Dissertations / Theses on the topic 'Olfactory nerve'
To see the other types of publications on this topic, follow the link: Olfactory nerve.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 37 dissertations / theses for your research on the topic 'Olfactory nerve.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse dissertations / theses on a wide variety of disciplines and organise your bibliography correctly.
1
Viswaprakash, Nilmini Vodyanoy Vitaly. "Enhancement, modulation and electrophysiological characterization of murine olfactory neurons to odorant stimulation in vitro." Auburn, Ala., 2006. http://hdl.handle.net/10415/1309.
Full text
2
Lee, I.-Hui. "On CNS injury and olfactory ensheathing cell engraftment strategies /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-551-8/.
Full text
3
Deckner, Maja-Lena. "Factors influencing the turnover of olfactory receptor neurons /." Stockholm : Karolinska Univ. Press, 2001. http://diss.kib.ki.se/2001/91-89428-05-6/.
Full text
4
冼振鋒 and Chun-fung Sin. "Olfactory ensheathing cell transplanation in spinal cord after contusion injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40738930.
Full text
5
Sin, Chun-fung. "Olfactory ensheathing cell transplanation in spinal cord after contusion injury." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40738930.
Full text
6
Thompson, Rebecca M. (Rebecca Mae). "Ultrastructural effects of chemical modification on olfactory receptors." Thesis, North Texas State University, 1987. https://digital.library.unt.edu/ark:/67531/metadc798163/.
Full textAbstract:
The ultrastructural effects of chemical modification on olfactory receptors were investigated with scanning electron microscopy, transmission electron microscopy and fluorescent microscopy. Mason and Morton (1984) hypothesized that a two-step chemical treatment would covalently modify receptor proteins. Their two-step protocol was modified in an attempt to label olfactory receptor proteins and the ultra structural effects of the original two-step protocol were examined.
7
Dombrowski, Mary A. "Sciatic nerve remyelination and nodal formation following olfactory ensheathing cell transplantation." Yale University, 2008. http://ymtdl.med.yale.edu/theses/available/etd-08092007-114648/.
Full textAbstract:
Transplantation of olfactory ensheathing cells (OECs) into injured spinal cord results in improved functional outcome through axonal regeneration, remyelination, and neuroprotection. However, because little is known of the fate of OECs transplanted into injured peripheral nerve, their myelin forming potential requires investigation. To study these issues OECs were isolated from the olfactory bulbs of adult green fluorescent protein (GFP)-expressing transgenic rats and transplanted into a sciatic nerve crush lesions. Five weeks to six months after transplantation the nerves were studied histologically and it was determined that GFP-expressing OECs survived in the lesion and distributed longitudinally across the lesion zone. Immunostaining revealed a high density of isoform Nav1.6 at the newly formed nodes of Ranvier which were flanked by paranodal Caspr staining. Immuno-electron microscopy for GFP revealed transplanted OECs form peripheral type myelin. These results indicate that transplanted OECs extensively integrate into transected peripheral nerve, form myelin on regenerated peripheral nerve fibers, and reconstruct nodes of Ranvier with proper sodium channel structure.
8
Vukovic, Jana. "An in vitro and in vitro study on the role of the glycoprotein fibulin-3 in olfactory nerve growth and repair." University of Western Australia. School of Anatomy and Human Biology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0182.
Full textAbstract:
The primary olfactory pathway in adult mammals has retained a remarkable potential for self-repair. Olfactory ensheathing cells (OECs), specialized glial cells within the olfactory nerve, are thought to play an important role in the ongoing growth and replenishment of sensory connections in this system. To gain insight into novel molecules that could mediate OEC-supported growth of axons within the olfactory nerve, gene expression profiling experiments revealed very high expression of the fibulin-3 glycoprotein in OECs. To date, research on fibulin-3 has been limited and mainly focused on its involvement in Doyne honeycomb retinal dystrophy, vasculogenesis and tumor formation. As the extracellular matrix associated with OECs is thought to be an important contributor to a growth-permissive environment, the main aim of this thesis was to define a putative role for fibulin-3 during olfactory receptor neuron replacement and regeneration. This hypothesis was investigated in a series of in vitro and in vivo experiments that involved lentiviral vectors to manipulate fibulin-3 gene expression in OECs as well as the use of knock-out mice. Using genetically-modified OECs, experimental data showed that increased levels of fibulin-3 induced morphological changes in OECs and also impeded their migration. Lentiviral vector-mediated expression of fibulin-3 in OECs also had an inhibitory effect on neurite outgrowth from dorsal root ganglion explants. On the other hand, knock-down of fibulin-3 levels via siRNA technology resulted in reduced proliferation. Comparative lesioning experiments in fibulin-3 knock-out and wild-type mice allowed for further assessment of a role for fibulin-3 in olfactory nerve repair in vivo. Two experimental injury models, i.e. epithelial (Triton-X) lesioning and olfactory bulbectomy, were employed. The results obtained were in line with in vitro observations. A lack of fibulin-3 in knock-out mice resulted in a seemingly augmented regeneration of the olfactory epithelium at 10 days post-injury. However, at the latest recovery time point of 42 days post-injury, an impaired recovery of the olfactory epithelium from the experimental insults was observed. Although the precise mechanism for the latter phenomenon is not yet fully understood, our data point towards several factors which include vascular abnormalities and altered cell proliferation within the olfactory epithelium. Additionally, the precise protein distribution of another wide-spread family of extracellular matrix molecules, the laminins, was investigated in this thesis. It was of interest to investigate the spatiotemporal expression of laminin isoforms during iii olfactory nerve development and regeneration as these molecules may have distinct roles in promoting olfactory sensory neuron growth and patterning. In situ hybridization and immunohistochemical studies concluded that laminin-211 and laminin-411 were the most likely candidates to play such a role. In summary, this thesis provides new insights into the role of the extracellular matrix, fibulin-3 in particular, in regulating cell migration, division and axonal growth in the primary olfactory pathway. Such knowledge also gives a greater understanding of the molecular mechanisms by which OEC transplants may enhance axonal regeneration elsewhere in the CNS.
9
McMonagle, Brent Anthony. "Nasal Derived Olfactory Ensheathing and Stem Cells in Peripheral Nerve Repair and Regeneration." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/366095.
Full textAbstract:
Damaged peripheral nerves are usually surgically repaired in an attempt to optimize recovery. The patient is stabilized and other potential life-threatening problems are managed. The wound area is thoroughly cleaned and devitalized tissue debrided, and any vascular injuries repaired. The nerve ends are trimmed, and if possible, sutured together using fine sutures using standard microsurgical techniques, provided there is no tension. There is often a gap between the ends of a damaged nerve, because of loss of nerve substance by the injury or resection of tumour, as well as retraction of the stumps because of the inherent elasticity of nerves. In certain circumstances, the nerve stumps may be mobilized to gain extra length, or sutured to other neighbouring nerves (see end-to side repair), but generally, a conduit is required to bridge the gap.
Various different conduits have been used to bridge this gap in an attempt to allow axons to regenerate across the gap to the distal nerve stump, align and enter the endoneurial tubes of the distal stump, elongate down these tubes, and finally assume a connection with the end-organs (e.g. motor end-plates, sensory receptors, etc.) of their previous peripheral targets.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
Full Text
10
Mallek, Jennifer de Toledo. "Hyaluronic acid-olfactory ensheathing cell compositions for spinal cord injury nerve regeneration." [Gainesville, Fla.] : University of Florida, 2006. http://purl.fcla.edu/fcla/etd/UFE0015880.
Full text
11
Amaya, Daniel Alejandro. "Integration of the Peripheral and Central Nervous System During Development of the Murine Olfactory Nerve." Thesis, Griffith University, 2016. http://hdl.handle.net/10072/367158.
Full textAbstract:
The need to develop therapies for neurodegenerative diseases and spinal cord injuries has led researchers to study the primary olfactory system, as it continuously renews itself throughout life, and completely regenerates after injury.
A pool of cells that line the basal surface of the olfactory epithelium gives rise to new olfactory neurons both during normal olfactory nervous system turnover and to a greater extent following injury. The unique, growth promoting olfactory system environment is crucial for this neurogenesis and regeneration. Significantly glial scarring (as is typically seen in neurodegeneration and neural damage elsewhere in the nervous system) is largely absent following injury to the olfactory tract. Thus replicating the favourable condition in the olfactory nervous system would be invaluable for developing these successful therapies. If we can mimic the cellular and molecular mechanisms responsible for maintenance andregeneration of the olfactory neurons, we can promote regeneration and facilitate the reestablishment of connectivity in damaged neural tracts. To model neural regeneratio n strategies in the olfactory nervous system we need to understand the normal olfactory system biology.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Natural Sciences
Science, Environment, Engineering and Technology
Full Text
12
Rayapureddi, S. "Characterisation and application of olfactory ensheathing cells for glaucoma induced optic nerve damage." Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1366899/.
Full textAbstract:
Glaucoma is the term used to describe a group diseases characterised by a specific type of damage to the optic nerve head (ONH) known as cupping and a characteristic type of visual field loss. This loss is associated with progressive atrophy and loss of the retinal ganglion cells. Glaucoma is a leading cause of irreversible blindness in the world. This project was aimed at investigating olfactory ensheathing cells (OEC), a population of radial glia proven to be neuroprotective in central and peripheral nerve injury models, and their potential to protect the retinal ganglion cells in glaucoma. We studied the interactions of RGC and OEC in culture. We show that OEC can straighten, ensheath and bundle RGC neurites as well as support the survival of RGC and their synapses in culture. We also show that OEC endocytose dead RGC in culture. We modified a rat model of glaucoma (where paramagnetic microbeads are injected into the anterior chamber of the rat eyes) and characterised the early and late functional changes in the glaucomatous retina. We showed that RGC function was compromised in the early stages of glaucoma, before histological changes set in. We injected OEC into glaucomatous rat eyes to study the effects of OEC on optic nerve damage. The presence of OEC in the vitreous cavity of the glaucomatous rat eye significantly reduced the optic nerve damage in glaucomatous eyes. In summary, the work presented in this thesis provides an insight into • The functional changes of RGC in the early stages of experimental glaucoma and • Protection of RGC in experimental glaucoma by introduction of OEC into the vitreous.
13
Zhao, Xiaoguang. "Probing biological structures with magnetic resonance imaging." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B40687478.
Full text
14
Tonsor, Michael M. "Interaction of apoE with estrogen in the olfactory system during nerve maintenance and recovery /." View online, 2009. http://repository.eiu.edu/theses/docs/32211131566909.pdf.
Full text
15
Bakos, Stephen. "The Expression of Matrix Metalloproteinase-9 and -2 in Olfactory Injury and Recovery." VCU Scholars Compass, 2010. http://scholarscompass.vcu.edu/etd/143.
Full textAbstract:
The olfactory system has the remarkable capacity for neurogenesis following injury. However, the molecular mechanisms important for reinnervation of the olfactory bulb (OB) remain unknown. The matrix metalloproteinases (MMPs) are important components in many central nervous system (CNS) injury paradigms, yet remain unexplored in olfactory injury and recovery. To address the role of MMPs, the temporal expressions of MMP-9 and MMP-2 were examined in 3 olfactory injury models: nerve transection (NTx), methyl bromide gas (MeBr) exposure, and nerve transection with Teflon barrier (NTx-TB). Each injury model represents a different degree of olfactory injury and neuronal recovery. In NTx, sensory axons are lesioned, leading to neuronal degeneration and subsequent reinnervation of the OB. MeBr exposure damages the cell bodies of sensory neurons in the peripheral olfactory epithelium (OE), leading to degeneration and reinnervation of the OB without direct trauma to the OB. In NTx-TB, sensory axons are lesioned and a barrier is inserted following injury that blocks regenerated neurons from reinnervation of the OB. Following NTx, MMP-9 increased immediately in the OB and was localized to neutrophils, an inflammatory leukocyte. The elevated levels of MMP-9 corresponded to neuronal degeneration. To confirm this relationship, MMP-9 expression was measured following MeBr injury. MMP-9 increased during neuronal degeneration in the OB and was localized to neutrophils in the area of sensory axon degradation. These experiments demonstrated that MMP-9 is important for both neuronal degeneration and the acute inflammatory response following olfactory injury. In NTx injury, MMP-2 expression peaked at day 7 and corresponded to the transition between degeneration and reinnervation of the OB. MMP-2 was localized to the granule cell and external plexiform layers in control and day 7 bulbs. Following NTx-TB, MMP-2 remained low and was not expressed by regenerated axons. The absence of a MMP-2 peak in the NTx-TB injury suggests that this peak depends on reinnervation of the OB. This study demonstrates a temporal correlation between MMP-9 and degeneration and MMP-2 and reinnervation following olfactory injury. These findings provide new insight into the molecular mechanisms underlying olfactory nerve injury. Modulation of MMPs could provide novel therapeutic interventions to improve neuronal recovery following injury.
16
Garraway, Richard. "The action of semiochemicals on olfactory nerve activity and behaviour of Deroceras reticulatum (Mull)." Thesis, University of Portsmouth, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.303955.
Full text
17
Zhao, Xiaoguang, and 赵晓光. "Probing biological structures with magnetic resonance imaging." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B40687478.
Full text
18
Winegar, Bruce D. (Bruce David). "Roles of Calcium Ions and Cyclic AMP in Olfactory Transduction." Thesis, North Texas State University, 1986. https://digital.library.unt.edu/ark:/67531/metadc331287/.
Full textAbstract:
The roles of Ca2 + and cAMP in olfactory transduction were explored using agents which affect calcium channels and second messenger systems. These agents were applied at certain calculated final concentrations onto olfactory epithelia of urethane-anesthetized frogs (Sana PiPlens) by two-sec aerosol spray. During extracellular recording, saturated vapors of isoamyl acetate were delivered every 100 sec in 0.3 sec pulses to produce an electroolfactogram (EOG). Inorganic cations that block inward calcium currents inhibit EOG responses with the following rank order: (La3+) > (Zn2+, Cd2+) > (Al3+, Ca2+, Sr2+) > (Co2+). Application of 7.5 mM La3+ eradicates £0G's, while Ba2+ (which can carry more current that Ca2+) initially produces significant enhancement (F=43.04, p<0.001, df=19). Magnesium ion has no effect on EOG's at 7.5 mM, while 1.5 X 10"4M Ca2+ is significantly inhibitory (F=5.74; p=0.0355; df=12). Control aerosol sprays of distilled water depress EOG's by an average of 5%. The organic calcium channel antagonists diltiazem and verapamil inhibit EOG's by 17% and 36X, respectively, at a concentration of 1.5 X 10~*M. Verapamil produces significant inhibition (F=17.17; p=0.002; df=ll) at 1.5 X 10" 5 M, while the 1,4-dihydropyridine calcium channel antagonists, nicardipine and nifedipine, do not inhibit beyond 1% DMSO controls. Several calmodulin antagonists decrease EOG's, but without correlation to their anti-calmodulin potency. Application of 1.5 X 10"*M chlorpromazine and N-(6-aminohexyl)-5-chloro-l-naphthalenesulfonamide inhibit EOG's by 31% and 27%, respectively, while trifluoperazine inhibits by 23%. Dibutyryl cAMP, a lipophilic mimic of cAMP, produces 54% inhibition at 1.5 X 10" *M. Dibutyryl cGMP, cGMP, cAMP, and adenosine all decrease EOG's by less than 15% compared to distilled water controls. Forskolin, a reversible activator of adenylate cyclase, inhibits EOG's by 57% at 1.5 X 10"5M, which is significant beyond the 1% DMSO controls (F=17.17; p=0.002; df=ll). These data support the hypothesis that Ca2+ participates in olfactory transduction. Calcium ions could serve as charge carriers, second messengers, or both. Cyclic AMP could be involved with the primary excitatory process or sensory adaptation, or both.
19
Jang, Woochan. "The presence of fos-like immunoreactivity in neurons in the vomeronasal epithelium of mice /." free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9842591.
Full text
20
Zaidi, Aliya Urooj. "Studies on the development of the olfactory nerve pathway in the sea lamprey, Petromyzon marinus L." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0012/NQ52741.pdf.
Full text
21
Koussa, Mounir Ahmad. "Development of a Glial Network in the Olfactory Nerve: Role of a Calcium and Neuronal Activity." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144555.
Full text
22
Fornazieri, Marco Aurelio. "Validação do teste de identificação do olfato da Universidade da Pensilvânia (UPSIT) para Brasileiros." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-10032014-090524/.
Full textAbstract:
INTRODUÇÃO: Apesar da fundamental importância da olfação para avaliação dos sabores dos alimentos ingeridos, percepção de vazamento de gases e de incêndios, sua avaliação clínica ainda não se encontra padronizada no Brasil. O Teste de Identificação do Olfato da Universidade da Pensilvânia (UPSIT) é um teste mundialmente utilizado e considerado por muitos como o padrão-ouro da avaliação olfatória. Originalmente em inglês, já foi traduzido para mais de 12 línguas. Esse trabalho se propôs a validar de forma inédita o UPSIT para outra cultura. O UPSIT versão em português foi validado para a população brasileira e tabelas normativas foram elaboradas para comparação do escore obtido segundo o sexo e idade do indivíduo. Secundariamente, procurou-se os fatores preditores de um melhor escore no teste. CASUÍSTICA E MÉTODOS: Estudo transversal realizado de dezembro de 2011 a agosto de 2012. A amostra utilizada foi não-probabilística por quotas e constituída por indivíduos presentes em uma instituição de atendimento público (Poupatempo São Paulo), de forma consecutiva, sem queixas olfatórias no dia do exame. Foi determinada a quota de 60 brasileiros(as) em cada faixa etária de cada sexo, a saber: 20-24, 25-30, 31-34, 35-40, 41-44, 45-50, 50-54, 55-59, 60-64, 65-69, 70-74, 75-79 e >= 80 anos. Após responderem questionário referente a dados demográficos e critérios de inclusão e exclusão do estudo, fizeram o UPSIT 782 indivíduos do sexo masculino e 796 do sexo feminino. Nos pacientes com idade igual ou superior a 65 anos foi realizado o Mini Exame do Estado Mental e se excluíram aqueles pacientes com escore inferior a 24 pontos pela possibilidade de quadro demencial. A versão do UPSIT aplicada nesse estudo foi resultado de dois estudos prévios para melhorar a aplicabilidade desse teste para a população brasileira. RESULTADOS: 1820 voluntários participaram do estudo, 1578 foram incluídos nas tabelas normativas. 242 foram excluídos no dia da entrevista por estarem com infecção das vias aéreas superiores, terem história de trauma crânio-encefálico, queixa de perda de olfato ou paladar e um escore menor de 24 no Mini Exame do Estado Mental. Verificou-se que entre os 1578 indivíduos analisados, o escore de UPSIT variou de 9 a 40, obtendo-se escore médio de 32,1 (desvio padrão: 5,3) e escore mediano igual a 33. Pela análise univariada (p < 0,01) e multivariada - regressão linear múltipla- (p < 0,05), observou-se que a idade, sexo, número de anos de estudo e renda mensal da família influíram no escore do teste. CONCLUSÕES: O UPSIT está agora validado para utilização na população brasileira. Disponibilizou-se tabelas normativas para avaliação olfatória e um modo rápido de obtê-las. Fatores de correção são necessários para uma perfeita equivalência entre as normas de todos os continentes, utilizando como padrão-ouro as normas do país onde a versão original do teste foi desenvolvida. Pior status econômico e educacional interferem negativamente na performance olfatóriaINTRODUCTION: Despite the fundamental importance of olfaction to assess the flavors of food, perception of gas leakage and fire, its clinical evaluation is not yet standardized in Brazil. The University of Pennsylvania Smell Identification Test of the (UPSIT) is a test used worldwide and considered by many as the gold standard of olfactory assessment. Originally in English, it has been translated into more than 12 languages. This study aimed to validate the UPSIT for another culture in a novel form. The portuguese version of UPSIT Portuguese version was validated for the Brazilian population and normative tables were prepared to compare the score obtained by sex and age of the individual. Secondarily, we sought the predictors of a better score on the test. PATIENTS AND METHODS: Cross-sectional study conducted from December 2011 to August 2012. The sample used was a non-probabilistic by quotas and consisted of individuals present in a public service institution (Poupatempo São Paulo), consecutively, without olfactory complaints on exam day. We determined the quota of 60 Brazilians in each age group for each sex, as follows: 20-24, 25-30, 31-34, 35-40, 41-44, 45-50, 50-54, 55 -59, 60-64, 65-69, 70-74, 75-79 and >= 80 years. After answering a questionnaire about demographics and inclusion and exclusion criteria of the study, 782 males and 796 females did the UPSIT. In patients aged over 65 years was held the Mini Mental State Examination and excluded those patients with a score less than 24 points for the possibility of dementia. The version of the UPSIT applied in this study was the result of two previous studies to enhance the applicability of this test for the Brazilian population. RESULTS: 1820 volunteers participated in the study, 1578 were included in the normative tables. 242 were excluded on the day of the interview for being with upper airway infection, having an history of head trauma, complaining of smell or taste losses and a score below 24 on the Mini Mental State Examination. It was found that among the 1578 subjects analyzed, the UPSIT scores ranged from 9 to 40, yielding a mean score of 32.1 (SD: 5.3) and a median 33. By univariate analysis (p < 0.01) and multivariate analysis - multiple linear regression-(p < 0.05), it was observed that the age, sex, years of schooling and family monthly income influenced the test scores. CONCLUSIONS: UPSIT is now validated for use in the Brazilian population. Normative tables for olfactory assessment and a fast way to obtain them were demonstrated. Correction factors are needed for a perfect equivalence between norms of all continents, using as gold standard norms of the country where the original version of the test was developed. Worse economic and educational status interfered negatively in olfactory performance
23
Walkden, Heidi. "Bacterial infection of the brain: how bacteria penetrate the CNS by invading peripheral nerves." Thesis, Griffith University, 2020. http://hdl.handle.net/10072/395110.
Full textAbstract:
Bacterial infections of the central nervous system (CNS), though uncommon, are associated with very high rates of morbidity and mortality. Recent research has also highlighted the correlation between pathogens and chronic diseases of the CNS, such as neurodegenerative disorders, particularly Alzheimer’s disease. Whilst some bacteria can cross the blood-brain/blood-cerebrospinal fluid barriers, to date, other pathways by which bacteria enter the CNS remain largely unknown. Identifying alternative paths by which pathogens can enter the CNS is thus important for developing novel strategies preventing CNS infection and potential long-term sequelae.
Novel evidence suggests some bacterial species (as well as certain viruses and amoebae) can enter the brain via the cranial nerves innervating the nasal cavity, particularly the olfactory nerve that mediates the sense of smell and connects the nasal cavity with the olfactory bulb in the forebrain. The trigeminal nerve also innervates the nasal cavity and constitutes another invasion path. Only a handful of pathogens are thought to use cranial nerves to reach the brain; certain Chlamydia species (spp.) being amongst these.
Chlamydia pneumoniae is to date the bacterium with the strongest established link to Alzheimer’s disease. Previous research by our laboratory has also demonstrated that the bacterium causing the tropical disease melioidosis, Burkholderia pseudomallei, can invade both the olfactory and trigeminal nerves, travel along these nerves, to then infect the CNS (the olfactory bulb and brainstem, respectively). We have also previously shown that in outbred mice, the olfactory nerve is resistant to B. pseudomallei infection. The nasal mucosa contains both innate and adaptive immune components and prevents many infections. If pathogens penetrate the mucosal barrier and reach nerves, glial cells of the nerves can also combat the infection. Whilst only a few macrophages are present inside the olfactory nerve fascicles, olfactory nerve glial cells, termed olfactory ensheathing cells (OECs), are powerful phagocytes with innate immune functions. Thus, in addition to the immune cells and other components of the immune system in the nasal mucosa, cranial nerve glia are thus thought to be key for preventing CNS infection, explaining why such infections are relatively rare. Some pathogens, however, can evade destruction by these cells and invade the nerves, however, it remains largely unknown which pathogens are capable of doing so. Furthermore, injuries to the nasal epithelium are common, and if the mucosal barrier is removed by injury, perhaps it is easier for pathogens to infect the underlying nerves (in particular the olfactory nerve) and then reach the CNS. With the exception of one bacterium (Staphylococcus aureus) for which injury has been shown to allow infection of the olfactory nerve, it also remains unknown whether epithelial injury increases the risk of pathogens invading the CNS via these paths. Thus, we need to determine which pathogens are capable of invading the CNS via nerves connecting the nasal cavity and the brain, and whether epithelial injury increases the risk of infection. Furthermore, determining the cellular mechanisms that protect against microbial invasion of the CNS via nerves, as well as why certain pathogens can evade destruction of the immune system may pave the way for the development of novel therapies preventing and treating CNS infections.
The key aims of this thesis were to determine (1) whether prior injury to the nasal epithelium could allow B. pseudomallei to invade the olfactory nerve and bulb in the mouse strain where this nerve is usually resistant to this infection, (2) whether the bacterium Chlamydia muridarum (which infects mice and is commonly used to study Chlamydia spp. infection in rodents) can utilise cranial nerves that innervate the nasal cavity to invade the CNS and, if C. muridarum can invade the CNS, to then determine whether the bacteria remained viable and (3) whether C. muridarum can infect OECs, and how OECs respond to C. muridarum in vitro.
This thesis demonstrated that injury to the olfactory epithelium allowed the invasion of the olfactory nerve and bulb by B. pseudomallei in S100β-DsRed Quackenbush mice, in which the olfactory nerve is otherwise typically resistant to infection. This work also showed that C. muridarum can rapidly (within 48 h) reach the CNS (olfactory bulb and cerebral cortex) via the olfactory nerve, as well as infect the trigeminal nerve, in mice. Immunohistochemistry showed the presence of C. muridarum inclusion bodies (membrane-bound components inside which the bacteria replicate intracellularly) and viable C. muridarum bacteria were also isolated from these regions. C. muridarum was shown to readily infect OECs in vitro, which led to the upregulation of a range of cytokines.
The outcomes from this project will contribute to an increased understanding of how bacteria can reach the CNS and has revealed that injury to the nasal epithelium may increase the risk of CNS bacterial invasion via the olfactory nerve. The outcomes also include an increased understanding of how olfactory nerve glia become infected by and respond to bacteria. This work may also contribute towards the growing body of knowledge regarding the link between pathogens and certain diseases of the CNS, such as Alzheimer’s disease. Furthermore, with an increased understanding of how glial cells respond to bacteria, new therapies may be developed that stimulate bacterial degradation by the glia. Such therapies may provide valid future alternatives to antibiotics, also combating the growing problem of antibiotic resistance. Thus, this work may contribute to the foundation required to develop therapies to treat diseases that are currently not curable, as well as to better diagnose and identify susceptibilities to certain conditions.Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Griffith Health
Full Text
24
Schultz, Jean Marie. "Characterization of olfactory nerves in Twirler mice a thesis submitted in partial fulfillment ... for the degree of Master of Science in Orthodontics ... /." 2000. http://catalog.hathitrust.org/api/volumes/oclc/68896419.html.
Full text
25
"Cell culture studies of olfactory receptor neurons." Chinese University of Hong Kong, 1991. http://library.cuhk.edu.hk/record=b5886941.
Full textAbstract:
by Long Wan Wong.Thesis (M.Phil.)--Chinese University of Hong Kong, 1991.
Bibliography: leaves 77-93.
ABSTRACT --- p.i
ACKNOWLEDGEMENTS --- p.iii
LIST OF TABLES --- p.vii
LIST OF FIGURES --- p.viii
LIST OF ABBREVIATIONS --- p.ix
INTRODUCTION --- p.1
ANATOMY OF OLFACTORY MUCOSA --- p.1
NEUROGENESIS AND DIFFERENTIATION OF OLFACTORY RECEPTOR NEURONS --- p.3
ANATOMY AND DEVELOPMENT OF THE NERVE FIBER LAYER OF THE OLFACTORY BULB --- p.4
FACTORS INFLUENCING NEURONAL DIFFERENTIATION --- p.6
Chapter (1) --- Extracellular Matrix Molecules
Chapter (2) --- Cell Adhesion Molecules
Chapter (3) --- Soluble Diffusible Molecules
ASTROCYTES AS A SUBSTRATUM FOR CELL CULTURE --- p.12
EXPERIMENTAL PURPOSE AND DESIGN --- p.15
MATERIALS AND METHODS --- p.16
PREPARATION OF CELLULAR SUBSTRATA --- p.16
Chapter (1) --- Cortical Astrocyte Monolayers
Chapter (2) --- OB Astrocyte Monolayers
Chapter (3) --- ONL Glial Cell Monolayers
Chapter (4) --- Skin Fibroblast Monolayers
DISSOCIATION OF OLFACTORY MUCOSA --- p.22
TRANSMISSION AND SCANNING ELECTRON MICROSCOPY --- p.23
IMMUNOFLUORESCENCE --- p.24
IMMUNOHISTOCHEMISTRY --- p.26
COUNTING OF ORNs BEARING NEURITES AND MEASUREMENT OF NEURITE LENGTH --- p.26
ANALYSIS OF CONDITIONED MEDIA --- p.27
Chapter (1) --- Preparation of Conditioned Media
Chapter (2) --- Ultrafiltration
Chapter (3) --- Heat Treatment
Chapter (4) --- Protein Assay
Chapter (5) --- Investigation of Concentration-Activity Relationship
TABLE 1 --- p.30
FIGURES 1-2 --- p.31
RESULTS --- p.36
TRANSMISSION AND SCANNING ELECTRON MICROSCOPY --- p.36
Chapter (1) --- Cortical Astrocytes
Chapter (2) --- ORNs on Cortical Astrocytes
"OLFACTORY NEURITE EXTENSION ON CORTICAL ASTROCYTES, OB ASTROCYTES, ONL GLIAL CELLS, AND FIBROBLASTS" --- p.38
Chapter (1) --- Morphology of the Cellular Substrata
Chapter (2) --- Morphology of ORNs on Various Cellular Substrata
Chapter (3) --- Quantitative Studies of Olfactory Neurite Extension on the Cellular Substrata
CELL ADHESION MOLECULES ON ASTROCYTES --- p.41
INFLUENCE OF SOLUBLE SUBSTANCES ON OLFACTORY NEURITE EXTENSION --- p.42
ANALYSIS OF MEDIA CONDITIONED BY FIBROBLASTS --- p.44
Chapter (1) --- Molecular Weight Range of the Inhibitory Substance(s)
Chapter (2) --- Culture of ORNs on Cortical Astrocytes in Heat-treated CMF
Chapter (3) --- Protein Assay
Chapter (4) --- Concentration-Activity Relationship
TABLES 2-8 --- p.46
FIGURES 3-9 --- p.53
DISCUSSION --- p.69
CONCLUSIONS --- p.76
REFERENCES --- p.77
26
Mountoufaris, George. "The Role of the Clustered Protocadherins in the Assembly of Olfactory Neural Circuits." Thesis, 2016. https://doi.org/10.7916/D89K4BBT.
Full textAbstract:
The clustered protocadherins (Pcdh α, β & γ) provide individual neurons with cell surface diversity. However, the importance of Pcdh mediated diversity in neural circuit assembly and how it may promote neuronal connectivity remains largely unknown. Moreover, to date, Pcdh in vivo function has been studied at the level of individual gene clusters; whole cluster-wide function has not been addressed. Here I examine the role of all three Pcdh gene clusters in olfactory sensory neurons (OSNs); a neuronal type that expressed all three types of Pcdhs and in addition I address the role of Pcdh mediate diversity in their wiring. When OSNs share a dominant single Pcdh identity (α, β & γ) their axons fail to form distinct glomeruli, suggestive of inappropriate self-recognition of neighboring axons (loss of non-self-discrimination). By contrast, deletion of the entire α, β,γ Pcdh gene cluster, but not of each individual cluster alone, leads to loss of self-recognition and self-avoidance thus, OSN axons fail to properly arborize. I conclude that Pcdh-expression is necessary for self-recognition in OSNs, whereas its diversity allows distinction between self and non-self. Both of these functions are required for OSNs to connect and assembly into functional circuits in the olfactory bulb. My results, also reveal neuron-type specific differences in the requirement of specific Pcdh gene clusters and demonstrate significant redundancy between Pcdh isoforms in the olfactory system.
27
Vincent, Adele Joan. "The morphological and molecular characterisation of olfactory ensheathing cells." Thesis, 2005. https://eprints.utas.edu.au/22147/1/whole_VincentAdeleJoan2005_thesis.pdf.
Full text
28
Davila, Nestor Gabriel Trombley Paul. "Characerization of dopamine and kainate receptors in olfactory bulb neurons and their effects on glutamatergic transmission." 2003. http://etd.lib.fsu.edu/theses/available/etd-11172003-231726/.
Full textAbstract:
Thesis (Ph. D.)--Florida State University, 2003.Advisor: Dr. Paul Trombley, Florida State University, School of Arts and Sciences, Dept. of Biological Science. Title and description from dissertation home page (viewed Feb. 26, 2004). Includes bibliographical references.
29
Wu, Po-Ju, and 吳帛儒. "Effects of spices on neuropeptide Y (NPY) expression in olfactory nerve cell and human plasma." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/42821795843262514703.
Full textAbstract:
碩士國立臺灣大學
食品科技研究所
97
Neuropeptide tyrosine (NPY), a 36-amino acid peptide, is widely present in the central and peripheral nervous system, especially abundant in the brain. NPY is the most important stimulator of food intake. On the other hand, essences such as limonene and linalool, which are respectively the major components of grapefruit oil and lavender oil, have been verified to influence (decrease/increase) appetite in rats. Therefore, we propose that appetite regulation effect of spices might be connected with the secretion of NPY. In a previous study, we had established a NPY expression screening model by culturing olfactory nerve cells Rolf B1.T for 2 days and treating cells with limonene and linalool for 10 min. Thus, in this study, we used this model to screen thirteen spices and expected to find potential spices that could stimulate NPY mRNA expression of Rolf B1.T cells. Furthermore, a clinical trial was implemented to study the effects of these spices on the human physiological indicators, including ear temperature, blood pressure, and plasma NPY secretion. Furthermore, leptin is synthesised by adipocytes in proportion to the levels of stored triglycerides, and is a key hormone in the regulation of food intake and energy expenditure. This research also analyzed the leptin content in plasma. In addition, personal’s questionnaire was used to further investigate the relationship between food intake and aroma components. In NPY expression screening model, our result indicated that octenol, pinene, and methyl phenylacetate significantly increased NPY mRNA levels in the Rolf B1.T cells. Moreover, the results of clinical trial were as follows: 1) when the experimental period was 10 min, limonene (negative control) decreased plasma NPY level, indicating that it might inhibit appetite, 2) when the experimental periods were 5, 10 min, linalool (positive control) increased plasma NPY level, indicating that it might stimulate appetite, 3) when the experimental periods were 5, 10 and 15 min, octenol could increase plasma NPY level, revealing that it might be a potent stimulator of food intake, 4) the plasma NPY level in the pinene group had no obviously changes at any experimental time. However, the results of plasma leptin concentrations were inconclusive. We suspected that it was influenced by other physiological factors. Blood pressure and ear temperature were not significantly changed at any experimental time.
30
Alvites, Rui Damazio. "Combined use of Olfactory Mucosa Mesenchymal Stem Cells and Biomaterials in Regenerative Therapies after Peripheral Nerve Injury." Doctoral thesis, 2021. https://hdl.handle.net/10216/134928.
Full text
31
Alvites, Rui Damazio. "Combined use of Olfactory Mucosa Mesenchymal Stem Cells and Biomaterials in Regenerative Therapies after Peripheral Nerve Injury." Tese, 2021. https://hdl.handle.net/10216/134928.
Full text
32
Wang, Yiliu. "Imposing structure on odor representations during learning in the prefrontal cortex." Thesis, 2019. https://doi.org/10.7916/d8-vnwq-8d62.
Full textAbstract:
Animals have evolved sensory systems that afford innate and adaptive responses to stimuli in the environment. Innate behaviors are likely to be mediated by hardwired circuits that respond to invariant predictive cues over long periods of evolutionary time. However, most stimuli do not have innate value. Over the lifetime of an animal, learning provides a mechanism for animals to update the predictive value of cues through experience. Sensory systems must therefore generate neuronal representations that are able to acquire value through learning. A fundamental challenge in neuroscience is to understand how and where value is imposed in brain during learning.
The olfactory system is an attractive sensory modality to study learning because the anatomical organization is concise in that there are relatively few synapses separating the sense organ from brain areas implicated in learning. Thus, the circuits for learned olfactory behaviors appear to be relatively shallow and therefore more experimentally accessible than other sensory systems. The goal of this thesis is to characterize the representation and function of neural circuits involved in olfactory associative learning. Odor perception is initiated by the binding of odors onto olfactory receptors expressed in the sensory epithelium. Each olfactory receptor neuron (ORN) expresses one of 1500 different receptor genes, the expression of which pushes the ORN to project with spatial specificity onto a defined loci within the olfactory bulb, the olfactory glomeruli. Therefore, each and every odor evokes a stereotyped map of glomerular activity in the bulb.
The projection neurons of the olfactory bulb, mitral and tufted (M/T) cells, send axons to higher brain areas, including a significant input to the primary olfactory cortex, the piriform cortex. Axons from M/T cells project diffusely to the piriform without apparent spatial preference; as a consequence, the spatial order of the bulb is discarded in the piriform. In agreement with anatomical data, electrophysiological and optical imaging studies also demonstrate that individual odorants activate sparse subsets of neurons across the piriform without any spatial order. Moreover, individual piriform neurons exhibit discontinuous receptive fields that defy chemical or perceptual categorization. These observations suggests that piriform neurons receive random subsets of glomerular input. Therefore, odor representations in piriform are unlikely to be hardwired to drive specific behaviors. Rather, this model suggests that value must be imposed upon the piriform through learning. Indeed, the piriform has been shown to be both sufficient and necessary for aversive olfactory learning without affecting innate odor responses. However, how value is imposed on odor representations in the piriform and downstream associational areas remain largely unknown.
We first developed a strategy to track neural activity in a population of neurons across multiple days in deep brain areas using 2-photon endoscopic imaging. This allowed us to assay changes in neural responses to odors during learning in piriform and in downstream associative areas. Using this technique, we first observe that piriform odor responses are unaffected by learning, so learning must therefore impose discernable changes in neural activity downstream of piriform. Piriform projects to multiple downstream areas that are implicated in appetitive associative learning, such as the orbitofrontal cortex (OFC). Imaging of neural activity in the OFC reveal that OFC neurons acquire strong responses to conditioned odors (CS+) during learning. Moreover, multiple and distinct CS+ odors activatethe same population of OFC neurons, and these responses are gated by context and internal state. Together, our imaging data shows that an external and sensory representation in the piriform is transformed into an internal and cognitive representation of value in the OFC. Moreover, we found that optogenetic silencing of the OFC impaired the ability of mice to acquire learned associations. Therefore, the robust representation of expected value of the odor cues is necessary for the formation of appetitive associations.
We made an important observation: once the task has been learned with a set of odors, the OFC representation decays after learning has plateaued and remains silent even when mice encounter novel odors they haven’t previously experienced. Moreover, silencing the OFC when it was not actively engaged during the subsequent learning of new odors had no effect on learning. These sets of imaging and silencing experiments reveal that the OFC is only important during initial learning; once task structure has been acquired, it is no longer needed. Task performance after initial task acquisition must therefore be accommodated by other brain regions that can store the learned association for long durations.
We therefore searched for other brain regions that held learned associations long-term. In the medial prefrontal cortex (mPFC), we observe that the learned representation persists throughout the entire course of training. Unlike the OFC, not only does this representation encode the positive expected value of CS+ odors, it also encodes the negative expected value of CS- odors in a non-overlapping ensemble of neurons. We further show through optogenetic silencing that this representation is necessary for task performance after the task structure has already been acquired. Therefore, while the OFC representation is required for initial task acquisition, the mPFC representation is required for subsequent appetitive learning and performance. Why would a learned representation vanish in the OFC and betransfered elsewhere? We hypothesize that the brain may allocate a portion of its real estate to be a cognitive playground where experimentation and hypothesis testing takes place. Once this area solves a task, it may unload what it has learned to storage units located elsewhere to free up space to learn new tasks.
We further imaged another associative area, the basolateral amygdala (BLA), and found a representation of positive value that appears to be generated from a Hebbian learning mechanism. However, the silencing of this representation during learning had no effect. This suggests that while multiple and distributed brain areas encode cues that predict the reward, not all may be necessary for the learning process or for task performance.
In summary, we have described a series of experiments that map the representation and function of different associational areas that underlie learning. The data and the techniques employed have the potential to significantly advance the understanding of learned behavior.
33
Boušová, Jiřina. "Změny v Srdeční Frekvenci Novorozenců v Reakci na Odoranty s Relativně Silnou a Slabou Trigeminální Komponentou." Master's thesis, 2017. http://www.nusl.cz/ntk/nusl-267850.
Full textAbstract:
The widely accepted view nowadays is that experiencing odours as rather pleasant or unpleasant is, to a certain degree, shaped on a daily basis through individual experience within one's culture via evaluative conditioning or, rather marginally so, via mere exposure to that certain odour. In other words, humans are not born with any fixed set of olfactory likes or dislikes but rather, they acquire them throughout their lifetime. However, olfactory sensation is not a "pure" percept, as odorant stimuli generally elicit a qualitative percept of an odorant - generated mainly by the olfactory nerve - as well as some degree of chemesthesis - a tactile confound of the odour generated mainly by the trigeminal nerve. The olfactory and trigeminal system exhibit complex interactions at both the peripheral and central level of chemosensory processing, which is also reflected in perceptual characteristics of the final percept, including perceived pleasantness (hedonics). If the olfactory contribution alone does not easily predict neonatal odour hedonics, due to newborns' limited previous exposure to chemosensory inputs, one may hypothesize that together with the strength of the trigeminal contribution they may form a significant factor affecting neonatal appetitive/aversive responses to odours. In the present...
34
Baßfeld, Eiko. "Imaging-Analyse dopaminerger Wirkungen am olfaktorischen Nerven von Xenopus-laevis-Larven." Doctoral thesis, 2013. http://hdl.handle.net/11858/00-1735-0000-0001-BC25-7.
Full text
35
Hour, Naussicca Lakena. "Étude anatomique de la relation entre les neurones exprimant l’hormone de relâche des gonadotrophines et le nerf terminal lors du développement postnatal de l’opossum (Monodelphis domestica)." Thèse, 2017. http://hdl.handle.net/1866/19557.
Full textAbstract:
Quoique très immature à la naissance, l’opossum grimpe de l’orifice urogénital de la mère jusqu’à une tétine à laquelle il s’accroche pour poursuivre sa maturation. Des informations sensorielles sont nécessaires pour que l’animal atteigne la tétine et que le réflexe d’attachement soit déclenché. Une modalité sensorielle envisagée est l’olfaction. Or, des expériences physiologiques effectuées au laboratoire sur des préparations in vitro suggèrent que le système olfactif central est trop immature pour influencer les comportements moteurs. Une étude immunohistochimique employant un marqueur de maturité axonique (NF200) a montré une absence de marquage dans le cerveau antérieur, à l’exception d’un mince faisceau reliant les bulbes olfactifs aux régions caudales du cerveau. L’implication de l’olfaction dans les comportements du nouveau-né est donc peu probable, mais la présence de ce faisceau est intrigante et l’étude de son développement est approfondie dans le présent travail. Le développement du faisceau exprimant NF200 est décrit de la naissance jusqu’à la fin de la 2e semaine postnatale, âge auquel le marquage NF200 n’est plus observé à ce niveau. Il est aussi montré que le trajet de ce faisceau se superpose à celui de fibres nerveuses exprimant GnRH1, une neurohormone exprimée par des neurones hypothalamiques chez l’adulte. Les résultats indiquent que ce faisceau est le nerf terminal et pourrait servir de voie pionnière pour la croissance des fibres GnRH1. Aucun marquage NF200 dans le cortex olfactif n’est observé avant P15, supportant l’idée que le système olfactif n’influence pas les comportements de l’opossum nouveau-né.While quite immature at birth, the opossum is nevertheless able to crawl from the urogenital opening to a mother's nipple to which it attaches to pursue its development. Sensory information are required to guide the newborn to the nipple and induce attachment. Olfaction is one of the sensory modalities often proposed. However, recent physiological experiments in the laboratory using in vitro preparations suggest that the olfactory system is too immature to influence the newborn behaviors. Furthermore, an immunohistochemical study using a marker of axonal maturity (neurofilament 200kDa, NF200) has shown that the prosencephalon is nearly devoid of mature fibers except for a thin fascicle running from the olfactory bulbs to more caudal areas of the brain. Olfaction is thus unlikely to guide the locomotion of the newborn, but the presence of this fascicle is intriguing and its development is studied in the present thesis. This fascicle is described from the day of birth to the end of the second postnatal week, when NF200 labeling is no more visible in this region. It is also shown that this fascicle superpose with fibers expressing GnRH1, a neurohormone characterizing hypothalamic neurons in the adult. The results indicate that this fascicle is the terminal nerve, and might serve as a pioneer pathway to GnRH1 fibers cells. Until P15, the olfactory cortex was devoid of NF200 projections, supporting that the olfactory systems is too immature to influence the behavior of newborn opossums.
36
Atallah, Elias. "Transmission des voies olfactives aux cellules réticulospinales de la lamproie." Thèse, 2011. http://hdl.handle.net/1866/7056.
Full textAbstract:
Les informations olfactives sont connues pour leur capacité à induire des comportements moteurs spécifiques. En dépit de nombreuses observations comportementales chez les vertébrés, on ne connaît toujours pas les mécanismes et les voies nerveuses qui sous-tendent ces phénomènes de transformation olfacto-locomotrices. Chez la lamproie, des travaux récents ont permis de décrire cette voie, et les mécanismes responsables de la transformation des entrées olfactives en activité locomotrice (Derjean et al., 2010). Cette voie prend origine dans la partie médiane du bulbe olfactif, et envoie des projections vers le tubercule postérieur, une région qui se trouve dans le diencéphale. De là, les neurones projettent directement vers la Région Locomotrice Mésencéphalique, connue pour envoyer des connexions vers les neurones réticulospinaux, et activer la locomotion.
L’objectif de cette étude était d’établir si l’ensemble des neurones réticulospinaux répond aux stimulations olfactives. Pour ce faire, nous avons utilisé sur une préparation de cerveau isolé de lamproie des techniques d’électrophysiologie et d’imagerie calcique.
La stimulation électrique des nerfs olfactifs, de la région médiane du bulbe olfactif ou du tubercule postérieur a provoqué une activation de toutes les cellules réticulospinales qui se retrouvent dans les quatre noyaux réticulaires (ARRN : Noyau Réticulaire Rhombencéphalique Antérieur; MRN : Noyau Réticulaire Mésencéphalique; MRRN : Noyau Réticulaire Rhombencéphalique Moyen; PRRN : Noyau Réticulaire Rhombencéphalique Postérieur). Seule la partie médiane du bulbe olfactif est impliquée dans le passage de l’information olfactive vers les neurones réticulospinaux. Nous avons aussi découvert que le blocage des récepteurs GABAergiques dans la partie médiane du bulbe olfactif augmentait les réponses olfactives de façon considérable dans les cellules réticulospinales. Nous avons montré ainsi qu’il existe un tonus inhibiteur impliqué dans la dépression modulatrice de la voie olfacto-locomotrice.
Ce travail a permis de montrer que la stimulation des afférences sensorielles olfactives active simultanément l’ensemble des populations de neurones réticulospinaux qui commandent la locomotion. De plus, il existerait un tonus inhibiteur GABAergique, au niveau de la partie médiane du bulbe olfactif, responsable d’une dépression modulatrice dans la voie olfacto-locomotrice.Olfactory inputs are known for their ability to induce specific motor behaviors. Despite numerous behavioral observations in vertebrates, the mechanisms and the neural pathways underlying the olfactory-locomotor transformation are still unknown. In lamprey, recent studies have described this pathway and the mechanism underlying the transformation of olfactory input into a locomotor activity (Derjean et al., 2010). This pathway originates in the medial part of the olfactory bulb, sends projections to the posterior tuberculum, a diencephalic region. From there, the neurons project directly to the mesencephalic locomotor region that is known to send projections to the reticulospinal neurons to activate locomotion. Using lamprey brain preparation, electrophysiology and calcium imaging, the aim of this study was to establish whether all reticulospinal neurons respond to olfactory stimuli. Electrical stimulation of the olfactory nerves, the medial part of the olfactory bulb or the posterior tuberculum activates all reticulospinal cells in the four reticular nuclei (ARRN: Anterior rhombencephalic reticular nucleus; MRN: middle mesencephalic reticular nucleus; MRRN: middle rhombencephalic reticular nucleus; PRRN: posterior rhombencephalic reticular nucleus). The medial part of the olfactory bulb is the only region that is implicated in transmitting the olfactory information to reticulospinal neurons. We also discovered that when blocking the GABAergic receptors in the medial part of the olfactory bulb, the reticulospinal neurons have a stronger response to olfactory stimulation. Thus we showed that a tonic inhibition is involved in the modulating depression of the olfacto-locomotor pathway. Altogether, this work shows that stimulation of the olfactory sensory inputs activates simultaneously the entire population of reticulospinal neurons that control locomotion. In addition, there is a GABAergic tonic inhibition at the level of the medial part of the olfactory bulb that causes a modulating depression in the olfacto-locomotor pathway.
37
Beauséjour, Philippe-Antoine. "Modulation dopaminergique dans le système olfactif." Thèse, 2016. http://hdl.handle.net/1866/18905.
Full textAbstract:
Les figures de neuroanatomie de ce mémoire peuvent être téléchargées en haute résolution.Une voie neuronale sous-tendant la locomotion induite par la détection d’odorants a été découverte chez la lamproie (Derjean et al., 2010). Le signal olfactif est relayé du bulbe olfactif médian au tubercule postérieur, puis à la région locomotrice mésencéphalique et enfin aux cellules réticulospinales qui activent les réseaux locomoteurs spinaux. Des études récentes démontrent que le bulbe olfactif médian est sous l’influence d’une inhibition GABAergique tonique qui régule les réponses des cellules réticulospinales à la stimulation du nerf olfactif (Daghfous et al., 2013). Des mécanismes de modulation supplémentaires pourraient exister dans le bulbe olfactif de Petromyzon marinus puisqu’il contient aussi des fibres dopaminergiques. Chez tous les vertébrés étudiés, la dopamine joue un rôle important dans le traitement olfactif. Des techniques anatomiques (traçage et immunofluorescence) et physiologiques (enregistrements intracellulaires) ont été utilisées pour étudier la modulation dopaminergique de la voie olfacto-motrice. L’immunofluorescence ciblant la dopamine a révélé des fibres plus nombreuses dans la partie médiane du BO et à proximité de neurones de projection et de fibres olfactives. De plus, aucun corps cellulaire immunopositif n’a été détecté dans le bulbe olfactif. L’enregistrement des réponses synaptiques des cellules réticulospinales à la stimulation du nerf olfactif a été réalisé dans le cerveau isolé in vitro. L’injection locale de dopamine dans le bulbe olfactif médian diminue de moitié l’amplitude de réponse. Sous l’effet d’un antagoniste des récepteurs GABAA dans le bain ou localement dans le bulbe olfactif médian, les dépolarisations soutenues enregistrées sont supprimées par l’injection de dopamine. Cependant, l’injection individuelle ou combinée dans le bulbe olfactif médian d’antagonistes sélectifs des récepteurs D1 ou D2, soit le SCH 23390 et l’éticlopride, demeure sans effet significatif sur les réponses olfacto-motrices, indiquant l’absence d’activité dopaminergique tonique. Pour localiser les neurones responsables de cette modulation, des injections de traceur axonal ont été combinées avec l’immunofluorescence ciblant la dopamine. Des cellules dopaminergiques projetant au BO médian ont été observées dans les noyaux dopaminergiques du tubercule postérieur et de l’hypothalamus périventriculaire. Dans l’ensemble, nos résultats montrent anatomiquement et physiologiquement la présence d’une innervation dopaminergique dans le bulbe olfactif médian qui a une action inhibitrice sur le traitement olfacto-moteur.
A neural substrate underlying odor-evoked locomotion was revealed in lampreys (Derjean et al., 2010), involving a neural pathway extending from the medial part of the olfactory bulb to the posterior tuberculum. The signal is then relayed to the mesencephalic locomotor region and eventually reaches reticulospinal cells that activate the spinal locomotor networks. Recent research in the lab (Daghfous et al., 2013) shows that the medial olfactory bulb, is under a tonic GABAergic inhibition gating reticulospinal cell responses to olfactory nerve stimulation. Additional modulatory mechanisms might exist in the olfactory bulb of Petromyzon marinus as it also contains dopaminergic fibers. In every vertebrate studied to date, dopamine plays an important role in olfactory processing. Anatomical (axonal tracers and immunofluorescence) and physiological (intracellular recordings) techniques were used to investigate the dopaminergic modulation of the olfacto-motor pathway. Dopamine immunofluorescence showed scarce innervation of the olfactory bulb that was most abundant in the medial part and in close vicinity to projection neurons and olfactory nerve fibers. Additionally, no dopamine-immunoreactive cell bodies were detected in the olfactory bulb. Synaptic responses of reticulospinal cells to olfactory nerve stimulation were recorded in the isolated brain. Local injection of dopamine in the medial olfactory bulb induces an almost two-fold decrease of the synaptic responses. When GABAA receptor antagonist GABAzine was also injected in the medial olfactory bulb, the effect of dopamine was much more evident and could suppress large bursts of action potentials. However, D1 (SCH 23390) and D2 (Eticlopride) receptor antagonists injection in the medial olfactory bulb failed to alter the amplitude of reticulospinal cell responses to olfactory nerve stimulation, indicating that this modulation is not tonic. To locate the neurons responsible for this modulation, tracer injections combined with dopamine immunofluorescence were performed. Dopaminergic cells projecting to the medial olfactory bulb were found in the dopaminergic nuclei of the posterior tuberculum and the periventricular hypothalamus. Altogether, our results show anatomically and physiologically the presence of a dopaminergic innervation within the medial olfactory bulb that mediates inhibitory effects on olfacto-motor signaling.