A Facilitation Action of Reserpine on the Central Nervous System

Chen, Graham; Ensor, Charles R.; Bohner, Barbara

doi:10.3181/00379727-86-21149

Cited by 173 publications

(37 citation statements)

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“…NE has long been known to display anticonvulsant properties, but little is known about the underlying mechanisms (Chen et al, 1954;Stanton, 1992;Stanton et al, 1992;Szot et al, 1999;Stoop et al, 2000;Weinshenker et al, 2001) The a 1A adrenoreceptor-mediated facilitation of GABA release in the BLA may be one of the mechanisms involved in the antiepileptic effects of NE in temporal lobe seizure disorders.…”

Section: Discussionmentioning

confidence: 99%

Stress Impairs α1A Adrenoceptor-Mediated Noradrenergic Facilitation of GABAergic Transmission in the Basolateral Amygdala

Braga

Aroniadou‐Anderjaska

Manion

et al. 2003

Neuropsychopharmacol

130

106

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Intense or chronic stress can produce pathophysiological alterations in the systems involved in the stress response. The amygdala is a key component of the brain's neuronal network that processes and assigns emotional value to life's experiences, consolidates the memory of emotionally significant events, and organizes the behavioral response to these events. Clinical evidence indicates that certain stressrelated affective disorders are associated with changes in the amygdala's excitability, implicating a possible dysfunction of the GABAergic system. An important modulator of the GABAergic synaptic transmission, and one that is also central to the stress response is norepinephrine (NE). In the present study, we examined the hypothesis that stress impairs the noradrenergic modulation of GABAergic transmission in the basolateral amygdala (BLA). In control rats, NE (10 mM) facilitated spontaneous, evoked, and miniature IPSCs in the presence of b and a 2 adrenoceptor antagonists. The effects of NE were not blocked by a 1D and a 1B adrenoceptor antagonists, and were mimicked by the a 1A agonist, A61603 (1 mM). In restrain/tail-shock stressed rats, NE or A61603 had no significant effects on GABAergic transmission. Thus, in the BLA, NE acting via presynaptic a 1A adrenoceptors facilitates GABAergic inhibition, and this effect is severely impaired by stress. This is the first direct evidence of stress-induced impairment in the modulation of GABAergic synaptic transmission. The present findings provide an insight into possible mechanisms underlying the antiepileptogenic effects of NE in temporal lobe epilepsy, the hyperexcitability and hyper-responsiveness of the amygdala in certain stress-related affective disorders, and the stress-induced exacerbation of seizure activity in epileptic patients.

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Section: Discussionmentioning

confidence: 99%

Stress Impairs α1A Adrenoceptor-Mediated Noradrenergic Facilitation of GABAergic Transmission in the Basolateral Amygdala

Braga

Aroniadou‐Anderjaska

Manion

et al. 2003

Neuropsychopharmacol

130

106

View full text Add to dashboard Cite

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“…PCA9 lacks any anticonvulsant activity, rather it showed a mild facilitation of metrazol-induced con vulsions and death. Chlorpromazine does not prevent the experimentally induced con vulsions (19) whereas reserpine enhances the susceptibility to seizures induced by electro shock or metrazol (20). PCA9 was effective in reducing amphetamine-induced hypera ctivity though it did not prevent the toxicity in aggregated mice.…”

Section: Acute Toxicitymentioning

confidence: 99%

PHARMACOLOGICAL STUDY OF 1-(β-PHENYLETHYL) TRIAZOLO (4, 5-c) PYRIDINE HYDROCHLORIDE, A TRANQUILLIZING AGENT

1967

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In an investigation of the pharmacological activities of a large number of substituted diaminopyridine and the corresponding imidazo and triazolo pyridines it was found that imidazo and triazolo (c) pyridines, in general, produced central depressant action and amongst these 1-((3-phenylethyl) triazolo (4,5-c) pyridine hydrochloride (PCA9) showed relatively better sedative and tranquillizing effects in mice (1, 2). In view of the tranquil lizing activity of PCA9 a study on some neuro-psychopharmacological and other phar macodynamic effects of this compound was carried out to elucidate the pattern of activity and the results of which are embodied in the present communication. MATERIALS AND METHODSSolution of 1-((3-phenylethyl) triazolo (4,5-c) pyridine hydrochloride (PCA9) was injected intraperitoneally (0.2 ml/20 g body weight) into white mice (16-20 g) and rats (100-140 g) of either sex from the C.D.R.I. colony. All experiments were conducted at room temperature 24±0.5°C or otherwise mentioned. Chlorpromazine and reserpine were used as the standards.1. Gross observation : Groups of mice and rats (5 in each group), after an hour observation, were injected with graded doses of PCA9. Treated animals were observed for 5 hours for behavioral, neurological, autonomic and toxic manifestations according to the method outlined by Irwin (3). Gross effects of PCA9 were also studied in rabbits and dogs.2. Effect on body temperature : Rectal temperature of mice was recorded before and at 1/4, 1/2, 1, 2, 3, and 4 hours after the administration of the test compounds using

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“…NE has long been known to display anticonvulsant properties, but Httle is known about the underlying mechanisms (Chen et al, 1954;Stanton, 1992;Stanton et al, 1992;Szot et al, 1999;Stoop et al, 2000;Weinshenker et al, 2001) The ajA adrenoreceptor-mediated facilitatipn of GABA release in the BLA may be one of the mechanisms involved in the antiepileptic effects of NE in temporal lobe seizure disorders.…”

Section: Ne Facilitates Gabaergic Transmission In the Bla Via Presynamentioning

confidence: 99%

Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala

Li¹,

Braga²,

Hough³

et al. 2005

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Public reporting burden for Ihis collection of information is estinnaled lo average 1 hour per response, including the time for reviewing inslojclions, searching existing data sources, gathering and malnlaining the data needed, and completing and reviewing this collection of Information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducing this burden to Washington Headquarters Services, Directorate for information Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Arlington, VA 22202-4302 and to the Office of Management and Budget,. Washington, DC 20503 AGENCY USE ONLY (Leave blank) REPORT DATEMarch 2 004 REPORT TYPE AND DATES COVEREDAnnual (1 Feb 2003 -1 Feb 2004 TITLE AND SUBTITLE Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala AUTHOR(S)He Li, M.D., Ph.D. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES)Henry SUPPLEMENTARY NOTESOriginal contains color plates: ALL DTIC reproductions will be in black and white 12a. DISTRIBUTION / AVAILABILITY STATEMENTApproved for Public Release; Distribution Unlimited ABSTRACT (Maximum 200 Words) 12b. DISTRIBUTION CODEPosttraumatic stress disorder (PTSD) is a syndrome of symptoms indicative of emotional dysfunction, which develop after exposure to life-threatening events. Prevalent symptoms are fear and anxiety, which become particularly intense during exposure to situations reminiscent of the traumatic events that precipitated the disease. The amygdala is a key component of the brain's neuronal network that determines the emotional significance of external events. Despite the central role of the amygdala in emotional behavior, little is known about the impact of stress on the amygdala's function. Clinical evidence indicates that norepinephrine and serotonin may participate in the synaptic plasticity phenomena that result in the memory of frightening events in PTSD. Our data indicate that the modulatory effects of norepinephrine and serotonin receptors on synaptic transmission, neuroplasticity and calcium homeostasis are altered in traumatically stressed rat amygdala. The results of this study may aid in the development of new strategies aimed at modifying and preventing the formation of traumatic memory, and thus could be useful for the treatment of combat PTSD in veterans. SUBJECT TERMS ~~~~Amygdala, post-traumatic stress disorder, serotonin, norepinephrine, calium signaling, adrenergic receptor, LTP, stress Conclusions 34References 35 Appendices 38 IntroductionIntense or chronic stress can have long-lasting consequences in an individual's health, and can be the cause of debiHtating mental ilhiesses. A very common mental ilhiess induced by traumatic stress is posttraumatic stress disorder (PTSD). PTSD is a syndrome of symptoms indicative of emotional dysfunction, which develop after exposure to life-threatening events, or very stressfiil situations of different nature. Prevalent symptoms are fear and anxiety, which become particularly intense during exposure to...

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A Facilitation Action of Reserpine on the Central Nervous System

Cited by 173 publications

References 1 publication

Stress Impairs α1A Adrenoceptor-Mediated Noradrenergic Facilitation of GABAergic Transmission in the Basolateral Amygdala

Stress Impairs α1A Adrenoceptor-Mediated Noradrenergic Facilitation of GABAergic Transmission in the Basolateral Amygdala

PHARMACOLOGICAL STUDY OF 1-(β-PHENYLETHYL) TRIAZOLO (4, 5-c) PYRIDINE HYDROCHLORIDE, A TRANQUILLIZING AGENT

Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala

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