutamatergic neurons that project to inhibitory granule cells of the main olfactory bulb (MOB). Local pharmacological and genetic manipulations revealed that endocannabinoids and exogenous cannabinoids increased odor detection and food intake in fasted mice by decreasing excitatory drive from olfactory cortex areas to the MOB. Consistently, cannabinoid agonists dampened in vivo optogenetically stimulated excitatory transmission in the same circuit. Our data indicate that cortical feedback projections to the MOB crucially regulate food intake via CB1 receptor signaling, linking the feeling of hunger to stronger odor processing. Thus, CB1 receptor-dependent control of cortical feedback projections in olfactory circuits couples internal states to perception and behavior

To explore the functional consequences of adult neurogenesis in the mouse olfactory bulb, we investigated plasticity at glutamatergic synapses onto GABAergic interneurons. We found that one subset of excitatory synapses onto adult-born granule cells showed long-term potentiation shortly after their arrival in the bulb. This property faded as the newborn neurons matured. These results indicate that recently generated adult-born olfactory interneurons undergo different experience-dependent synaptic modifications compared with their pre-existing mature neighbors and provide a possible substrate for adult neurogenesis-dependent olfactory learning.

In the olfactory bulb (OB), odorants induce oscillations in the ␥ range (20 -80 Hz) that play an important role in the processing of sensory information. Synaptic transmission between dendrites is a major contributor to this processing. Glutamate released from mitral cell dendrites excites the dendrites of granule cells, which in turn mediate GABAergic inhibition back onto mitral cells. Although this reciprocal synapse is thought to be a key element supporting oscillatory activity, the mechanisms by which dendrodendritic inhibition induces and maintains ␥ oscillations remain unknown. Here, we assessed the role of the dendrodendritic inhibition, using mice lacking the GABA A receptor ␣1-subunit, which is specifically expressed in mitral cells but not in granule cells. The spontaneous inhibitory postsynaptic current frequency in these mutants was low and was consistent with the reduction of GABA A receptor clusters detected by immunohistochemistry. The remaining GABA A receptors in mitral cells contained the ␣3-subunit and supported slower decaying currents of unchanged amplitude. Overall, inhibitory-mediated interactions between mitral cells were smaller and slower in mutant than in WT mice, although the strength of sensory afferent inputs remained unchanged. Consequently, both experimental and theoretical approaches revealed slower ␥ oscillations in the OB network of mutant mice. We conclude, therefore, that fast oscillations in the OB circuit are strongly constrained by the precise location, subunit composition and kinetics of GABA A receptors expressed in mitral cells.␣1 knockout ͉ GABAA receptor ͉ olfaction ͉ reciprocal synapses I n the olfactory bulb (OB), ␥ frequency (20-80 Hz) oscillations of local field potentials (LFP) reflect synchronized spike discharges of principal neurons (i.e., mitral/tufted cells), and may be part of the encoding of sensory information (reviewed in refs. 1 and 2). In line with this assumption, the strength of ␥ oscillations correlates with both discrimination abilities (3) and learning capacities (4, 5) in rodents.In vivo experimental approaches revealed that ␥ oscillations are intrinsic to the OB circuitry (5-7) and are even preserved in slice preparations (8, 9), which suggests that intrinsic properties of the OB connectivity are sufficient to give rise to large-scale synchronization. Analysis of the mechanisms involved has focused almost exclusively on the excitatory principal neurons (i.e., mitral cells) and included intrinsic subthreshold oscillations (10, 11) or mutual excitation through electrical coupling and glutamate spillover between mitral cells sharing the same glomerulus (12-14). As a result, relatively little is known about the role of local inhibitory interneurons in generating and maintaining network oscillations, although pioneering studies proposed dendrodendritic inhibition as a key element for inducing fast rhythms (15)(16)(17). This assumption is also supported by the fact that interneurons constitute the main target of excitatory centrifugal fibers (18,19) k...