Mouse olfactory receptor proteins have relatively broad odorant tuning profiles, so single odorants typically activate a substantial subset of glomeruli in the main olfactory bulb, resulting in stereotyped odorant- and concentration-dependent glomerular input maps. One of the functions of the olfactory bulb may be to reduce the extent of this rather widespread activation before transmitting the information to higher olfactory centers. Two circuits have been studied in vitro that could perform center-surround inhibition in the olfactory bulb, one circuit acting between glomeruli, the other through the classical reciprocal synapses between the lateral dendrites of mitral cells and the dendrites of granule cells. One unanswered question from these in vitro measurements was how these circuits would affect the response to odorants in vivo. We made measurements of the odorant-evoked increase in calcium concentration in the olfactory receptor neuron terminals in the anesthetized mouse to evaluate the role of presynaptic inhibition in reshaping the input to the olfactory bulb. We compared the glomerular responses in 2- to 4-wk-old mice before and after suppressing presynaptic inhibition onto the receptor neuron terminals with the GABAB antagonist, CGP46381. We find that the input maps are modified by an apparent center-surround inhibition: strongly activated glomeruli appear to suppress the release from receptor neurons terminating in surrounding glomeruli. This form of lateral inhibition has the effect of increasing the contrast of the sensory input map.
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http://dx.doi.org/10.1152/jn.00918.2005 | DOI Listing |
Sci Rep
January 2025
The Department of Cellular and Integrative Physiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX, USA.
Fragile X syndrome (FXS) is a neurodevelopmental disorder oftentimes associated with abnormal social behaviors and altered sensory responsiveness. It is hypothesized that the inappropriate filtering of sensory stimuli, including olfaction, can lead to aberrant social behavior in FXS. However, previous studies investigating olfaction in animal models of FXS have shown inconsistent results.
View Article and Find Full Text PDFZool Res
January 2025
School of Basic Medicine, Institute of Brain Science and Disease, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Brain Diseases, Qingdao University, Qingdao, Shandong, 266071, China. E-mail:
Iron is the most abundant transition metal in the brain and is essential for brain development and neuronal function; however, its abnormal accumulation is also implicated in various neurological disorders. The olfactory bulb (OB), an early target in neurodegenerative diseases, acts as a gateway for environmental toxins and contains diverse neuronal populations with distinct roles. This study explored the cell-specific vulnerability to iron in the OB using a mouse model of intranasal administration of ferric ammonium citrate (FAC).
View Article and Find Full Text PDFNat Commun
January 2025
Cold Spring Harbor Laboratory, Cold Spring Harbor, NY, USA.
While animals readily adjust their behavior to adapt to relevant changes in the environment, the neural pathways enabling these changes remain largely unknown. Here, using multiphoton imaging, we investigate whether feedback from the piriform cortex to the olfactory bulb supports such behavioral flexibility. To this end, we engage head-fixed male mice in a multimodal rule-reversal task guided by olfactory and auditory cues.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Autonomic Neuroscience, Tokyo Metropolitan Institute for Geriatrics and Gerontology, 35-2 Sakaecho, Itabashi-ku, 173-0015, Tokyo, Japan.
The olfactory bulb receives cholinergic basal forebrain inputs as does the neocortex. With a focus on nicotinic acetylcholine receptors (nAChRs), this review article provides an overview and discussion of the following findings: (1) the nAChRs-mediated regulation of regional blood flow in the neocortex and olfactory bulb, (2) the nAChR subtypes that mediate their responses, and (3) their activity in old rats. The activation of the α4β2-like subtype of nAChRs produces vasodilation in the neocortex, and potentiates olfactory bulb vasodilation induced by olfactory stimulation.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Developmental and Regenerative Neurobiology, Institute of Brain Science, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan.
In the ventricular-subventricular-zone (V-SVZ) of the postnatal mammalian brain, immature neurons (neuroblasts) are generated from neural stem cells throughout their lifetime. These V-SVZ-derived neuroblasts normally migrate to the olfactory bulb through the rostral migratory stream, differentiate into interneurons, and are integrated into the preexisting olfactory circuit. When the brain is injured, some neuroblasts initiate migration toward the lesion and attempt to repair the damaged neuronal circuitry, but their low regeneration efficiency prevents functional recovery.
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