Olfactory cortex and Olfactory bulb volume alterations in patients with post-infectious Olfactory loss
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Voxel-based morphometry
Orbitofrontal cortex
Anterior olfactory nucleus
Anterior olfactory nucleus
Piriform cortex
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ABSTRACT Impaired olfaction has been described as an early symptom in Alzheimer's disease (AD). Neuroanatomical changes underlying this deficit in the olfactory system are largely unknown. Given that interneuron populations are crucial in olfactory information processing, we have quantitatively analyzed somatostatin‐ (SOM), parvalbumin‐ (PV), and calretinin‐expressing (CR) cells in the olfactory bulb, anterior olfactory nucleus, and olfactory tubercle in PS1 x APP double transgenic mice model of AD. The experiments were performed in wild type and double transgenic homozygous animal groups of 2, 4, 6, and 8 months of age to analyze early stages of the pathology. In addition, beta‐amyloid (Aβ) expression and its correlation with SOM cells have been quantified under confocal microscopy. The results indicate increasing expressions of Aβ with aging as well as an early fall of SOM and CR expression, whereas PV was decreased later in the disease progression. These observations evidence an early, preferential vulnerability of SOM and CR cells in rostral olfactory structures during AD that may be useful to unravel neural basis of olfactory deficits associated to this neurodegenerative disorder. Anat Rec, 296:1413‐1423, 2013. © 2013 Wiley Periodicals, Inc.
Anterior olfactory nucleus
Calretinin
Olfactory marker protein
Olfactory ensheathing glia
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Abstract Reduced olfactory function (hyposmia) is one of the most common non-motor symptoms experienced by those living with Parkinson’s disease (PD), however, the underlying pathology of the dysfunction is unclear. Recent evidence indicates that α-synuclein (α-syn) pathology accumulates in the anterior olfactory nucleus of the olfactory bulb years before the motor symptoms are present. It is well established that neuronal cells in the olfactory bulb are affected by α-syn, but the involvement of other non-neuronal cell types is unknown. The occurrence of intracellular α-syn inclusions were quantified in four non-neuronal cell types – microglia, pericytes, astrocytes and oligodendrocytes as well as neurons in the anterior olfactory nucleus of post-mortem human PD olfactory bulbs (n = 11) and normal olfactory bulbs (n = 11). In the anterior olfactory nucleus, α-syn inclusions were confirmed to be intracellular in three of the four non-neuronal cell types, where 7.78% of microglia, 3.14% of pericytes and 1.97% of astrocytes were affected. Neurons containing α-syn inclusions comprised 8.60% of the total neuron population. Oligodendrocytes did not contain α-syn. The data provides evidence that non-neuronal cells in the PD olfactory bulb contain α-syn inclusions, suggesting that they may play an important role in the progression of PD.
Anterior olfactory nucleus
Hyposmia
Olfactory ensheathing glia
Olfactory nerve
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Anterior olfactory nucleus
Rhinencephalon
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Anterior olfactory nucleus
Piriform cortex
Olfactory nerve
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Anterior olfactory nucleus
Piriform cortex
Olfactory nerve
Axoplasmic transport
Entorhinal cortex
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Abstract The purpose of the study was to determine the morphology and distribution of vasoactive intestinal polypeptide‐ and peptide histidine isoleucineimmunoreactive (VIP‐ and PHI‐ir) neurons and innervation patterns in the main and accessory olfactory bulb, anterior olfactory nucleus, and piriform cortex of the adult cat. In these centers, VIP‐ and PHI‐immunoreactive material are present in the same neuronal types, respectively, therefore summarized as VIP/PHI‐ir neurons. In the main olfactory bulb, the majority of VIP/PHI‐ir neurons are localized in the external plexiform layer. These neurons give rise to two or more locally branching axons. They form boutons on mitral and external tufted cell bodies. According to the morphology and location, we have classified these neurons as Van Gehuchten cells. Some VIP/PHI‐ir neurons are present in the glomerular layer. They have small somata and give rise to dendrites branching exclusively into glomeruli. We have classified these neurons as periglomerular cells . In the granule cell layer, neurons with long apical dendrites and one locally projecting axon are present. In the accessory olfactory bulb, VIP/PHI‐ir neurons are localized in the mixed external/mitral/internal plexiform layer. They represent Van Gehuchten cells. In the anterior olfactory nucleus and piriform cortex, VIP/PHI‐ir bipolar basket neurons are present. They are localized mainly in layers II/III. These neurons are characterized by a bipolar dendritic pattern and by locally projecting axons forming basket terminals on large immunonegative cell somata. Because of their common morphological features, we summarize them as the retrobulbar VIP/PHI‐ir interneuron population. The PHI‐ir neurons display the same morphology as the VIP‐ir cells. However, they are significantly lower in number with a ratio of VIP‐ir to PHI‐ir cells about 2:1 in the main and accessory olfactory bulb and in the anterior olfactory nucleus. By contrast, in the piriform cortex the ratio is about 1:1.
Anterior olfactory nucleus
Piriform cortex
Granule cell
Vomeronasal organ
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Olfactory memory
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Abstract A study was made of the normal and experimental anatomy of the olfactory system of the young adult male rhesus monkey. The cytoarchitecture of the central olfactory areas was studies with cell and fiber stains, while the extent and pattern of the projections of the olfactory bulb were determined by the Fink‐Heimer and autoradiographic methods. The brain of one animal that had sustained damage to the olfactory bulb two days prior to sacrifice, and of one that had a transection of the olfactory tract ten days prior to sacrifice, were processed with the Fink‐Heimer technique. The first of these and four others received injections of 3 H‐proline or 3 H‐leucine into the olfactory bulb, and following a survival period of 18 hours, or 2, 4, 12, or 20 days, their brains were proceessed with the autoradiographic technique. The results were the same for both experimenal methods and for all survivalperiods. The projections of the olfactory bulb in this microsmatic animal are entirely ipsilateral. All of the structures that receive direct olfactory afferents have a laminar organization except for the anterior olfactory necleus, which is laminated only in its anterior, peduncular, portion. While the olfactory bulb projects to the entire extent and depth of the naterior olfactory nucleus, the olfactory afferents of all other structures are confined to layer IA of the plexiform layer. These structures are: all divisions of the olfactory tubercle; the frontal and temporal prepiriform cortices; the oral, medial, and dorsal divisions of the superficial amygdaloid nucleus; and polar and anterior entorhinal cortex. The rhesus monkey does not have a recognizable accessory olfactory bulb, and no projectiosns were seen to the taenia ecta or the ventral division of the superficial amygdaloid nucleus. With these exceptions, the projections of the olfactory bulb in the rhesus monkey are similar to those in macrosmatic species.
Cytoarchitecture
Anterior olfactory nucleus
Laminar organization
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Abstract Electrophysiological and anatomical observations suggest that terminals of olfactory bulb mitral cells ending in rat primary olfactory cortex exert certain postsynaptic effects via an excitatory amino acid neurotransmitter. Recent anatomical studies have shown that several peptides, most notably corticotropin‐releasing factor (CRF) (Imaki et al., '89) (Brain Res., 496:35–44), are also localized within rat olfactory bulb projection neurons, thus raising the possibility that there is a peptide cotransmitter in this system. In contrast to the availability of data for rodents, very little is known about the distribution of peptides and other putative transmitters in the olfactory systems of primate species. In the present study, sections through the olfactory bulb and its target areas were obtained from two monkey species ( Saimiri sciureus and Macaca fascicularis ) and processed for immunohistochemistry with a well‐characterized polyclonal antiserum directed against the human form of CRF. Virtually identical results were obtained in the two species. Within the olfactory bulb, nearly all mitral and many tufted cells contained CRF‐like immunoreactivity. CRF‐positive fibers were seen within the olfactory tract and olfactory stria, which contain the axons of mitral and tufted cells. Within the anterior olfactory nucleus and layer Ia of the olfactory tubercle and piriform cortex, immunoreactivity was seen within fine processes, as well as in coarse, varicose fibers and isolated puncta. CRF‐positive cells were seen within layer III of the olfactory tubercle and piriform cortex. Immunoreactive fibers and varicosities were also seen within olfactory‐recipient regions of the amygdala and entorhinal cortex. These observations suggest that CRF may act as a transmitter and/or neuromodulator in primate olfactory system.
Piriform cortex
Anterior olfactory nucleus
Anterior commissure
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