scholarly journals Neurobiology of mammalian olfactory learning that occurs during sensitive periods

2010 ◽  
Vol 56 (6) ◽  
pp. 819-833 ◽  
Author(s):  
Hideto Kaba
Keyword(s):  
Olfactory Bulb ◽  
Neural Plasticity ◽  
Critical Role ◽  
Olfactory Learning ◽  
Mitral Cells ◽  
Somatosensory Stimulation ◽  
Release Of Noradrenaline ◽  
Functional Changes ◽  
Sensitive Periods ◽  
Circuit Function

Abstract This review examines the organizational principles underlying olfactory learning in three specialized contexts that occur during sensitive periods of enhanced neural plasticity and emphasizes some of their common features. All three forms of olfactory learning are associated with neural changes in the olfactory bulb (OB) at the first stage of sensory processing. These changes require the association of the olfactory and somatosensory signals in the OB. They all depend on somatosensory stimulation- induced release of noradrenaline that induces structural and functional changes at mitral-granule cell reciprocal synapses in the OB, resulting in increases in inhibitory transmission. In the accessory olfactory bulb, this represents the enhanced self-inhibition of mitral cells, which selectively disrupts the transmission of the mating male's pregnancy-blocking signal at this level. In contrast, an extensive network of secondary dendrites of mitral cells in the main olfactory bulb probably results in a sharpening of the odor-induced pattern of activity, due to increases in lateral inhibition, leading to offspring recognition in sheep and neonatal learning in rats and rabbits. These findings show that inhibitory interneurons play a critical role in olfactory learning. Further work on how these neurons shape olfactory circuit function could provide important clues to understand memory functions of interneurons in other systems. Moreover, recent research has suggested that three forms of olfactory learning are controlled by synergistic, redundant, and distributed neural mechanisms. This has general implications regarding the mechanisms that may contribute to the robustness of memories.

scholarly journals The role of astrocyte‐mediated plasticity in neural circuit development and function

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Nelson A. Perez-Catalan ◽  
Chris Q. Doe ◽  
Sarah D. Ackerman
Keyword(s):  
Nervous System ◽  
Neural Plasticity ◽  
Neural Circuit ◽  
System Development ◽  
Critical Role ◽  
Nervous System Development ◽  
Functional Changes ◽  
Sensory Evoked ◽  
And Function

AbstractNeuronal networks are capable of undergoing rapid structural and functional changes called plasticity, which are essential for shaping circuit function during nervous system development. These changes range from short-term modifications on the order of milliseconds, to long-term rearrangement of neural architecture that could last for the lifetime of the organism. Neural plasticity is most prominent during development, yet also plays a critical role during memory formation, behavior, and disease. Therefore, it is essential to define and characterize the mechanisms underlying the onset, duration, and form of plasticity. Astrocytes, the most numerous glial cell type in the human nervous system, are integral elements of synapses and are components of a glial network that can coordinate neural activity at a circuit-wide level. Moreover, their arrival to the CNS during late embryogenesis correlates to the onset of sensory-evoked activity, making them an interesting target for circuit plasticity studies. Technological advancements in the last decade have uncovered astrocytes as prominent regulators of circuit assembly and function. Here, we provide a brief historical perspective on our understanding of astrocytes in the nervous system, and review the latest advances on the role of astroglia in regulating circuit plasticity and function during nervous system development and homeostasis.

scholarly journals Adrenergic Receptor-Mediated Disinhibition of Mitral Cells Triggers Long-Term Enhancement of Synchronized Oscillations in the Olfactory Bulb

2010 ◽  
Vol 104 (2) ◽  
pp. 665-674 ◽  
Author(s):  
Sruthi Pandipati ◽  
David H. Gire ◽  
Nathan E. Schoppa
Keyword(s):  
Olfactory Bulb ◽  
Granule Cells ◽  
Gamma Oscillations ◽  
Olfactory Learning ◽  
Inhibitory Synapses ◽  
Mitral Cells ◽  
Acute Effects ◽  
Long Term Effects ◽  
Gamma Frequency

Norepinephrine (NE) is widely implicated in various forms of associative olfactory learning in rodents, including early learning preference in neonates. Here we used patch-clamp recordings in rat olfactory bulb slices to assess cellular actions of NE, examining both acute, short-term effects of NE as well as the relationship between these acute effects and long-term cellular changes that could underlie learning. Our focus for long-term effects was on synchronized gamma frequency (30–70 Hz) oscillations, shown in prior studies to be enhanced for up to an hour after brief exposure of a bulb slice to NE and neuronal stimulation. In terms of acute effects, we found that a dominant action of NE was to reduce inhibitory GABAergic transmission from granule cells (GCs) to output mitral cells (MCs). This disinhibition was also induced by clonidine, an agonist specific for α2 adrenergic receptors (ARs). Acute NE-induced disinhibition of MCs appeared to be linked to long-term enhancement of gamma oscillations, based, first, on the fact that clonidine, but not agonists specific for other AR subtypes, mimicked NE's long-term actions. In addition, the α2 AR-specific antagonist yohimbine blocked the long-term enhancement of the oscillations due to NE. Last, brief exposure of the slice to the GABAA receptor antagonist gabazine, to block inhibitory synapses directly, also induced the long-term changes. Acute disinhibition is a plausible permissive effect of NE leading to olfactory learning, because, when combined with exposure to a specific odor, it should lead to neuron-specific increases in intracellular calcium of the type generally associated with long-term synaptic modifications.

γ-Frequency Excitatory Input to Granule Cells Facilitates Dendrodendritic Inhibition in the Rat Olfactory Bulb

2003 ◽  
Vol 90 (2) ◽  
pp. 644-654 ◽  
Author(s):  
Brian Halabisky ◽  
Ben W. Strowbridge
Keyword(s):  
Olfactory Bulb ◽  
Nmda Receptors ◽  
Lateral Inhibition ◽  
Granule Cells ◽  
Critical Role ◽  
Recurrent Inhibition ◽  
Granule Cell Layer ◽  
Gabaergic Interneurons ◽  
Mitral Cells ◽  
Dendrodendritic Synapses

Recurrent and lateral inhibition play a prominent role in patterning the odor-evoked discharges in mitral cells, the output neurons of the olfactory bulb. Inhibitory responses in this brain region are mediated through reciprocal synaptic connections made between the dendrites of mitral cells and GABAergic interneurons. Previous studies have demonstrated that N-methyl-d-aspartate (NMDA) receptors on interneurons play a critical role in eliciting GABA release at reciprocal dendrodendritic synapses. In acute olfactory bulb slices, these receptors are tonically blocked by extracellular Mg2+, and recurrent inhibition is disabled. In the present study, we examined the mechanisms by which this tonic blockade could be reversed. We demonstrate that near-coincident activation of an excitatory pathway to the proximal dendrites of GABAergic interneurons relieves the Mg2+ blockade of NMDA receptors at reciprocal dendrodendritic synapses and greatly facilitates recurrent inhibition onto mitral cells. Gating of recurrent and lateral inhibition in the presence of extracellular Mg2+ requires γ-frequency stimulation of glutamatergic axons in the granule cell layer. Long-range excitatory axon connections from mitral cells innervated by different subpopulations of olfactory receptor neurons may provide a gating input to granule cells, thereby facilitating the mitral cell lateral inhibition that contributes to odorant encoding.

Mitral Cells of Olfactory Bulb Are Capable of Encoding Odor Location*

2011 ◽  
Vol 38 (11) ◽  
pp. 1020-1026 ◽  
Author(s):  
Xiang LI ◽  
An-An LI ◽  
Ling GONG ◽  
Qing LIU ◽  
Fu-Qiang XU
Keyword(s):  
Olfactory Bulb ◽  
Mitral Cells

Group I Metabotropic Glutamate Receptors Are Differentially Expressed by Two Populations of Olfactory Bulb Granule Cells

2007 ◽  
Vol 97 (4) ◽  
pp. 3136-3141 ◽  
Author(s):  
Thomas Heinbockel ◽  
Kathryn A. Hamilton ◽  
Matthew Ennis
Keyword(s):  
Olfactory Bulb ◽  
Glutamate Receptors ◽  
Metabotropic Glutamate Receptors ◽  
Granule Cells ◽  
Mitral Cell ◽  
Mitral Cells ◽  
Patch Clamp Recording ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Bath Application

In the main olfactory bulb, several populations of granule cells (GCs) can be distinguished based on the soma location either superficially, interspersed with mitral cells within the mitral cell layer (MCL), or deeper, within the GC layer (GCL). Little is known about the physiological properties of superficial GCs (sGCs) versus deep GCs (dGCs). Here, we used patch-clamp recording methods to explore the role of Group I metabotropic glutamate receptors (mGluRs) in regulating the activity of GCs in slices from wildtype and mGluR−/− mutant mice. In wildtype mice, bath application of the selective Group I mGluR agonist DHPG depolarized and increased the firing rate of both GC subtypes. In the presence of blockers of fast synaptic transmission (APV, CNQX, gabazine), DHPG directly depolarized both GC subtypes, although the two GC subtypes responded differentially to DHPG in mGluR1−/− and mGluR5−/− mice. DHPG depolarized sGCs in slices from mGluR5−/− mice, although it had no effect on sGCs in slices from mGluR1−/− mice. By contrast, DHPG depolarized dGCs in slices from mGluR1−/− mice but had no effect on dGCs in slices from mGluR5−/− mice. Previous studies showed that mitral cells express mGluR1 but not mGluR5. The present results therefore suggest that sGCs are more similar to mitral cells than dGCs in terms of mGluR expression.

Mitral and Tufted Cells Differ in the Decoding Manner of Odor Maps in the Rat Olfactory Bulb

2004 ◽  
Vol 91 (6) ◽  
pp. 2532-2540 ◽  
Author(s):  
Shin Nagayama ◽  
Yuji K. Takahashi ◽  
Yoshihiro Yoshihara ◽  
Kensaku Mori
Keyword(s):  
Olfactory Bulb ◽  
Spike Activity ◽  
Homologous Series ◽  
Morphological Difference ◽  
Aliphatic Acid ◽  
Mitral Cells ◽  
Firing Rates ◽  
Aliphatic Acids ◽  
Projection Pattern ◽  
Tufted Cells

Mitral and tufted cells in the mammalian olfactory bulb are principal neurons, each type having distinct projection pattern of their dendrites and axons. The morphological difference suggests that mitral and tufted cells are functionally distinct and may process different aspects of olfactory information. To examine this possibility, we recorded odorant-evoked spike responses from mitral and middle tufted cells in the aliphatic acid- and aldehyde-responsive cluster at the dorsomedial part of the rat olfactory bulb. Homologous series of aliphatic acids and aldehydes were used for odorant stimulation. In response to adequate odorants, mitral cells showed spike responses with relatively low firing rates, whereas middle tufted cells responded with higher firing rates. Examination of the molecular receptive range (MRR) indicated that most mitral cells exhibited a robust inhibitory MRR, whereas a majority of middle tufted cells showed no or only a weak inhibitory MRR. In addition, structurally different odorants that activated neighboring clusters inhibited the spike activity of mitral cells, whereas they caused no or only a weak inhibition in the middle tufted cells. Furthermore, responses of mitral cells to an adequate excitatory odorant were greatly inhibited by mixing the odorant with other odorants that activated neighboring glomeruli. In contrast, odorants that activated neighboring glomeruli did not significantly inhibit the responses of middle tufted cells to the adequate excitatory odorant. These results indicate a clear difference between mitral and middle tufted cells in the manner of decoding the glomerular odor maps.

scholarly journals Odor enrichment sculpts the abundance of olfactory bulb mitral cells

2013 ◽  
Vol 541 ◽  
pp. 173-178 ◽  
Author(s):  
Melissa Cavallin Johnson ◽  
K.C. Biju ◽  
Joshua Hoffman ◽  
Debra Ann Fadool
Keyword(s):  
Olfactory Bulb ◽  
Mitral Cells

Role of olfactory bulb serotonin in olfactory learning in the greater short-nosed fruit bat, Cynopterus sphinx (Chiroptera: Pteropodidae)

2010 ◽  
Vol 1352 ◽  
pp. 108-117 ◽  
Author(s):  
Ambigapathy Ganesh ◽  
Wieslaw Bogdanowicz ◽  
Moritz Haupt ◽  
Ganapathy Marimuthu ◽  
Koilmani Emmanuvel Rajan
Keyword(s):  
Olfactory Bulb ◽  
Olfactory Learning ◽  
Fruit Bat ◽  
Cynopterus Sphinx

scholarly journals Acute small intestinal inflammation results in persistent lymphatic alterations

2018 ◽  
Vol 314 (3) ◽  
pp. G408-G417 ◽  
Author(s):  
Sonia Rehal ◽  
Matthew Stephens ◽  
Simon Roizes ◽  
Shan Liao ◽  
Pierre-Yves von der Weid
Keyword(s):  
Dendritic Cell ◽  
Lymphatic System ◽  
Intestinal Inflammation ◽  
Critical Role ◽  
Lymphatic Vessels ◽  
Lymphoid Tissues ◽  
Functional Changes ◽  
Increased Risk ◽  
Small Intestinal ◽  
Acute Ileitis

Inflammatory bowel disease (IBD) has a complex pathophysiology with limited treatments. Structural and functional changes in the intestinal lymphatic system have been associated with the disease, with increased risk of IBD occurrence linked to a history of acute intestinal injury. To examine the potential role of the lymphatic system in inflammation recurrence, we evaluated morphological and functional changes in mouse mucosal and mesenteric lymphatic vessels, and within the mesenteric lymph nodes during acute ileitis caused by a 7-day treatment with dextran sodium sulfate (DSS). We monitored whether the changes persisted during a 14-day recovery period and determined their potential consequences on dendritic cell (DC) trafficking between the mucosa and lymphoid tissues. DSS administration was associated with marked lymphatic abnormalities and dysfunctions exemplified by lymphangiectasia and lymphangiogenesis in the ileal mucosa and mesentery, increased mesenteric lymphatic vessel leakage, and lymphadenopathy. Lymphangiogenesis and lymphadenopathy were still evident after recovery from intestinal inflammation and correlated with higher numbers of DCs in mucosal and lymphatic tissues. Specifically, a deficit in CD103+ DCs observed during acute DSS in the lamina propria was reversed and further enhanced during recovery. We concluded that an acute intestinal insult caused alterations of the mesenteric lymphatic system, including lymphangiogenesis, which persisted after resolution of inflammation. These morphological and functional changes could compromise DC function and movement, increasing susceptibility to further gastrointestinal disease. Elucidation of the changes in mesenteric and intestinal lymphatic function should offer key insights for new therapeutic strategies in gastrointestinal disorders such as IBD. NEW & NOTEWORTHY Lymphatic integrity plays a critical role in small intestinal homeostasis. Acute intestinal insult in a mouse model of acute ileitis causes morphological and functional changes in mesenteric and intestinal lymphatic vessels. While some of the changes significantly regressed during inflammation resolution, others persisted, including lymphangiogenesis and altered dendritic cell function and movement, potentially increasing susceptibility to the recurrence of gastrointestinal inflammation.

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