The Deakin/Graeff hypothesis: Focus on serotonergic inhibition of panic
2014-11-27
org.kosen.entty.User@e9a2370
정승호(hopejsh)
분야
뇌과학
개최일
October 2014
신청자
정승호(hopejsh)
개최장소
URL
첨부파일
행사&학회소개
Abstract
1. Introduction to panic disorder
1.1. Symptomatology and epidemiology of panic disorder
1.2. Experimentally induced panic: putative panicogenic agents
1.3. Toward a panic disorder hypothesis: hyperventilation theories, exaggerated fear networks, and false suffocation alarms
1.4. Bilateral focal lesions of the amygdala lead to increased vulnerability to CO2-evoked panic
1.5. Functional topography of midbrain serotonergic systems: recent advances and new opportunities
2. A putative panic inhibition system involving the amygdala, dorsal raphe nucleus and periaqueductal gray
2.1. The DPAG mediates panic-/escape-like physiological and behavioral responses
2.2. Evidence for a suffocation alarm system in the PAG
2.3. Serotonin acts in the DPAG to inhibit panic-/escape-like physiological and behavioral responses.
2.4. Chronic treatment with antidepressant drugs acts to potentiate the anti-panic effects of serotonin in the DPAG
3. The DRVL/VLPAG serotonergic system, a critical node in panic physiology
3.1. DRVL/VLPAG serotonergic neurons form part of a sympathomotor command center
3.2. DRVL/VLPAG and medullary serotonergic neurons are central chemosensory receptors
3.3. DRVL/VLPAG serotonergic neurons are activated by panicogenic agents and altered in rodent models of chronic anxiety states
3.4. A CE/DRVL/VLPAG circuit mediating expression of contextual fear (freezing) and inhibition of panic-/escape-like physiological and behavioral responses
4. Neuropeptide modulation of the panic inhibition system
4.1. CRH projections from the CE activate DRVL/VLPAG serotonergic neurons via CRHR2
4.2. BnST CRH neurons activate the conflict anxiety facilitation system
4.3. Interactions between CRH, hypocretinergic/orexinergic, and serotonergic systems: implications for anxiety and panic
4.3.1. Hypothalamic hypocretinergic/orexinergic and extended amygdala CRH neurons comprise a stress-sensitive circuit
4.3.2. A hypocretinergic/orexinergic-serotonergic circuit implicated in stress, anxiety and panic
5. Panicogenic agents activate a distributed network of anxiety-, fear- and panic-related brain regions
5.1. Acid-sensing ion channels in the amygdala: implications for fear and panic
5.2. Acid-sensing ion channels are expressed throughout the panic inhibition system
5.3. Sodium lactate-induced panic activates angiotensin II neurons
5.4. Serotonergic neurons express two-pore domain K+ TASK channels capable of sensing fluctuations in extracellular pH
6. conclusion
1. Introduction to panic disorder
1.1. Symptomatology and epidemiology of panic disorder
1.2. Experimentally induced panic: putative panicogenic agents
1.3. Toward a panic disorder hypothesis: hyperventilation theories, exaggerated fear networks, and false suffocation alarms
1.4. Bilateral focal lesions of the amygdala lead to increased vulnerability to CO2-evoked panic
1.5. Functional topography of midbrain serotonergic systems: recent advances and new opportunities
2. A putative panic inhibition system involving the amygdala, dorsal raphe nucleus and periaqueductal gray
2.1. The DPAG mediates panic-/escape-like physiological and behavioral responses
2.2. Evidence for a suffocation alarm system in the PAG
2.3. Serotonin acts in the DPAG to inhibit panic-/escape-like physiological and behavioral responses.
2.4. Chronic treatment with antidepressant drugs acts to potentiate the anti-panic effects of serotonin in the DPAG
3. The DRVL/VLPAG serotonergic system, a critical node in panic physiology
3.1. DRVL/VLPAG serotonergic neurons form part of a sympathomotor command center
3.2. DRVL/VLPAG and medullary serotonergic neurons are central chemosensory receptors
3.3. DRVL/VLPAG serotonergic neurons are activated by panicogenic agents and altered in rodent models of chronic anxiety states
3.4. A CE/DRVL/VLPAG circuit mediating expression of contextual fear (freezing) and inhibition of panic-/escape-like physiological and behavioral responses
4. Neuropeptide modulation of the panic inhibition system
4.1. CRH projections from the CE activate DRVL/VLPAG serotonergic neurons via CRHR2
4.2. BnST CRH neurons activate the conflict anxiety facilitation system
4.3. Interactions between CRH, hypocretinergic/orexinergic, and serotonergic systems: implications for anxiety and panic
4.3.1. Hypothalamic hypocretinergic/orexinergic and extended amygdala CRH neurons comprise a stress-sensitive circuit
4.3.2. A hypocretinergic/orexinergic-serotonergic circuit implicated in stress, anxiety and panic
5. Panicogenic agents activate a distributed network of anxiety-, fear- and panic-related brain regions
5.1. Acid-sensing ion channels in the amygdala: implications for fear and panic
5.2. Acid-sensing ion channels are expressed throughout the panic inhibition system
5.3. Sodium lactate-induced panic activates angiotensin II neurons
5.4. Serotonergic neurons express two-pore domain K+ TASK channels capable of sensing fluctuations in extracellular pH
6. conclusion
보고서작성신청
급격하게 변화하고 있는 사회에서 살고 있는 현대인들에게 가장 쉽게 발견할 수 있는 정신질환들 중의 하나는 바로 공황장애일 것이다. 많은 연애인들이 공황장애(panic disorder)를 겪고 있다고 밝히고 있지만, 아직까지 정확한 기전에 대한 명확한 설명이 부족한 것이 신경과학계의 현실이다. 본 리뷰 논문은 이러한 패닉에 대하여 1990년대 초반에 Deakin과 Graeff에 의해 제시된 세로토닌 신경 subtype의 비율에 기초한 이론을 자세히 설명하고 있다. 특히, 이론이 제시된 이후 현재까지 제시된 다양한 과학적, 신경생물학적 증거들을 깊이 있게 다룬 리뷰논문으로, 이러한 전공분야에 종사하고 있는 과학자들에게 좋은 리뷰논문이라 생각된다.