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Journal articles on the topic 'Bulbectomie'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

Tashev, Roman E., Galya Tz Stavreva, and Margarita St Velikova. "Subchronic Central Administration of Cannabinoid Ligands Modulates Nociception in Bulbectomized Rats." Folia Medica 61, no. 4 (December 31, 2019): 540–44. http://dx.doi.org/10.3897/folmed.61.e47957.

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Introduction: Endocannabinoid system is involved in neuropsychiatric disorders such as major depression. The bilaterally olfactory bulbectomized rat is widely used as an animal model of depression. The removal of the olfactory bulbs produces behavioural, physiological, and neurochemical alterations resembling clinical depression. There is increasing evidence that highlights the important role of cannabinoid signalling in depression and nociception. Aim: To investigate the effect of CB1 receptor agonist HU 210 and CB1 receptor antagonist SR 141716A administered icv subchronically (for 7 days) on nociception of rats with model of depression - bilateral olfactory bulbectomy (OBX). Material and methods: Experimental model of depression - bilateral olfactory bulbectomy (OBX). Bilaterally olfactory bulbectomized rats were used as an experimental model of depression. HU 210 (5 µg) or SR 141716A (3 µg) were infused icv for 7 consecutive days, starting 15 days after the olfactory bulbectomy. Nociception was examined by applying paw pressure test (analgesy-meter) evaluating the rat pain threshold. On day 7, five minutes after the last microinjection, the rats were tested in an analgesy-meter and their mechanically evoked pain responses were measured in arbitrary units (AU). Results: Microinjections of HU 210 (5 µg) significantly decreased the pain threshold in olfactory bulbectomized rats, while SR 141716A (3 µg) exerted antinociceptive effect by increasing the pain threshold. Conclusions: Data point to an involvement of CB1 receptors in depression-like behaviour and nociception in olfactory bulbectomized rats and support the data for the association between depressive disorder and pain pathways.

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2

Conley, David B., Alan M. Robinson, Michael J. Shinners, and Robert C. Kern. "Age-Related Olfactory Dysfunction: Cellular and Molecular Characterization in the Rat." American Journal of Rhinology 17, no. 3 (May 2003): 169–75. http://dx.doi.org/10.1177/194589240301700311.

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Background Olfactory receptor neurons (ORNs) undergo apoptosis at a baseline rate even in the absence of obvious disease. Although the precise triggers of the apoptotic cascade are unclear, ORNs are exposed directly to the external environment, making them susceptible to injury. As an adaptive mechanism, mammals have the ability to replace lost ORNs throughout adult life from neuronal precursors within the olfactory epithelium (OE). In humans, this process fails with age as the surface area of the OE and the number of ORNs decline, coupled with a loss of clinical olfactory function. The question addressed in this study is whether this age-related failure of olfactory sensation is a result of a decrease in neuronal proliferation or an increase in ORN cell death. Methods To begin to address this question the ribonuclease protection assay was used to assess expression of apoptosisrelated genes in rat OE as a function of age. Second, the terminal deoxynucleotide transferase end labeling assay was used to assess the percentage of ORNs undergoing apoptosis (apoptotic index) in three groups of animals: young (12 weeks), old (32 months), and bulbectomized rats. Bulbectomy is a standard model for ORN injury associated with a massive increase in ORN apoptosis and serves as a positive control. Results Ribonuclease protection assay data indicate an age-related increase in Bax, Bcl-xL, and procaspase-3 messenger RNA expression in aged compared with young rats. A similar but more pronounced increase in expression of these apoptotic-related genes is seen after bulbectomy. The terminal deoxynucleotide transferase end labeling assay also showed a statistically significant increase in the apoptotic index with both age and bulbectomy. Conclusion Taken together, the current results indicate that aging and injury induce parallel changes in OE. Furthermore, these findings support the hypothesis that age-related olfactory dysfunction is, at least in part, related to an increase in ORN cell death.

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3

Bansal, Y., A. Kuhad, R. Singh, and P. Saroj. "Targeting Kynurenine Pathway in Olfactory Bulbectomised Mice: Inflammatory and Neurodegerative Pathway of Depression." European Psychiatry 41, S1 (April 2017): s140. http://dx.doi.org/10.1016/j.eurpsy.2017.01.1972.

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Aims and objectivesThe aim of study was to evaluate the pharmacotherapeutic efficacy of NDGA in experimental paradigm of depression i.e. olfactory bulbectomy (OB) specifically targeting kynurenine pathway.Materials and methodDepression like behaviours was induced in OB mice and evaluated by assessment of various behavioural (olfactory deficit test, forced swim test, splash test, open field test, sucrose preference test), biochemical (catalase, reduced glutathione, SOD, nitrite, MAO-A, MDA, corticosterone), inflammatory cytokines (TNF- α, IL-1β, IL-6, IFN-γ) levels and alterations in delta sleep was recorded using EEG. Kynurenine pathway metabolites were determined in plasma and brain using HPLC method. After 14 days post-surgery, olfactory bulbectomized (OBX) mice were administered nordihydroguaiaretic acid (5 mg/kg, 10 mg/kg and 25 mg/kg) daily i.p.ResultsWe have developed a new HPLC method for simultaneous estimation of monoamines and kynurenine pathway metabolites in plasma and brain samples of mice. Chronic treatment with nordihydroguaiaretic acid significantly restored all behavioural, biochemical and neurochemical alterations in OBX mice and increase in quinolinic acid and decrease in kynurenic acid point out the neurodegeneration hypothesis of depression.ConclusionNordihydroguaiaretic acid showed potent neuropharmacotherapeutic effect in OBX mice by virtue of its strong anti-oxidant, anti-inflammatory, anti-stress and by restoring quinolinic acid levels.

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4

Makino, N., S. Ookawara, S. Madoiwa, Y. Ohta, T. Ishikawa, K. Katoh, S. Takigami, et al. "Morphological assessment of the luminal surface of olfactory epithelium in mice deficient in tissue plasminogen activator following bulbectomy." Journal of Laryngology & Otology 126, no. 11 (September 19, 2012): 1114–20. http://dx.doi.org/10.1017/s002221511200206x.

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AbstractObjective:This study aimed to investigate the function of tissue plasminogen activator in the olfactory epithelium of mice following neural injury.Method:Transmission electron microscopy was used to study the changes in the morphology of the olfactory epithelium 1–7 days after surgical ablation of the olfactory bulb (bulbectomy).Results:Prior to bulbectomy, a uniformly fine material was observed within some regions of the olfactory epithelium of mice deficient in tissue plasminogen activator. At 2–3 days after bulbectomy, there were degenerative changes in the olfactory epithelium. At 5–7 days after bulbectomy, we noted drastic differences in olfactory epithelium morphology between mice deficient in tissue plasminogen activator and wild-type mice (comparisons were made using findings from a previous study). The microvilli seemed to be normal and olfactory vesicles and receptor neuron dendrites were largely intact in the olfactory epithelium of mice deficient in tissue plasminogen activator.Conclusion:The tissue plasminogen activator plasmin system may inhibit the regeneration of the olfactory epithelium in the early stages following neural injury.

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5

Burke, Nikita N., Yan Li, Daniel R. Deaver, David P. Finn, Michelle Roche, David J. Eyerman, Connie Sanchez, and John P. Kelly. "Chronic administration of buprenorphine in combination with samidorphan produces sustained effects in olfactory bulbectomised rats and Wistar-Kyoto rats." Journal of Psychopharmacology 33, no. 12 (September 12, 2019): 1620–27. http://dx.doi.org/10.1177/0269881119872203.

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Background: The combination of buprenorphine, a partial mu-opioid receptor agonist and a functional kappa-opioid receptor antagonist, with samidorphan, a functional mu-opioid receptor antagonist, is being developed as an adjunct therapy for major depressive disorder, in order to harness the mood-enhancing effects of opioids without unwanted side-effects such as a risk of addiction. Acute and subacute administration of the combination of buprenorphine and samidorphan is effective in reducing forced swim immobility in the Wistar-Kyoto rat, but the chronic effects have not been examined. Aims and methods: The purpose of this study was to assess if chronic (14-day) administration of buprenorphine (0.1 mg/kg, subcutaneous) alone or in combination with samidorphan (0.3 mg/kg, subcutaneous) maintains antidepressant-like activity in the olfactory bulbectomised rat model and the Wistar-Kyoto rat, two models that exhibit ongoing behavioural deficits in tests commonly used to study effects of antidepressants. Results: Olfactory bulbectomised-induced hyperactivity was attenuated by chronic administration of buprenorphine alone and in combination with samidorphan, to that of sham control activity levels. Neither buprenorphine nor samidorphan altered stress-associated defecation in sham or olfactory bulbectomised rats in the open field. In Wistar-Kyoto rats, buprenorphine alone significantly reduced forced swim immobility and increased locomotor activity three hours post-final dosing. Buprenorphine plus samidorphan significantly reduced forced swim immobility without changing locomotor activity at this time point. Buprenorphine alone also significantly reduced forced swim immobility 24 h post-final dosing. Conclusion: Chronic treatment of buprenorphine alone or buprenorphine plus samidorphan is effective in reversing behavioural deficits in distinct non-clinical paradigms. These non-clinical results complement the antidepressant effect of this combination observed in clinical studies.

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6

Slotnick, B. "Olfaction in Olfactory Bulbectomized Rats." Journal of Neuroscience 24, no. 41 (October 13, 2004): 9195–200. http://dx.doi.org/10.1523/jneurosci.1936-04.2004.

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7

Novoselova, E. G., N. V. Bobkova, O. A. Sinotova, V. B. Ogai, O. V. Glushkova, N. I. Medvinskaya, and A. N. Samokhin. "The Immune State of Bulbectomized Mice." Doklady Biological Sciences 393, no. 1-6 (November 2003): 505–7. http://dx.doi.org/10.1023/b:dobs.0000010308.59629.c0.

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8

Novoselova, E. G., N. V. Bobkova, O. V. Glushkova, O. A. Sinotova, V. B. Ogai, N. I. Medvinskaya, and A. N. Samokhin. "Immunodepressed Status of Mice after Bulbectomy." Biology Bulletin 31, no. 6 (November 2004): 613–19. http://dx.doi.org/10.1023/b:bibu.0000049734.07925.d8.

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9

Grecksch, Gisela, and Axel Becker. "Alterations of reward mechanisms in bulbectomised rats." Behavioural Brain Research 286 (June 2015): 271–77. http://dx.doi.org/10.1016/j.bbr.2015.03.015.

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10

Perret, M., and A. Schilling. "Response to short photoperiod and spontaneous sexual recrudescence in the lesser mouse lemur: role of olfactory bulb removal." Journal of Endocrinology 137, no. 3 (June 1993): 511–18. http://dx.doi.org/10.1677/joe.0.1370511.

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ABSTRACT The body weight and sexual activity of the male lesser mouse lemur, a prosimian primate, undergo cyclic changes that are photoperiod-dependent. Exposure to long daylength (LD; 14 h light/day) led to sustained sexual activity, fully developed testes and high plasma testosterone concentrations (228 ±25 nmol/l, n = 10). After 14 weeks under LD, a marked decrease in testosterone levels occurred. Gonadal regression was completed within 20 weeks under LD without concomitant changes in body weight. Exposure to short daylength (SD; 8 h light/day) reinforced the sexual quiescence and was associated with a high ponderal gain (from 60 to 110 g). However, independent of the date of gonadal arrest, the sexual activity of males spontaneously resumed at a fixed time after exposure to SD. The testes developed, testosterone concentrations increased to 155 nmol/l and the body weight decreased (from 110 to 80 g) within 20 weeks under SD exposure. The timing for refractoriness appeared very similar under inhibitory and stimulatory photoperiods. This is consistent with the hypothesis that the perception of a critical daylength is used to regulate the timing of the following sexual phase through a mechanism involving photorefractoriness. Contrary to cricetid rodents, a direct response to photoperiodic signals for both body weight and sexual activity were not prevented by olfactory bulb removal in male mouse lemurs. In bulbectomized males (n = 12), sexual activity was stimulated by LD and inhibited by SD. Their plasma testosterone levels, however, significantly differed from those of controls in both photoperiods. Likewise, ponderal cycles remained intact but the fattening phase was delayed and reduced. Finally, whereas the sexual recrudescence of bulbectomized males occurred under SD with a delay of only 2–4 weeks, spontaneous testicular regression under exposure to LD did not appear in our experimental photoperiodic conditions. Journal of Endocrinology (1993) 137, 511–518

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11

Brunjes, Peter C. "Lessons from lesions: the effects of olfactory bulbectomy." Chemical Senses 17, no. 6 (1992): 729–63. http://dx.doi.org/10.1093/chemse/17.6.729.

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12

Moffitt, Julia A., Angela J. Grippo, Philip V. Holmes, and Alan Kim Johnson. "Olfactory bulbectomy attenuates cardiovascular sympathoexcitatory reflexes in rats." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (December 1, 2002): H2575—H2583. http://dx.doi.org/10.1152/ajpheart.00164.2002.

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Bilateral removal of the olfactory lobes in rats produces a number of behavioral, endocrine, and neurochemical alterations in the brain. Little is known, however, regarding the effects of this treatment on cardiovascular function and autonomic reflexes. Male Sprague-Dawley rats underwent bilateral surgical ablation of the olfactory bulbs ( n = 10) or were sham operated ( n = 8). After 3 wk of recovery, animals were instrumented with femoral catheters and a lumbar sympathetic nerve recording electrode. After 24 h of recovery, cardiovascular responses to arterial baroreflex manipulation, air jet stress, and smoke exposure were recorded. Olfactory bulbectomized rats demonstrated attenuated sympathoexcitatory responses to hypotension, air jet stress, and smoke exposure, as well as elevated basal blood pressure, compared with sham-operated rats. These data indicate that the integrity of the olfactory bulbs in rats is important for the elicitation of normal cardiovascular and autonomic responses to a number of evocative stimuli.

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13

MORRISON, EDWARD E., PASQUALE P. C. GRAZIADEI, and RICHARD M. COSTANZO. "Degeneration-Regeneration of the Olfactory Neuroepithelium Following Bulbectomy." Annals of the New York Academy of Sciences 510, no. 1 Olfaction and (November 1987): 512–14. http://dx.doi.org/10.1111/j.1749-6632.1987.tb43608.x.

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14

Coppola, David M., and R. Parrish Waters. "The olfactory bulbectomy disease model: A Re-evaluation." Physiology & Behavior 240 (October 2021): 113548. http://dx.doi.org/10.1016/j.physbeh.2021.113548.

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15

Song, Cai, and Brian E. Leonard. "The olfactory bulbectomised rat as a model of depression." Neuroscience & Biobehavioral Reviews 29, no. 4-5 (January 2005): 627–47. http://dx.doi.org/10.1016/j.neubiorev.2005.03.010.

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16

Ivanova, Margarita, Stiliana Belcheva, Iren Belcheva, and Roman Tashev. "Locomotor responses to vasoactive intestinal peptide in bulbectomized rats." Scripta Scientifica Medica 45, no. 4 (December 19, 2013): 31. http://dx.doi.org/10.14748/ssm.v45i4.230.

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17

Tews, Jean K., Joyce J. Repa, Hoang Nguyen, and Alfred E. Harper. "Avoidance of GABA-containing diets by olfactory bulbectomized rats." Physiology & Behavior 34, no. 6 (June 1985): 983–86. http://dx.doi.org/10.1016/0031-9384(85)90024-1.

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18

Risser, Judith M., and Burton M. Slotnick. "Nipple attachment and survival in neonatal olfactory bulbectomized rats." Physiology & Behavior 40, no. 4 (January 1987): 545–49. http://dx.doi.org/10.1016/0031-9384(87)90042-4.

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19

Zueger, M., A. Urani, S. Chourbaji, C. Zacher, M. Roche, A. Harkin, and P. Gass. "Olfactory bulbectomy in mice induces alterations in exploratory behavior." Neuroscience Letters 374, no. 2 (February 2005): 142–46. http://dx.doi.org/10.1016/j.neulet.2004.10.040.

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20

Mucignat-Caretta, Carla, Michela Bondí, and Antonio Caretta. "Time course of alterations after olfactory bulbectomy in mice." Physiology & Behavior 89, no. 5 (December 2006): 637–43. http://dx.doi.org/10.1016/j.physbeh.2006.08.003.

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21

Clancy, Andrew N., Bruce D. Goldman, Andrzej Bartke, and Foteos Macrides. "Reproductive Effects of Olfactory Bulbectomy in the Syrian Hamster1." Biology of Reproduction 35, no. 5 (December 1, 1986): 1202–9. http://dx.doi.org/10.1095/biolreprod35.5.1202.

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22

Fulk, L. J., H. S. Stock, J. M. Davis, P. R. Burghardt, and G. A. Hand. "EXERCISE TRAINING REDUCES OLFACTORY BULBECTOMY-INDUCED ANXIETY IN RATS." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S178. http://dx.doi.org/10.1097/00005768-200105001-01012.

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23

Gary, Devin S., Thomas V. Getchell, Marilyn L. Getchell, and Mark P. Mattson. "Olfactory Bulbectomy Protects Hippocampal Pyramidal Neurons against Excitotoxic Death." Experimental Neurology 176, no. 1 (July 2002): 266–68. http://dx.doi.org/10.1006/exnr.2002.7925.

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24

Chambers, R. Andrew, Teige Sheehan, and Jane R. Taylor. "Locomotor sensitization to cocaine in rats with olfactory bulbectomy." Synapse 52, no. 3 (2004): 167–75. http://dx.doi.org/10.1002/syn.20017.

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25

Lumia, Augustus R., Martin H. Teicher, Frederic Salchli, Elise Ayers, and Bernard Possidente. "Olfactory bulbectomy as a model for agitated hyposerotonergic depression." Brain Research 587, no. 2 (August 1992): 181–85. http://dx.doi.org/10.1016/0006-8993(92)90995-l.

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26

Suzuki, Yuko, Joshua Schafer, and Albert I. Farbman. "Phagocytic Cells in the Rat Olfactory Epithelium after Bulbectomy." Experimental Neurology 136, no. 2 (December 1995): 225–33. http://dx.doi.org/10.1006/exnr.1995.1099.

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27

Inamitsu, Mayumi, Tadashi Nakashima, and Takuya Uemura. "Immunopathology of olfactory mucosa following injury to the olfactory bulb." Journal of Laryngology & Otology 104, no. 12 (December 1990): 959–64. http://dx.doi.org/10.1017/s0022215100114483.

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AbstractRemoval of the olfactory bulb was performed on rats in an attempt to elucidate the processes of olfactory dysfunction following head injury. Degeneration and regeneration of the olfactory mucosa were examined, histopathologically and immunohistochemically. We used antisera to olfactory marker protein (OMP) and neuron specific enolase (NSE) as a marker of the mature olfactory receptor neurons. Following rapid degeneration after bulbectomy, the olfactory receptor neurons regenerated. OMP and NSE containing cells re-appeared 49 days later. However, the cell population of the neuroepithelium did not revert to the numbers observed in the non-operated neuroepithelium, even three months later. The lack of a connection between regenerated axons and the olfactory bulb may result in immature neuronal replacement and reduce the number of olfactory receptor neurons.

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28

Velikova, Margarita, Dobrinka Doncheva, and Roman Tashev. "EFFECTS OF RIMONABANT ON ACTIVE AVOIDANCE LEARNING IN BULBECTOMIZED RATS." Journal of IMAB - Annual Proceeding (Scientific Papers) 26, no. 1 (February 24, 2020): 2936–41. http://dx.doi.org/10.5272/jimab.2020261.2936.

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29

YAMAMOTO, Yui, Norifumi SHIODA, Feng HAN, Shigeki MORIGUCHI, and Kohji FUKUNAGA. "Donepezil-induced Neuroprotection of Acetylcholinergic Neurons in Olfactory Bulbectomized Mice." YAKUGAKU ZASSHI 130, no. 5 (May 1, 2010): 717–21. http://dx.doi.org/10.1248/yakushi.130.717.

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30

Pawar, AnilT, GayatriD Gaikwad, and BhanudasS Kuchekar. "Antidepressant effect of Hedyotis corymbosa extract in olfactory bulbectomy rats." Pharmacognosy Research 10, no. 2 (2018): 213. http://dx.doi.org/10.4103/pr.pr_118_17.

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31

NAGATANI, Tadashi, Tsuneyuki YAMAMOTO, Katsuyuki TAKAO, Taisuke SUGIHARA, and Showa UEKI. "β-CCM Inhibits Muricide Induced by Olfactory Bulbectomy in Rats." Japanese Journal of Pharmacology 52, no. 3 (1990): 441–47. http://dx.doi.org/10.1016/s0021-5198(19)40037-1.

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32

Primeaux, Stefany Deprato, and Philip V. Holmes. "Role of Aversively Motivated Behavior in the Olfactory Bulbectomy Syndrome." Physiology & Behavior 67, no. 1 (August 1999): 41–47. http://dx.doi.org/10.1016/s0031-9384(99)00027-x.

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33

Ra?ekov�, Enik�, Judita Orend�?ov�, Marcela Marton?ikov�, Tanja Zigova, Gabriela Sekerkova, and Jozef Mar?ala. "Developmental characteristics in adult forebrain following neonatal unilateral olfactory bulbectomy." Neuroscience Research Communications 31, no. 1 (July 2002): 1–9. http://dx.doi.org/10.1002/nrc.10032.

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34

Suzuki, Yuko, Masako Takeda, and Albert I. Farbman. "Supporting cells as phagocytes in the olfactory epithelium after bulbectomy." Journal of Comparative Neurology 376, no. 4 (December 23, 1996): 509–17. http://dx.doi.org/10.1002/(sici)1096-9861(19961223)376:4<509::aid-cne1>3.0.co;2-5.

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35

Jiang, Yifei, Raymund Y. K. Pun, Katrina Peariso, Katherine D. Holland, Qingquan Lian, and Steve C. Danzer. "Olfactory Bulbectomy Leads to the Development of Epilepsy in Mice." PLOS ONE 10, no. 9 (September 14, 2015): e0138178. http://dx.doi.org/10.1371/journal.pone.0138178.

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36

NAGATANI, Tadashi, Tsuneyuki YAMAMOTO, Katsuyuki TAKAO, Taisuke SUGIHARA, and Showa UEKI. ".BETA.-CCM inhibits muricide induced by olfactory bulbectomy in rats." Japanese Journal of Pharmacology 52, no. 3 (1990): 441–47. http://dx.doi.org/10.1254/jjp.52.441.

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37

Kang, Hye-Min, Jizi Jin, Seungjoo Lee, Jonghoon Ryu, and Chan Park. "A novel method for olfactory bulbectomy using photochemically induced lesion." NeuroReport 21, no. 3 (February 2010): 179–84. http://dx.doi.org/10.1097/wnr.0b013e328334884c.

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38

Slotkin, Theodore A., and Frederic J. Seidler. "Cholinergic receptor subtypes in the olfactory bulbectomy model of depression." Brain Research Bulletin 68, no. 5 (January 2006): 341–45. http://dx.doi.org/10.1016/j.brainresbull.2005.09.005.

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39

Konzelmann, S., Diane Saucier, Jörg Strotmann, Heinz Breer, and Liliane Astic. "Decline and recovery of olfactory receptor expression following unilateral bulbectomy." Cell and Tissue Research 294, no. 3 (November 3, 1998): 421–30. http://dx.doi.org/10.1007/s004410051193.

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40

Bissette, Garth. "Effects of sertraline on regional neuropeptide concentrations in olfactory bulbectomized rats." Pharmacology Biochemistry and Behavior 69, no. 1-2 (May 2001): 269–81. http://dx.doi.org/10.1016/s0091-3057(01)00513-5.

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41

Kelly, J. P., A. S. Wrynn, and B. E. Leonard. "The olfactory bulbectomized rat as a model of depression: An update." Pharmacology & Therapeutics 74, no. 3 (January 1997): 299–316. http://dx.doi.org/10.1016/s0163-7258(97)00004-1.

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42

Nakagawasai, Osamu, Kotaro Yamada, Takayo Odaira, Wakana Sakuma, Wataru Nemoto, Hidetomo Sakurai, and Koichi Tan-No. "Liver hydrolysate produces antidepressant and antidementia effects in olfactory bulbectomized mice." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO3–1–16. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po3-1-16.

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43

Odaira, Takayo, Osamu Nakagawasai, Wataru Nemoto, Kohei Takahashi, Wakana Sakuma, Ryotaro Ono, and Koichi Tan-No. "Hippocampal AMPK activation suppresses depressive-like behavior in olfactory bulbectomized mice." Proceedings for Annual Meeting of The Japanese Pharmacological Society WCP2018 (2018): PO3–1–31. http://dx.doi.org/10.1254/jpssuppl.wcp2018.0_po3-1-31.

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44

Aleksandrova, I. Yu, V. V. Kuvichkin, I. A. Kashparov, N. I. Medvinskaya, I. V. Nesterova, S. M. Lunin, A. N. Samokhin, and N. V. Bobkova. "Increased Level of β-Amyloid in the Brain of Bulbectomized Mice." Biochemistry (Moscow) 69, no. 2 (February 2004): 176–80. http://dx.doi.org/10.1023/b:biry.0000018948.04559.ab.

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45

Komori, T., M. Yamamoto, T. Matsumoto, K. Zhang, and Y. Okazaki. "Effects of Imipramine on T Cell Subsets in Olfactory Bulbectomized Mice." Neuropsychobiology 46, no. 4 (2002): 194–96. http://dx.doi.org/10.1159/000067811.

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46

Redmond, A. M., J. P. Kelly, and B. E. Leonard. "The NMDA receptor and the olfactory bulbectomised rat model of depression." European Neuropsychopharmacology 6 (September 1996): S4–87—S4–88. http://dx.doi.org/10.1016/0924-977x(96)83239-1.

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47

Mar, Adam, Emma Spreekmeester, and Joseph Rochford. "Antidepressants preferentially enhance habituation to novelty in the olfactory bulbectomized rat." Psychopharmacology 150, no. 1 (May 24, 2000): 52–60. http://dx.doi.org/10.1007/s002130000400.

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48

Uzunova, Veska, Aileen S. Wrynn, Anu Kinnunen, Melanie Ceci, Christian Kohler, and Doncho P. Uzunov. "Chronic antidepressants reverse cerebrocortical allopregnanolone decline in the olfactory-bulbectomized rat." European Journal of Pharmacology 486, no. 1 (February 2004): 31–34. http://dx.doi.org/10.1016/j.ejphar.2003.12.002.

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Takahashi, Kohei, Osamu Nakagawasai, Takeharu Nakajima, Myu Okubo, Yuki Nishimura, Wakana Sakuma, Ryota Yamagata, et al. "Dopamine D2 receptor supersensitivity in the hypothalamus of olfactory bulbectomized mice." Brain Research 1746 (November 2020): 147015. http://dx.doi.org/10.1016/j.brainres.2020.147015.

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Gomita, Yutaka, Nobuya Ogawa, and Showa Ueki. "Effects of psychotropic drugs on discrimination conditioning in olfactory bulbectomized rats." Pharmacology Biochemistry and Behavior 22, no. 5 (May 1985): 717–22. http://dx.doi.org/10.1016/0091-3057(85)90519-2.

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