Activation of adrenal preganglionic neurons during autonomic dysreflexia in the chronic spinal cord-injured rat
Identifieur interne : 005611 ( PascalFrancis/Corpus ); précédent : 005610; suivant : 005612Activation of adrenal preganglionic neurons during autonomic dysreflexia in the chronic spinal cord-injured rat
Auteurs : Samuel Leman ; Henrique SequeiraSource :
- Autonomic neuroscience : basic & clinical [ 1566-0702 ] ; 2002.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Autonomic dysreflexia (AD) occurs in a majority of high paraplegic and quadriplegic patients and is particularly characterized by a paroxysmal hypertension elicited by somatic or visceral stimuli. We have previously shown that plasma adrenaline and noradrenaline levels were significantly increased during episodes of AD in the 30-day spinal cord-injured (SCI) rats, suggesting the participation of adrenal catecholamines in the cardiovascular changes associated to AD. Thus, adrenal sympathetic preganglionic neurons (SPN) could be activated by visceral afferences leading to AD. The aim of this study was then to demonstrate whether visceral stimulation that induces AD activates adrenal SPN in chronic SCI rats. To this end, a retrograde tracer, the cholera toxin B subunit (CTB), was combined with the immunocytochemical detection of Fos protein after visceral stimulation. Chronic SCI rats received a CTB injection into the adrenal gland and, 3 days later, were stimulated by repetitive distension of the colon. Results showed that this stimulation elicited typical hypertensive episodes of AD and a significant increase in the number of double-labeled neurons (CTB/Fos immunoreactive neurons) in the thoracic spinal cord below the level of injury (T4 segment) when compared to the stimulated non-SCI rats. In conclusion, visceral stimulations in the chronic SCI rats activate adrenal SPN, which could induce release of catecholamines by the adrenal medulla. The present study brings new data on the spinal mechanisms of AD cardiovascular dysfunctions.
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Format Inist (serveur)
NO : | PASCAL 02-0498681 INIST |
---|---|
ET : | Activation of adrenal preganglionic neurons during autonomic dysreflexia in the chronic spinal cord-injured rat |
AU : | LEMAN (Samuel); SEQUEIRA (Henrique); PILOWSKY (Paul M.); GIBBINS (I.) |
AF : | Laboratoire de Neurosciences du Comportement, SN4-1, Université de Lille 1/59655, Villeneuve d'Ascq/France (1 aut., 2 aut.); Research Laboratory, Central Autonomic Neuroscience, Royal North Shore Hospital, Block 3, Ground Floor/St. Leonards 2065/Australie (1 aut.) |
DT : | Publication en série; Congrès; Niveau analytique |
SO : | Autonomic neuroscience : basic & clinical; ISSN 1566-0702; Pays-Bas; Da. 2002; Vol. 98; No. 1-2; Pp. 94-98; Bibl. 27 ref. |
LA : | Anglais |
EA : | Autonomic dysreflexia (AD) occurs in a majority of high paraplegic and quadriplegic patients and is particularly characterized by a paroxysmal hypertension elicited by somatic or visceral stimuli. We have previously shown that plasma adrenaline and noradrenaline levels were significantly increased during episodes of AD in the 30-day spinal cord-injured (SCI) rats, suggesting the participation of adrenal catecholamines in the cardiovascular changes associated to AD. Thus, adrenal sympathetic preganglionic neurons (SPN) could be activated by visceral afferences leading to AD. The aim of this study was then to demonstrate whether visceral stimulation that induces AD activates adrenal SPN in chronic SCI rats. To this end, a retrograde tracer, the cholera toxin B subunit (CTB), was combined with the immunocytochemical detection of Fos protein after visceral stimulation. Chronic SCI rats received a CTB injection into the adrenal gland and, 3 days later, were stimulated by repetitive distension of the colon. Results showed that this stimulation elicited typical hypertensive episodes of AD and a significant increase in the number of double-labeled neurons (CTB/Fos immunoreactive neurons) in the thoracic spinal cord below the level of injury (T4 segment) when compared to the stimulated non-SCI rats. In conclusion, visceral stimulations in the chronic SCI rats activate adrenal SPN, which could induce release of catecholamines by the adrenal medulla. The present study brings new data on the spinal mechanisms of AD cardiovascular dysfunctions. |
CC : | 002B16B |
FD : | Neurone préganglionnaire; Chronique; Animal; Traumatisme; Moelle épinière; Système nerveux sympathique pathologie; Rat; Dysreflexie autonome |
FG : | Système nerveux central; Système nerveux central pathologie; Rodentia; Mammalia; Vertebrata |
ED : | Preganglionic neuron; Chronic; Animal; Trauma; Spinal cord; Autonomic neuropathy; Rat |
EG : | Central nervous system; Central nervous system disease; Rodentia; Mammalia; Vertebrata |
SD : | Neurona preganglionar; Crónico; Animal; Traumatismo; Médula espinal; Sistema nervioso simpático patología; Rata |
LO : | INIST-18294.354000101650340210 |
ID : | 02-0498681 |
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<front><div type="abstract" xml:lang="en">Autonomic dysreflexia (AD) occurs in a majority of high paraplegic and quadriplegic patients and is particularly characterized by a paroxysmal hypertension elicited by somatic or visceral stimuli. We have previously shown that plasma adrenaline and noradrenaline levels were significantly increased during episodes of AD in the 30-day spinal cord-injured (SCI) rats, suggesting the participation of adrenal catecholamines in the cardiovascular changes associated to AD. Thus, adrenal sympathetic preganglionic neurons (SPN) could be activated by visceral afferences leading to AD. The aim of this study was then to demonstrate whether visceral stimulation that induces AD activates adrenal SPN in chronic SCI rats. To this end, a retrograde tracer, the cholera toxin B subunit (CTB), was combined with the immunocytochemical detection of Fos protein after visceral stimulation. Chronic SCI rats received a CTB injection into the adrenal gland and, 3 days later, were stimulated by repetitive distension of the colon. Results showed that this stimulation elicited typical hypertensive episodes of AD and a significant increase in the number of double-labeled neurons (CTB/Fos immunoreactive neurons) in the thoracic spinal cord below the level of injury (T4 segment) when compared to the stimulated non-SCI rats. In conclusion, visceral stimulations in the chronic SCI rats activate adrenal SPN, which could induce release of catecholamines by the adrenal medulla. The present study brings new data on the spinal mechanisms of AD cardiovascular dysfunctions.</div>
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<server><NO>PASCAL 02-0498681 INIST</NO>
<ET>Activation of adrenal preganglionic neurons during autonomic dysreflexia in the chronic spinal cord-injured rat</ET>
<AU>LEMAN (Samuel); SEQUEIRA (Henrique); PILOWSKY (Paul M.); GIBBINS (I.)</AU>
<AF>Laboratoire de Neurosciences du Comportement, SN4-1, Université de Lille 1/59655, Villeneuve d'Ascq/France (1 aut., 2 aut.); Research Laboratory, Central Autonomic Neuroscience, Royal North Shore Hospital, Block 3, Ground Floor/St. Leonards 2065/Australie (1 aut.)</AF>
<DT>Publication en série; Congrès; Niveau analytique</DT>
<SO>Autonomic neuroscience : basic & clinical; ISSN 1566-0702; Pays-Bas; Da. 2002; Vol. 98; No. 1-2; Pp. 94-98; Bibl. 27 ref.</SO>
<LA>Anglais</LA>
<EA>Autonomic dysreflexia (AD) occurs in a majority of high paraplegic and quadriplegic patients and is particularly characterized by a paroxysmal hypertension elicited by somatic or visceral stimuli. We have previously shown that plasma adrenaline and noradrenaline levels were significantly increased during episodes of AD in the 30-day spinal cord-injured (SCI) rats, suggesting the participation of adrenal catecholamines in the cardiovascular changes associated to AD. Thus, adrenal sympathetic preganglionic neurons (SPN) could be activated by visceral afferences leading to AD. The aim of this study was then to demonstrate whether visceral stimulation that induces AD activates adrenal SPN in chronic SCI rats. To this end, a retrograde tracer, the cholera toxin B subunit (CTB), was combined with the immunocytochemical detection of Fos protein after visceral stimulation. Chronic SCI rats received a CTB injection into the adrenal gland and, 3 days later, were stimulated by repetitive distension of the colon. Results showed that this stimulation elicited typical hypertensive episodes of AD and a significant increase in the number of double-labeled neurons (CTB/Fos immunoreactive neurons) in the thoracic spinal cord below the level of injury (T4 segment) when compared to the stimulated non-SCI rats. In conclusion, visceral stimulations in the chronic SCI rats activate adrenal SPN, which could induce release of catecholamines by the adrenal medulla. The present study brings new data on the spinal mechanisms of AD cardiovascular dysfunctions.</EA>
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