31 research outputs found
Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli
<p>Abstract</p> <p>Background</p> <p>Vertebrates sense chemical stimuli through the olfactory receptor neurons whose axons project to the main olfactory bulb. The main projections of the olfactory bulb are directed to the olfactory cortex and olfactory amygdala (the anterior and posterolateral cortical amygdalae). The posterolateral cortical amygdaloid nucleus mainly projects to other amygdaloid nuclei; other seemingly minor outputs are directed to the ventral striatum, in particular to the olfactory tubercle and the islands of Calleja.</p> <p>Results</p> <p>Although the olfactory projections have been previously described in the literature, injection of dextran-amines into the rat main olfactory bulb was performed with the aim of delimiting the olfactory tubercle and posterolateral cortical amygdaloid nucleus in our own material. Injection of dextran-amines into the posterolateral cortical amygdaloid nucleus of rats resulted in anterograde labeling in the ventral striatum, in particular in the core of the nucleus accumbens, and in the medial olfactory tubercle including some islands of Calleja and the cell bridges across the ventral pallidum. Injections of Fluoro-Gold into the ventral striatum were performed to allow retrograde confirmation of these projections.</p> <p>Conclusion</p> <p>The present results extend previous descriptions of the posterolateral cortical amygdaloid nucleus efferent projections, which are mainly directed to the core of the nucleus accumbens and the medial olfactory tubercle. Our data indicate that the projection to the core of the nucleus accumbens arises from layer III; the projection to the olfactory tubercle arises from layer II and is much more robust than previously thought. This latter projection is directed to the medial olfactory tubercle including the corresponding islands of Calleja, an area recently described as critical node for the neural circuit of addiction to some stimulant drugs of abuse.</p
Neurodegeneration and astrogliosis in the entorhinal cortex in Alzheimer鈥檚 disease: Stereological layer-specific assessment and proteomic analysis
Introduction: The entorhinal cortex is among the earliest areas involved in Alzheimer鈥檚
disease. Volume reduction and neural loss in this area have been widely reported.
Human entorhinal cortex atrophy is, in part, due to neural loss, but microglial and/or
astroglial involvement in the different layers remains unclear. Additionally, -omic
approaches in the human entorhinal cortex are scarce.
Methods: Herein, stereological layer-specific and proteomic analyses were carried out
in the human brain.
Results: Neurodegeneration, microglial reduction, and astrogliosis have been demonstrated, and proteomic data have revealed relationships with up- (S100A6, PPP1R1B,
BAG3, and PRDX6) and downregulated (GSK3B, SYN1, DLG4, and RAB3A) proteins.
Namely, clusters of these proteins were related to synaptic, neuroinflammatory, and
oxidative stress processes.
Discussion: Differential layer involvement among neural and glial populations determined by proteinopathies and identified proteins related to neurodegeneration and
astrogliosis could explain how the cortical circuitry facilitates pathological spreading
within the medial temporal lobe.Introducci贸n
La corteza entorrinal se encuentra entre las primeras 谩reas involucradas en la enfermedad de Alzheimer. La reducci贸n de volumen y la p茅rdida neural en esta 谩rea han sido ampliamente reportadas. La atrofia de la corteza entorrinal humana se debe, en parte, a la p茅rdida neural, pero la participaci贸n microglial y/o astroglial en las diferentes capas sigue sin estar clara. Adem谩s, los enfoques -贸micos en la corteza entorrinal humana son escasos.
M茅todos
En este documento, se llevaron a cabo an谩lisis prote贸micos y espec铆ficos de capa estereol贸gica en el cerebro humano.
Resultados
Se ha demostrado la neurodegeneraci贸n, la reducci贸n microglial y la astrogliosis, y los datos prote贸micos han revelado relaciones con prote铆nas reguladas al alza (S100A6, PPP1R1B, BAG3 y PRDX6) y a la baja (GSK3B, SYN1, DLG4 y RAB3A). Es decir, los grupos de estas prote铆nas estaban relacionados con procesos de estr茅s oxidativo, neuroinflamatorio y sin谩ptico.
Discusi贸n
La participaci贸n de capas diferenciales entre poblaciones neurales y gliales determinada por proteinopat铆as y prote铆nas identificadas relacionadas con la neurodegeneraci贸n y la astrogliosis podr铆a explicar c贸mo el circuito cortical facilita la propagaci贸n patol贸gica dentro del l贸bulo temporal medial
Neuronal and glial characterization in the rostrocaudal axis of the human anterior olfactory nucleus: Involvement in Parkinson鈥檚 disease
Hyposmia is one of the prodromal symptoms of Parkinson鈥檚 disease (PD) and a red flag in clinical diagnosis. Neuropathologically, this sign correlates with 伪-synuclein involvement in the anterior olfactory nucleus (AON). Neurodegeneration, microgliosis, and astrogliosis in AON are poorly studied, and bulbar AON is the focus of these studies with contradictory results. Additionally, male sex is a risk marker for developing PD, but sexual dimorphism of neural and glial populations in the AON has rarely been considered. The aim of this study was to analyze the density of NeuN, Iba-1, GFAP, and Lewy bodies (LBs), as well as the relationship of these cell type markers with pathology along the rostrocaudal axis of the AON (bulbar, retrobulbar, cortical anterior, and posterior divisions). Cavalieri, optical fractionator, and area fraction fractionator stereological approaches were used for the volume, cell populations and LBs densities, area fraction, and percentage of overlap. Iba-1 and 伪-syn intensities were measured using ImageJ. In non-PD (NPD) cases, the volume was lower in the AON at the extremes of the rostrocaudal axis than in the intermediate divisions. Cortical anterior AON volume decreased in PD compared with NPD cases. NeuN density decreased rostrocaudally in AON portions in NPD and PD cases. This occurred similarly in Iba-1 but only in PD samples. Iba-1 intensity significantly increased in bulbar AON between PD and NPD. No changes were found in astrocytes. Eight percent of NeuN, 0.1% of Iba-1, and 0.1% of GFAP areas overlapped with LBs area along the AON portions. The data indicate that bulbar AON, which is the most rostral portion in this axis, could play a major role in the pathology. This could be related to the larger area occupied by LBs in these divisions
Editorial: 50th Anniversary of Adult Neurogenesis: Olfaction, Hippocampus, and Beyond
Peer reviewedPeer Reviewe
Septal complex of the telencephalon of lizards: III. Efferent connections and general discussion
Differential Effects of Parkinson鈥檚 Disease on Interneuron Subtypes within the Human Anterior Olfactory Nucleus
Synucleinopathies (including 伪-synucleinopathies), which include Parkinson鈥檚 disease (PD), manifest themsevles early on (stage 1) in the olfactory system; preferentially in the anterior olfactory nucleus (AON). In particular, the non-motor, early manifestations of PD include hyposmia, which is the partial loss of the sense of smell. The neural basis of hyposmia in PD, however, is poorly understood; but the AON appears to be a key structure in the disease鈥檚 progression. We analyzed whether 伪-synuclein was involved in the differential interneuron vulnerability associated with PD in the retrobulbar, cortical anterior and cortical posterior divisions of the AON. First, we determined the expression of the calcium binding interneuron markers, calretinin, calbindin and parvalbumin, as well as non-calcium binding interneuron marker, somatostatin, in neuronal cell bodies alone (cells/mm2) and in neuronal cell bodies and neurites (% of area fraction) of post-mortem tissue from PD cases and age-matched controls (n = 4 for each) by immunofluorescent confocal microscopy. Results indicated that parvalbumin expression was upregulated in neuronal cell bodies throughout the anterior olfactory nucleus of PD cases compared with controls. Furthermore, there was increased calbindin, calretinin and parvalbumin expression in the cell bodies and neurites of neurons in the retrobulbar division and also increased parvalbumin expression in the neurites of neurons in the cortical division; calretinin expression was also increased in neuronal cell bodies and neurites in the cortical posterior division. Second, we analyzed the co-localization of the above markers with 伪-synuclein, with results indicating that 伪-synuclein co-localized with the calcium-binding proteins, but only partially with somatostatin. Taken together, these results indicate differential expression levels among different neural markers in the divisions of the AON in PD cases and point to several possibilities, among them: possible neuroprotective mechanisms of calcium-binding proteins against 伪-synuclein; and the differential involvement of somatostatin in 伪-synuclein-positive cell bodies and neurites
伪-Synucleinopathy in the Human Amygdala in Parkinson Disease: Differential Vulnerability of Somatostatin- and Parvalbumin-Expressing Neurons
Neurodegeneration and contralateral 伪-synuclein induction after intracerebral 伪-synuclein injections in the anterior olfactory nucleus of a Parkinson鈥檚 disease A53T mouse model
Abstract Parkinson鈥檚 disease is characterized by a proteinopathy that includes aggregates of 伪-synuclein. A recent hypothesis proposes a prion-like spreading mechanism for this 伪-synucleinopathy. Early neuropathological deposits occur, among others, in the anterior olfactory nucleus (AON). This study investigates the anterograde and/or retrograde transmissibility of exogenous 伪-synuclein inoculated in the right AON of the A53T model of Parkinson鈥檚 disease and wild-type mice as well as neuronal and glial involvement. Seven experimental groups were established: wild-type injected with tracers; A53T mice injected with either 伪-synuclein or saline 2鈥塵onths beforehand; wild-type injected with either 伪-synuclein or saline 2鈥塵onths beforehand; and wild-type injected with either 伪-synuclein or saline 4鈥塵onths beforehand. Weight and behavioral changes were analyzed. Immunohistochemistry against 伪-synuclein, NeuN, Iba-1 and GFAP was performed. Volume and marker distributions in the olfactory bulb (OB), AON and piriform cortex were analyzed using unbiased stereology. The behavioral analyses reveal higher levels of hyperactivity in transgenic as compared to wild-type mice. Tract-tracing experiments show that the main contralateral afferent projections to the dorsal AON come from the AON and secondarily from the OB. In saline-injected transgenic animals, 伪-synuclein expression in the OB and the AON is higher in the left hemisphere than in the right hemisphere, which could be due to basal interhemispheric differences. 伪-synuclein injection could provoke a significant increase in the left hemisphere of the transgenic mice鈥檚 OB, compared to saline-injected animals. Neuronal loss was observed in saline-injected transgenic mice relative to the saline-injected wild-type group. There were no overall differences in neuron number following injection of聽伪-synuclein into either wild-type or transgenic mice, however some neuron loss was apparent in specific regions of 伪-synuclein injected wild-types.聽Microglia labeling appeared to be correlated with surgery-induced inflammation. Astroglial labeling was higher in transgenic animals, which could be due to endogenous 伪-synucleinopathy. This study suggests 伪-synucleinopathy induction, via retrograde and contralateral projections, within the olfactory system of transgenic animals