دورية أكاديمية
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Cerebellar modulation of memory encoding in the periaqueductal grey and fear behaviour.

التفاصيل البيبلوغرافية
العنوان: Cerebellar modulation of memory encoding in the periaqueductal grey and fear behaviour.
المؤلفون: Lawrenson C; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom., Paci E; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom., Pickford J; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom., Drake RAR; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom., Lumb BM; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom., Apps R; School of Physiology, Pharmacology & Neuroscience, University of Bristol, Bristol, United Kingdom.
المصدر: ELife [Elife] 2022 Mar 15; Vol. 11. Date of Electronic Publication: 2022 Mar 15.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: eLife Sciences Publications, Ltd Country of Publication: England NLM ID: 101579614 Publication Model: Electronic Cited Medium: Internet ISSN: 2050-084X (Electronic) Linking ISSN: 2050084X NLM ISO Abbreviation: Elife Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Cambridge, UK : eLife Sciences Publications, Ltd., 2012-
مواضيع طبية MeSH: Fear*/physiology , Periaqueductal Gray*/physiology, Animals ; Cerebellum/physiology ; Conditioning, Classical/physiology ; Conditioning, Operant/physiology ; Male ; Rats
مستخلص: The pivotal role of the periaqueductal grey (PAG) in fear learning is reinforced by the identification of neurons in male rat ventrolateral PAG (vlPAG) that encode fear memory through signalling the onset and offset of an auditory-conditioned stimulus during presentation of the unreinforced conditioned tone (CS+) during retrieval. Some units only display CS+ onset or offset responses, and the two signals differ in extinction sensitivity, suggesting that they are independent of each other. In addition, understanding cerebellar contributions to survival circuits is advanced by the discovery that (i) reversible inactivation of the medial cerebellar nucleus (MCN) during fear consolidation leads in subsequent retrieval to (a) disruption of the temporal precision of vlPAG offset, but not onset responses to CS+, and (b) an increase in duration of freezing behaviour. And (ii) chemogenetic manipulation of the MCN-vlPAG projection during fear acquisition (a) reduces the occurrence of fear-related ultrasonic vocalisations, and (b) during subsequent retrieval, slows the extinction rate of fear-related freezing. These findings show that the cerebellum is part of the survival network that regulates fear memory processes at multiple timescales and in multiple ways, raising the possibility that dysfunctional interactions in the cerebellar-survival network may underlie fear-related disorders and comorbidities.
Competing Interests: CL, EP, JP, RD, BL, RA No competing interests declared
(© 2022, Lawrenson et al.)
References: J Neurophysiol. 2007 May;97(5):3421-31. (PMID: 17360820)
J Neurosci Methods. 1985 Aug;14(3):149-67. (PMID: 2864480)
Sci Rep. 2019 Mar 14;9(1):4522. (PMID: 30872749)
J Neurophysiol. 1953 Jul;16(4):397-413. (PMID: 13070051)
Eur J Neurosci. 2020 Feb;51(3):866-880. (PMID: 31376295)
Nat Rev Neurosci. 2015 Oct;16(10):642. (PMID: 26333516)
J Vis Exp. 2011 Mar 10;(49):. (PMID: 21445033)
Anesth Analg. 2008 Jul;107(1):309-17. (PMID: 18635502)
Proc Natl Acad Sci U S A. 2008 Feb 26;105(8):3117-22. (PMID: 18287060)
Learn Mem. 2018 Sep 17;25(10):544-549. (PMID: 30224557)
Exp Brain Res. 1985;58(2):379-91. (PMID: 3996501)
Neuroscientist. 2005 Jun;11(3):217-27. (PMID: 15911871)
Proc Natl Acad Sci U S A. 2013 Sep 3;110(36):14795-800. (PMID: 23959880)
PLoS Biol. 2019 Aug 30;17(8):e3000417. (PMID: 31469831)
Curr Protoc Neurosci. 2017 Jul 5;80:8.40.1-8.40.21. (PMID: 28678397)
Neuron. 1997 Sep;19(3):613-24. (PMID: 9331352)
Neuroscience. 2003;116(3):897-912. (PMID: 12573728)
J Comp Physiol Psychol. 1969 Mar;67(3):370-5. (PMID: 5787388)
Neuroreport. 2004 Jul 19;15(10):1565-9. (PMID: 15232284)
Neurosci Lett. 2015 Sep 14;604:173-7. (PMID: 26219987)
Handb Clin Neurol. 2018;154:85-108. (PMID: 29903454)
Indian J Physiol Pharmacol. 1999 Oct;43(4):449-57. (PMID: 10776460)
Nat Neurosci. 2017 Jan;20(1):90-97. (PMID: 27842071)
Prog Brain Res. 2000;124:141-72. (PMID: 10943123)
Behav Brain Funct. 2016 Feb 24;12(1):8. (PMID: 26912001)
Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8406-11. (PMID: 12034877)
Nat Commun. 2020 Oct 15;11(1):5207. (PMID: 33060630)
Braz J Med Biol Res. 2012 Apr;45(4):337-48. (PMID: 22437483)
Annu Rev Psychol. 2012;63:129-51. (PMID: 22129456)
Neuroreport. 2001 Dec 21;12(18):4109-12. (PMID: 11742247)
Lab Anim. 2006 Apr;40(2):180-5. (PMID: 16600077)
Nat Rev Neurosci. 2015 Jun;16(6):317-31. (PMID: 25991441)
Elife. 2019 Sep 30;8:. (PMID: 31566567)
Eur J Neurosci. 2007 May;25(9):2875-84. (PMID: 17466022)
Proc Natl Acad Sci U S A. 2013 May 7;110(19):7892-7. (PMID: 23610391)
Eur J Neurosci. 2010 Feb;31(4):599-612. (PMID: 20384807)
Cerebellum. 2016 Apr;15(2):122-38. (PMID: 25808751)
Physiol Behav. 1987;39(5):579-86. (PMID: 3588702)
Brain Res. 1982 Jul 22;244(1):1-8. (PMID: 7116161)
Trends Neurosci. 2011 Jun;34(6):283-92. (PMID: 21549434)
PLoS One. 2012;7(1):e30151. (PMID: 22272290)
Learn Mem. 2013 Oct 16;20(11):633-41. (PMID: 24131794)
Elife. 2017 Oct 13;6:. (PMID: 29027903)
Cell Rep. 2019 Apr 16;27(3):872-885.e7. (PMID: 30995483)
Brain Struct Funct. 2019 Jul;224(6):2153-2165. (PMID: 31165919)
Curr Opin Behav Sci. 2016 Apr;8:53-59. (PMID: 26949723)
Brain Res. 1990 Feb 12;509(1):17-23. (PMID: 2306634)
Exp Brain Res. 2007 Jun;180(2):355-65. (PMID: 17256160)
Front Behav Neurosci. 2011 May 19;5:25. (PMID: 21637320)
PLoS One. 2010 Dec 21;5(12):e15500. (PMID: 21203536)
J Neurosci. 2006 May 31;26(22):5990-5. (PMID: 16738241)
Behav Brain Res. 2016 Jul 15;308:196-204. (PMID: 27102341)
Exp Brain Res. 2007 May;179(2):291-9. (PMID: 17146647)
Neuron. 2010 Feb 11;65(3):412-21. (PMID: 20159453)
Biol Psychiatry. 2018 Sep 15;84(6):401-412. (PMID: 29478701)
Brain Struct Funct. 2019 Jul;224(6):2121-2142. (PMID: 31165301)
J Comp Neurol. 1998 Nov 30;401(4):455-79. (PMID: 9826273)
J Physiol. 2014 May 15;592(10):2197-213. (PMID: 24639484)
Nat Rev Neurosci. 2021 Nov;22(11):674-684. (PMID: 34545241)
Nat Neurosci. 2018 Sep;21(9):1146-1147. (PMID: 30127429)
Trends Neurosci. 2014 Aug;37(8):455-64. (PMID: 24929864)
Neurobiol Learn Mem. 2005 Nov;84(3):228-40. (PMID: 16115784)
J Neurosci. 1987 Jan;7(1):271-8. (PMID: 3806198)
Nature. 2016 Jun 01;534(7606):206-12. (PMID: 27279213)
Braz J Med Biol Res. 2003 May;36(5):557-66. (PMID: 12715074)
Neuroscience. 2005;131(1):1-11. (PMID: 15680687)
J Neurosci. 2016 Dec 14;36(50):12707-12719. (PMID: 27974618)
Science. 2009 Jul 10;325(5937):210-3. (PMID: 19590004)
Front Psychol. 2017 Apr 07;8:456. (PMID: 28439244)
Sci Rep. 2019 Jul 3;9(1):9581. (PMID: 31270350)
J Neurosci. 2002 Mar 15;22(6):2343-51. (PMID: 11896173)
Int Rev Neurobiol. 1997;41:555-73. (PMID: 9378608)
Exp Neurol. 2009 Apr;216(2):375-82. (PMID: 19162011)
Behav Brain Res. 2006 Jan 30;166(2):271-80. (PMID: 16213033)
Brain Res. 1980 Mar 17;186(1):83-97. (PMID: 7357452)
Nat Neurosci. 2010 Aug;13(8):979-86. (PMID: 20601946)
Neuron. 2014 May 21;82(4):797-808. (PMID: 24768300)
Elife. 2019 Mar 07;8:. (PMID: 30843787)
Neuroscience. 1997 May;78(1):165-77. (PMID: 9135098)
Proc Natl Acad Sci U S A. 2013 Aug 27;110(35):14124-31. (PMID: 23912185)
Physiol Behav. 1987;39(3):333-9. (PMID: 3575473)
Pol J Pharmacol. 2002 Sep-Oct;54(5):423-31. (PMID: 12593529)
Biol Psychiatry. 1999 Apr 1;45(7):806-16. (PMID: 10202567)
J Physiol. 2006 Oct 15;576(Pt 2):547-56. (PMID: 16916903)
Annu Rev Neurosci. 2009;32:413-34. (PMID: 19555291)
Neurosci Lett. 2014 Apr 30;566:162-6. (PMID: 24607928)
Mol Pain. 2018 Jan-Dec;14:1744806918804441. (PMID: 30209982)
Neuroscience. 2009 Sep 1;162(3):756-62. (PMID: 19409218)
Nat Neurosci. 2014 Nov;17(11):1607-12. (PMID: 25282614)
Elife. 2020 Mar 24;9:. (PMID: 32207681)
معلومات مُعتمدة: United Kingdom WT_ Wellcome Trust; BB/MO19616/1 United Kingdom BB_ Biotechnology and Biological Sciences Research Council; 203775/Z/16/Z United Kingdom WT_ Wellcome Trust
فهرسة مساهمة: Keywords: PAG; cerebellum; fear; neuroscience; rat; survival circuits; timing
Local Abstract: [plain-language-summary] Anxiety disorders are a cluster of mental health conditions characterised by persistent and excessive amounts of fear and worry. They affect millions of people worldwide, but treatments can sometimes be ineffective and have unwanted side effects. Understanding which brain regions are involved in fear and anxiety-related behaviours, and how those areas are connected, is the first step towards designing more effective treatments. A region known as the periaqueductal grey (or PAG) sits at the centre of the brain’s fear and anxiety network, regulating pain, encoding fear memories and responding to threats and stressors. It also controls survival behaviours such as the ‘freeze’ response, when an animal is frightened. A more recent addition to the fear and anxiety network is the cerebellum, which sits at the base of the brain. Two-way connections between this region and the PAG have been well described, but how the cerebellum might influence fear and anxiety-related behaviours remains unclear. To explore this role, Lawrenson, Paci et al. investigated whether the cerebellum modulates brain activity within the PAG and if so, how this relates to fear behaviours. Rats had electrodes implanted in their brains to record the activity of nerve cells within the PAG. A common fear-conditioning task was then used to elicit ‘freeze’ responses: a sound was paired with mild foot shocks until the animals learned to fear the auditory signal. In the rats, a subset of neurons within the PAG responded to the tone, consistent with those cells encoding a fear memory. But when a drug blocked the cerebellum’s output during fear conditioning, the timing of the PAG response was less precise and the rats’ freeze response lasted longer. Lawrenson, Paci et al. concluded that the cerebellum, through its interactions with the brain’s fear and anxiety network, might be responsible for coordinating the most appropriate behavioural response to fear, and how long ‘freezing’ lasts. In summary, these findings show that the cerebellum is a part of the brain’s survival network which regulates fear-memory processes. It raises the possibility that disruption of the cerebellum might underlie anxiety and other fear-related disorders, thereby providing a new target for future therapies.
تواريخ الأحداث: Date Created: 20220315 Date Completed: 20220429 Latest Revision: 20220716
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC8923669
DOI: 10.7554/eLife.76278
PMID: 35287795
قاعدة البيانات: MEDLINE
الوصف
تدمد:2050-084X
DOI:10.7554/eLife.76278