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

The prodromes of Parkinson's disease.

"This is the peer reviewed version of the following article: Rees RN, Noyce AJ, Schrag A. The prodromes of Parkinson's disease. Eur J Neurosci. 2018;00:1–8. https://doi.org/10.1111/ejn.14269, which has been published in final form at https://doi.org/10.1111/ejn.14269. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Use of Self-Archived Versions."Whilst the diagnosis of Parkinson’s disease (PD) relies on the motor triad of bradyki-nesia, rigidity and tremor, the underlying pathological process starts many years be-fore these signs are overt. In this prodromal phase of PD, a diverse range of non- motor and motor features can occur. Individually they do not allow a diagnosis of PD, but when considered together, they reflect the gradual development of the clinical syn-drome. Different subgroups within the prodromal phase may exist and reflect different underlying pathology. Here, we summarise the evidence on the prodromal phase of PD in patient groups at increased risk of PD with well described prodromal features: patients with idiopathic rapid eye movement sleep behaviour disorder, patients with idiopathic anosmia and families with monogenic mutations that are closely linked to PD pathology. In addition, we discuss the information on prodromal features from ongoing studies aimed at detecting prodromal PD in the general population. It is likely that better delineation of the clinical prodromes of PD and their progression in these high- risk groups will improve understanding of the underlying pathophysiology.Parkinson’s UK, Grant/Award Number: G1606; Barts Charity (Preventive Neurology Grant); National Institute for Health Research University College London Hospitals Biomedical Research Centr

Differential Effects of Parkinson’s Disease on Interneuron Subtypes within the Human Anterior Olfactory Nucleus

Synucleinopathies (including α-synucleinopathies), which include Parkinson’s 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’s progression. We analyzed whether α-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 α-synuclein, with results indicating that α-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 α-synuclein; and the differential involvement of somatostatin in α-synuclein-positive cell bodies and neurites

Neurodegeneration and contralateral α-synuclein induction after intracerebral α-synuclein injections in the anterior olfactory nucleus of a Parkinson’s disease A53T mouse model

Abstract Parkinson’s disease is characterized by a proteinopathy that includes aggregates of α-synuclein. A recent hypothesis proposes a prion-like spreading mechanism for this α-synucleinopathy. Early neuropathological deposits occur, among others, in the anterior olfactory nucleus (AON). This study investigates the anterograde and/or retrograde transmissibility of exogenous α-synuclein inoculated in the right AON of the A53T model of Parkinson’s 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 α-synuclein or saline 2 months beforehand; wild-type injected with either α-synuclein or saline 2 months beforehand; and wild-type injected with either α-synuclein or saline 4 months beforehand. Weight and behavioral changes were analyzed. Immunohistochemistry against α-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, α-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. α-synuclein injection could provoke a significant increase in the left hemisphere of the transgenic mice’s 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 α-synuclein into either wild-type or transgenic mice, however some neuron loss was apparent in specific regions of α-synuclein injected wild-types. Microglia labeling appeared to be correlated with surgery-induced inflammation. Astroglial labeling was higher in transgenic animals, which could be due to endogenous α-synucleinopathy. This study suggests α-synucleinopathy induction, via retrograde and contralateral projections, within the olfactory system of transgenic animals

The Effect of Visualization Techniques on Students of Occupational Therapy during the First Visit to the Dissection Room

Background: Part of the basic teaching of human anatomy are prosection sessions with a human corpse, which may generate stress or anxiety among students. The objective of this work was to study how, through the visualization technique (a coping technique), these levels could be reduced before starting prosection classes. Methods: A cross-sectional pilot study was conducted involving first-year students who had never participated in screening sessions. Prior to the visit, occupational therapy students underwent a viewing session (visualization technique). On the day of the visit, before and after the screening session, an anonymous questionnaire was distributed to find out about aspects of the students’ experiences, such as their feelings and perceptions. The State–Trait Anxiety Inventory was used to assess anxiety. Results: The baseline levels of anxiety measured remained stable (from 18.5 to 18.2 points), with no differences being found (p > 0.05). The levels of emotional anxiety measured fell from 15.2 to 12.6 points (p p < 0.05). Conclusions: Sessions in a dissection room can cause stressful experiences and change the emotional balances of some students. The results obtained and published here showed no significant differences after the visualization technique. We found that the students believed that the prosection sessions were very useful for teaching anatomy

Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli-2

<p><b>Copyright information:</b></p><p>Taken from "Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli"</p><p>http://www.biomedcentral.com/1471-2202/8/103</p><p>BMC Neuroscience 2007;8():103-103.</p><p>Published online 29 Nov 2007</p><p>PMCID:PMC2216080.</p><p></p>) of the posterolateral cortical amygdaloid nucleus, respectively. For abbreviations, see list. Calibration bar: A, C 400 μm; B, D 200 μm

Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli-4

<p><b>Copyright information:</b></p><p>Taken from "Projections from the posterolateral olfactory amygdala to the ventral striatum: neural basis for reinforcing properties of chemical stimuli"</p><p>http://www.biomedcentral.com/1471-2202/8/103</p><p>BMC Neuroscience 2007;8():103-103.</p><p>Published online 29 Nov 2007</p><p>PMCID:PMC2216080.</p><p></p>xtran-amine injection into the main olfactory bulb (A). For abbreviations, see list. Calibration bar: A 1250 μm; B, C, E 400 μm; D, F 100 μm