Gotowa bibliografia na temat „Fear-potentiated startle”
Utwórz poprawne odniesienie w stylach APA, MLA, Chicago, Harvard i wielu innych
Zobacz listy aktualnych artykułów, książek, rozpraw, streszczeń i innych źródeł naukowych na temat „Fear-potentiated startle”.
Przycisk „Dodaj do bibliografii” jest dostępny obok każdej pracy w bibliografii. Użyj go – a my automatycznie utworzymy odniesienie bibliograficzne do wybranej pracy w stylu cytowania, którego potrzebujesz: APA, MLA, Harvard, Chicago, Vancouver itp.
Możesz również pobrać pełny tekst publikacji naukowej w formacie „.pdf” i przeczytać adnotację do pracy online, jeśli odpowiednie parametry są dostępne w metadanych.
Artykuły w czasopismach na temat "Fear-potentiated startle"
Paschall, Gayla Y., i Michael Davis. "Olfactory-mediated fear-potentiated startle." Behavioral Neuroscience 116, nr 1 (2002): 4–12. http://dx.doi.org/10.1037/0735-7044.116.1.4.
Pełny tekst źródłaHamm, Alfons O., Mark K. Greenwald, Margaret M. Bradley, Bruce N. Cuthbert i Peter J. Lang. "The fear potentiated startle effect". Integrative Physiological and Behavioral Science 26, nr 2 (kwiecień 1991): 119–26. http://dx.doi.org/10.1007/bf02691034.
Pełny tekst źródłaMccaughran, James A., James Bell i Robert J. Hitzemann. "Fear-Potentiated Startle Response in Mice". Pharmacology Biochemistry and Behavior 65, nr 2 (luty 2000): 301–12. http://dx.doi.org/10.1016/s0091-3057(99)00216-6.
Pełny tekst źródłaPatrick, Christopher J., Bryan D. Berthot i J. David Moore. "Diazepam blocks fear-potentiated startle in humans." Journal of Abnormal Psychology 105, nr 1 (luty 1996): 89–96. http://dx.doi.org/10.1037/0021-843x.105.1.89.
Pełny tekst źródłaDAVIS, MICHAEL. "Neural Systems Involved in Fear-Potentiated Startle". Annals of the New York Academy of Sciences 563, nr 1 Modulation of (czerwiec 1989): 165–83. http://dx.doi.org/10.1111/j.1749-6632.1989.tb42197.x.
Pełny tekst źródłaPaschall, G. Y. "Second-Order Olfactory-Mediated Fear-Potentiated Startle". Learning & Memory 9, nr 6 (1.11.2002): 395–401. http://dx.doi.org/10.1101/lm.50602.
Pełny tekst źródłaMorgan, C. A., Christian Grillon, Steven M. Southwick, Michael Davis i Dennis S. Charney. "Fear-potentiated startle in posttraumatic stress disorder". Biological Psychiatry 38, nr 6 (wrzesień 1995): 378–85. http://dx.doi.org/10.1016/0006-3223(94)00321-s.
Pełny tekst źródłaSilva, R. C. B., A. P. M. Cruz, V. Avanzi, J. Landeira-Fernandez i M. L. Brandão. "Distinct Contributions of Median Raphe Nucleus to Contextual Fear Conditioning and Fear-Potentiated Startle". Neural Plasticity 9, nr 4 (2002): 233–47. http://dx.doi.org/10.1155/np.2002.233.
Pełny tekst źródłaJovanovic, Tanja, Megan Keyes, Ana Fiallos, Karyn M. Myers, Michael Davis i Erica J. Duncan. "Fear Potentiation and Fear Inhibition in a Human Fear-Potentiated Startle Paradigm". Biological Psychiatry 57, nr 12 (czerwiec 2005): 1559–64. http://dx.doi.org/10.1016/j.biopsych.2005.02.025.
Pełny tekst źródłaFalls, William A., i Michael Davis. "Fear-potentiated startle using three conditioned stimulus modalities". Animal Learning & Behavior 22, nr 4 (grudzień 1994): 379–83. http://dx.doi.org/10.3758/bf03209157.
Pełny tekst źródłaRozprawy doktorskie na temat "Fear-potentiated startle"
Pissiota, Anna. "Fear, Startle, and Fear-Potentiated Startle : Probing Emotion in the Human Brain". Doctoral thesis, Uppsala University, Department of Psychology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3479.
Pełny tekst źródłaThe present thesis explored the neurobiological basis of three aspects of defense behaviors in humans. Positron emission tomography methodology was used, and changes in regional cerebral blood flow (rCBF) were measured as an index of neural activity. Firstly, brain function was studied in a group of patients suffering from combat-related posttraumatic stress disorder, using a symptom provocation paradigm with combat sounds in order to elicit fear. Exposure to auditory trauma reminders relative to neutral sounds was associated with increased rCBF in sensorimotor areas, the cerebellar vermis, the periaqueductal gray matter, and the right amygdala, whereas decreased activity was observed in the retrosplenial area of the posterior cingulate cortex. Secondly, the neural circuitry mediating the acoustic startle response and its habituation was studied in a group of healthy subjects. During acoustic startle stimulation as compared to a resting condition, increased rCBF was found in a medial posterior area of the pons corresponding to the nucleus reticularis pontis caudalis. As a result of startle repetition, altered activity was found in the cerebellum, pointing to its involvement in startle habituation. Thirdly, neural activity associated with startle modulation by phobic fear was studied in a group of subjects with specific animal phobias during exposure to pictures of their feared and non-feared objects, paired and unpaired with acoustic startle stimuli. As a result of startle potentiation, increased rCBF was found in the left amygdaloid-hippocampal region, and medially in the affective division of the anterior cingulate cortex. In conclusion, these results provide evidence for the involvement of limbic and paralimbic brain areas during fear provocation and fear-potentiated startle and for a similar neurocircuitry underlying startle in humans and animals.
Yap, Carol Sue Lynn Psychology Faculty of Science UNSW. "An analysis of late-developing learning and memory systems in rats: fear-potentiated startle and context-specific latent inhibition and extinction". Awarded by:University of New South Wales. Psychology, 2006. http://handle.unsw.edu.au/1959.4/24374.
Pełny tekst źródłaGreba, Quentin Matthew Luke. "The involvement of amygdala neurons and amygdaloid dopaminergic and glutamatergic receptors in the acquisition and reinstatement of fear-potentiated startle in rats". Thesis, University of Canterbury. Psychology, 2005. http://hdl.handle.net/10092/6174.
Pełny tekst źródłaColombo, Ana Caroline. "Papel dos receptores dopaminérgicos D1 e D2 do colículo inferior na expressão de respostas incondicionadas e condicionadas de medo". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-11042014-095621/.
Pełny tekst źródłaThe inferior colliculus (IC) is a structure primarily involved in acoustic information processing, but it also participates in the integration of the sensory, autonomic and behavioral aspects of the defensive reaction to threatening situations. Furthermore, this structure has a high concentration of dopamine receptors, and dopamine is one of the most active neuromodulators in the mechanisms underlying states of fear and anxiety. Thus, the aim of this study was to evaluate the role of IC dopamine receptors (D1 and D2) in the expression of unconditioned and conditioned defensive responses. For this purpose, male Wistar rats (±270 g, n=186) were implanted with bilateral guide cannuli directed to the IC. These animals received intraIC quinpirole (D2 agonist), sulpiride (D2 antagonist), SKF 38393 (D1 agonist) or SCH 23390 (D1 antagonist) at different doses, and were tested in the elevated plus maze (EPM) and the open field tests. A single dose of sulpiride was also evaluated in the fear potentiated startle test (FPS). In the EPM test, it was observed that only sulpiride decreased the numbers of entries and time spent in the open arms of the maze, suggesting an ansiogenic-like effect. The other drugs did not influence these defensive responses. Impairment in motor performance was observed with intraIC quimpirole (decrease in closed arm entries) and SCH 23390 (decrease in locomotion in the open field test). In the FPS test, no significant effects in the amplitude of the startle response and freezing behavior were observed. The data point to an involvement of IC dopaminergic D2-like receptors in the expression of unconditioned fear responses. Dopamine in the IC, therefore, seems to be important for regulating the expression of these responses. On the other hand, there was no evidence that this modulation in the IC is involved in the expression of conditioned fear responses. Therefore, the influence of the dopaminergic neurotransmission in the IC on the expression of defensive responses appears to occur via D2-like receptors, which selectively modulate unconditional fear responses.
Borowski, Thomas Brian. "The role of ventral tegmental dopamine neurons and the effects of central and peripheral dopamine agonists on fear motivation as measured by the potentiated acoustic startle reflex in rats". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq24006.pdf.
Pełny tekst źródłaOliveira, Amanda Ribeiro de. "Mecanismos dopaminérgicos na aquisição e expressão do medo condicionado: envolvimento de receptores D1 e D2". Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-30032006-144132/.
Pełny tekst źródłaThe increase in the startle reflex in the presence of a stimulus that has been previously paired to footshock is taken as an index of fear and named fear potentiated startle (FPS). Freezing behavior, a cessation of all observable movements, except those associated with respiration, has also been used as an index of fear in rats. A growing body of evidence has suggested that dopaminergic mechanisms are implicated in different aspects of affective memory, namely its formation, expression or retrieval. However, the results of studies that have examined how, and through which receptors, dopaminergic mechanisms influence fear have been inconsistent. This work is aimed at examining the involvement of dopaminergic receptors in the acquisition and expression of conditioned fear to ligth-CS. We evaluated the effects of systemic administration of the D1 antagonist, SCH 23390, the D1 agonist, SKF 38393, the D2 antagonist, sulpiride, and the D2 agonist, quinpirole before and after conditioning on FPS and freezing. The motor activity of the animals was also evaluated in an open field test. SCH 23390, SKF 38393, sulpiride and quinpirole, injected before conditioning sessions, did not produce any effect on FPS, but SCH 23390 decreased freezing. Injections of SCH 23390, SKF 38393 and sulpiride before testing session did not produce any effect on FPS or freezing. Quinpirole, injected at doses acting at presynaptic level, caused significant reduction in FPS and freezing, when injected before testing. Drugs action was not due to nonspecific effects since they had no effect in the open field test. Our findings indicate that DA mechanisms are involved in the acquisition and expression of conditioned fear using light-CS. Dopaminergic mechanisms mediated by postsynaptic D1 receptors seem to be involved in the acquisition of conditioned freezing to light-CS, but not in FPS. On the other hand, dopaminergic mechanisms mediated by presynaptic D2 receptors seem to be involved in the expression of conditioned fear to light-CS.
Oliveira, Amanda Ribeiro de. "Envolvimento de receptores dopaminérgicos da área tegmental ventral e do complexo basolateral da amígdala na aquisição e na expressão do medo condicionado". Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-18022010-093027/.
Pełny tekst źródłaOLIVEIRA, A.R. Involvement of dopaminergic receptors of ventral tegmental area and basolateral amygdala in the acquisition and expression of conditioned fear. 2010. 93 p. Thesis (Doctoral) Faculdade de Filosofia, Ciências e Letras de Ribeirão Preto, Universidade de São Paulo. The Pavlovian fear conditioning is one of the most used paradigms to study the biological basis of emotion, as well as of learning and memory. Dopamine (DA) is one of the most important neurotransmitters involved in mechanisms underlying states of fear and anxiety. A growing body of evidence supports the hypothesis that excitation of the mesocorticolimbic pathway, originating from DA neurons in the ventral tegmental area (VTA), is particularly sensitive to fear-arousing stimuli. Among the forebrain regions innervated by this pathway, the basolateral amygdala (BLA) is an essential component of the neural circuitry of conditioned fear. The present study explored the involvement of VTA and BLA DA receptors, using DA agonists and antagonists, in the acquisition and expression of conditioned fear to a light conditioned stimulus (CS). None of the drugs used produced significant effects on fear-potentiated startle (FPS) when injected in VTA before conditioning, indicating that VTA DA receptors are not involved in the acquisition of conditioned fear to a light-CS. In contrast, when injected before the test session, intra-VTA quinpirole (D2 agonist) significantly reduced FPS, whereas the other drugs had no effect. Intra-BLA SCH 23390 (D1 antagonist) did not produce significant effects on FPS, indicating that BLA D1 receptors do not appear to be involved in the expression of FPS. On the other hand, intra-BLA sulpiride (D2 antagonist) inhibited FPS produced by light-CS previously paired with footshocks. Also, conditioned fear was associated with increased freezing and DA levels in the BLA, both inhibited by intra-VTA quinpirole. Quinpirole\'s ability to decrease FPS and conditioned freezing may be the result of an action on VTA D2 presynaptic autoreceptors. The activation of those receptors decreases dopamine levels in terminal fields of the mesocorticolimbic pathway. Sulpirides results stress the importance of BLA D2 receptors in the fear-activating effects of the Pavlovian conditioning.
Reimer, Adriano Edgar. "Envolvimento de mecanismos glutamatérgicos da substância cinzenta periaquedutal dorsal e do hipotálamo medial no medo condicionado à luz". Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/59/59134/tde-27112012-140923/.
Pełny tekst źródłaThe dorsal periaqueductal gray matter (dPAG) and the medial hypothalamus (MH) are two brain structures that are involved in the elaboration of aversive states and expression of defensive responses. Electrical stimulation of the dPAG or MH produces a series of behavioral responses that resemble those defensive responses triggered in the presence of a predator. These same behaviors can be elicited with the local microinjection of glutamate agonists into these structures, indicating the involvement of excitatory amino acids in the expression of unconditioned fear responses. Nevertheless, the involvement of these structures in fear conditioning is still unknown. The objective of this study was to evaluate the involvement of glutamatergic mediation of the dPAG and MH nuclei anterior nucleus (AH) and dorsal pre-mammillary nucleus (PMd) in the expression of conditioned fear to the light. Thus, we evaluated the effects of glutamatergic agonists and antagonists (AMPA/Kainate and NMDA) administered into these structures in fear potentiated startle (FPS) and conditioned freezing responses to the light. Male Wistar rats with guide-cannulae implanted in the dPAG, AH or PMd were subjected to aversive conditioning (light+shock pairings). Twenty-four hours later, the animals were injected intra-dPAG, AH or PMd with NMDA or kainic acid (NMDA and AMPA/Kainate agonists, respectively) or AP7 or NBQX (NMDA and AMPA/Kainate antagonists, respectively) and were subjected to the FPS test. The conditioned freezing response was measured in the same session. Potential motor effects were evaluated with the open-field test. The administration of glutamate agonists into the dPAG promoted pro-aversive effects in the FPS and conditioned freezing. NBQX produced no significant effect per se, whereas AP7 only decreased conditioned freezing. Both antagonists blocked the effects of the respective agonist. On the other hand, the administration of glutamatergic agonists and antagonists into AH and PMd, in doses that did not affect motor activity, produced no significant effects on conditioned fear responses. The present results suggest the involvement of mechanisms mediated by excitatory amino acids of the dPAG, but not of the MH, in the expression of conditioned fear responses to light.
Yeh, Shiu-Hwa, i 葉修華. "Involvement of NF-kB in fear potentiated startle". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/49337555578826748939.
Pełny tekst źródła國立成功大學
基礎醫學研究所
93
Learning and memory is the basis for the survival and development of creatures, however, aversive experience of fear leads to anxiety. With the changes of the society, anxious complications happen commonly in the modern life. Therefore, the problems of anxiety can be solved by an understanding of emotional fear in terms of its underlying cellular and molecular mechanisms. NF-kB, originally identified as a regulator of immunoglobulin k light chain gene expression, is a DNA-binding factor that functions as a dimer. Recent studies indicate that NF-kB played an important role in the synaptic plasticity. Therefore, we used fear-potentiated startle paradigm to identify the role of NF-kB signaling pathway in memory formation. The results show that p50 and p65 subunits of NF-kB were selectively activated in the amygdala following fear conditioning through the signal-induced activation of PI-3 kinase, IKK and subsequent proteolytic degradation of IkB-a in the cytoplasm. This allows NF-kB to translocate into the nucleus where it binds to specific�nkB DNA consensus sequences in the enhancer region of�n�羠-responsive genes. Pharmacological blockade of NF-kB impairs fear memory in a dose-dependent manner. In in vitro slice preparation, bath application of kB decoy DNA attenuates tetanus-induced L-LTP in the amygdala. Therefore, a novel role of NF-kB in fear conditioning and synaptic plasticity has been demonstrated here. CBP/p300 contains histone acetyltransferase that has been implicated in the regulation of gene expression. Recent studies show that the action of NF-kB is regulated by reversible acetylation. We found that the expression of acetyl-p65 subunit was selectively increased in the amygdala following fear conditioning through the increase associated with CBP (CREB binding protein). Pharmacological blockade of histone deacetylase further increase DNA binding activity of NF-kB and fear memory in a dose-dependent manner. In in vitro slice preparation, bath application of histone deacetylase inhibitor increases the degree of forskolin-induced L-LTP in the amygdala. Therefore, a novel role of NF-kB in fear conditioning and synaptic plasticity has been demonstrated. These results suggest that HDAC-mediated deacetylation functions as an intranuclear molecular switch culminating in the termination of NF-kB transcriptional response. AMPA receptors mediate the majority of the fast excitatory synaptic transmission. One recently identified mechanism contributing to synaptic plasticity is the regulated trafficking of AMPA receptors in and out of synapses. Receptors with long cytoplasmic tails (GluR4/2 and GluR1/2) are driven into synapses in an activity-dependent manner. Our results show that synaptoneurosome membrane expression of GluR1 was selectively increased in the amygdala following fear conditioning through the signal-induced activation of PI-3 kinase, NMDA receptor and NF-kB. Pharmacological blockade of histone deacetylase further increases conditioning-induced membrane expression of GluR1 in NF-kB-dependent manner. Furthermore, fear training-induced increase in GluR1 was reversed when animal was exposed to the memory extinction protocol. The reversal of GluR1 increase was also blocked by D-APV and anisomycin treatment. The similar pattern of changes in GluR1 was observed in the amygdala slices after delivery of high-frequency stimulation (HFS) or HFS followed by low-frequency stimulation (LFS) that elicited long-term potentiation (LTP) and depotentiation respectively. These results suggest that long-term synaptic plasticity and memory formation are correlated with the changes in modification of GluR1 expression, and surface expression of GluR1 is a potential effector that contributes at least in part to the expression of fear memory.
Lee, Ching-Fen, i 李淨芬. "Studies on the molecular mechanisms of fear-potentiated startle". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/52675027710070246763.
Pełny tekst źródła國立成功大學
藥理學研究所
91
Accumulated evidence indicate that the amygdala is a crucial neuronal locus for the induction and expression of fear memory. Fear conditioning induces associative long-term potentiation in the amygdala and protein phosphorylation is a powerful regulator of long-term synaptic plasticity. Protein phosphorylation is also a direct and rapid modulator of exocytosis in neurons. Previous studies indicate that protein kinases play an important role in mediating the release of synaptic vesicles from the reserve pool and the synaptic-vesicle-associated phosphoprotein, synapsin I, is a key kinase substrate in this process. Hence, my study is to prove whether fear conditioning induces phosphorylation of synapsin I and whether this effect is subjected to regulate by memory extinction. In this study, I have shown that synapsin I is phosphorylated after fear training and phosphorylated synapsin I is subsequently dephosphorylated when animals receive extinction training. Previous studies in our laboratory demonstrated that L-CCG-induced long-term depotentiation ( LTD ) leads to a long-lasting decrease in transmitter release which was induced by presynaptically group II metabotropic glutamate receptor ( mGluRII )-mediated inhibition of Ca2+-sensitive adenylyl cyclase, resulting in a decrease in cAMP formation and PKA activation. Therefore, I used the mGluRII agonist, (2S, 2R,3R)-2-(2,3-Dicarboxycyclopropyl)glycine ( DCG-IV ), to examine its effect on the phosphorylation of synapsin I and used the antagonist, LY341495, to test whether it could reverse the effect of DCG-IV. The results revealed that DCG-IV decreased the phosphorylation of synapsin I that was reversed by LY341495 . Finally, I determined the different phosphorylation site of synapsin I in fear conditioning and found that the phosphorylation of PKA/CaMKI phosphorylation site, CaMKII phosphorylation site, and cdk5 phosphorylation site were increased following fear conditioning. By using the specific kinase inhibitor to block synapsin I phosphorylation, I found that these inhibitors reduced the phosphorylation of different synapsin I phosphorylation site and inhibited the fear-potentiated startle.
Części książek na temat "Fear-potentiated startle"
Verster, Joris C., Thomas M. Tzschentke, Kieran O’Malley, Francis C. Colpaert, Bart Ellenbroek, Bart Ellenbroek, R. Hamish McAllister-Williams i in. "Fear-Potentiated Startle". W Encyclopedia of Psychopharmacology, 533. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_3269.
Pełny tekst źródłaHamm, Alfons O. "Fear-Potentiated Startle". W International Encyclopedia of the Social & Behavioral Sciences, 860–67. Elsevier, 2015. http://dx.doi.org/10.1016/b978-0-08-097086-8.55023-5.
Pełny tekst źródła"Focus: Learning and the Auditory System — Fear-Potentiated Startle Studies". W Handbook of Mouse Auditory Research, 105–10. CRC Press, 2001. http://dx.doi.org/10.1201/9781420038736-11.
Pełny tekst źródłaDavis, Michael. "Neural systems involved in fear and anxiety based on the fear-potentiated startle test". W Neurobiology of Learning and Memory, 381–425. Elsevier, 2007. http://dx.doi.org/10.1016/b978-012372540-0/50013-3.
Pełny tekst źródłaDavis, Michael, Janice M. Hitchcock i Jeffrey B. Rosen. "Anxiety and the Amygdala: Pharmacological and Anatomical Analysis of the Fear-Potentiated Startle Paradigm". W Psychology of Learning and Motivation, 263–305. Elsevier, 1988. http://dx.doi.org/10.1016/s0079-7421(08)60031-6.
Pełny tekst źródłaDAVIS, MICHAEL. "ANIMAL MODELS OF ANXIETY BASED ON CLASSICAL CONDITIONING: THE CONDITIONED EMOTIONAL RESPONSE AND THE FEAR-POTENTIATED STARTLE EFFECT". W Psychopharmacology of Anxiolytics and Antidepressants, 187–212. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-040698-5.50013-2.
Pełny tekst źródłaRaporty organizacyjne na temat "Fear-potentiated startle"
Rosen, Jeff. Oxytocin and Social Support as Synergistic Inhibitors of Aversive Fear Conditioning and Fear-Potentiated Startle in Male Rats. Fort Belvoir, VA: Defense Technical Information Center, maj 2011. http://dx.doi.org/10.21236/ada554060.
Pełny tekst źródłaRosen, Jeffrey B. Oxytocin and Social Support as Synergistic Inhibitors of Aversive Fear Conditioning and Fear-Potentiated Startle in Male Rats. Fort Belvoir, VA: Defense Technical Information Center, wrzesień 2010. http://dx.doi.org/10.21236/ada555016.
Pełny tekst źródła