Effects of acute and chronic treatment with amitryptyline on the sleep-wake activity of rats

Obál, F.; Benedek, György; Lelkes, Z.

doi:10.1016/0028-3908(85)90078-4

Cited by 20 publications

(10 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, it is known that antidepressant medications including tricyclic antidepressants, can induce a loss or severe reduction in REM sleep. 64,65 In our clinical practice, we note that the addition of a small dose of amitriptyline (10 mg) at night can serve to disrupt the sleep cycle and postpone the first REM-associated CH attack by a few hours (unpublished observations).…”

Section: -Hydroxytryptamine (5ht Serotonin)mentioning

confidence: 98%

Primary Headache Disorders and Circadian Biology: A Clinical, Imaging, and Therapy Perspective

Cohen

Kaube

2005

Headache Currents

View full text Add to dashboard Cite

Primary headache syndromes such as hypnic headache, and trigeminal autonomic cephalgias (TACs) such as cluster headache, paroxysmal hemicrania, and SUNCT (Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing), are associated with varying degrees with attacks that occur with circadian rhythmicity. In hypnic headache, the attacks occur exclusively during sleep, and in cluster headache the attacks predominate in sleep in 75% of patients. The TACs, especially cluster headache and SUNCT, have been associated on functional imaging with activation of the hypothalamus during attacks. There is also evidence in patients with cluster headache of altered secretory rhythms of a variety of hypophyseal hormone systems including melatonin, cortisol, and others. Given the role of the suprachiasmatic nucleus in the diurnal cycle, the hypothalamus is implicated as a generator of headaches with a prominent circadian rhythm. This article discusses the physiological and biochemical mechanisms that implicate the hypothalamus in the generation of a variety of primary headache disorders.Abbreviations: CH = cluster headache, ECH = episodic cluster headache, CCH = chronic cluster headache, TAC = trigeminal autonomic cephalgia, OSA = obstructive sleep apnea, REM = rapid eye movement, NREM = non rapid eye movement, 5HT = 5-hydroxytryptamine, PH = paroxysmal hemicrania, SUNCT = Short-lasting Unilateral Neuralgiform headache attacks with Conjunctival injection and Tearing

show abstract

Section: -Hydroxytryptamine (5ht Serotonin)mentioning

confidence: 98%

Primary Headache Disorders and Circadian Biology: A Clinical, Imaging, and Therapy Perspective

Cohen

Kaube

2005

Headache Currents

View full text Add to dashboard Cite

show abstract

“…The range of doses, 0.04-10 mg/ kg, was large. The influence of a low dose was included since-at least upon chronic administration-the effects of antidepressants upon sleep patterns may be expressed at low doses relative to those exerting a positive influence upon mood (see Obal et al 1985).…”

Section: Drugsmentioning

confidence: 99%

“…Upon discontinuation of long-term administration of these classes of antidepressant, further, there is usually a rebound elevation in PS (Staner et al 1995;Trivedi et al 1999). Mimicking these clinical findings, chronic (and acute) treatment of rats with various tricyclic agents (Hill et al 1980;Obal et al 1985), SSRIs or NARIs (Kafi de Saint Hilaire et al 1984;Kleinlogel and Burki 1987;Sommerfelt and Ursin 1991;Neckelmann et al 1996;Ursin 2002), is similarly followed by a marked decrease in PS, together with a rebound elevation in PS following withdrawal of treatment (Kafi de Saint Hilaire et al 1984;Maudhuit et al 1994). In addition, milnacipran, a mixed serotonin and noradrenaline reuptake blocker (SNRI), was recently suggested to decrease PS in rats when administered at the onset of the light phase for a period of 21 days (Gervasoni et al 2002).…”

Section: Introductionmentioning

confidence: 96%

Acute administration of the novel serotonin and noradrenaline reuptake inhibitor, S33005, markedly modifies sleep–wake cycle architecture in the rat

et al. 2005

View full text Add to dashboard Cite

show abstract

“…& 1978Polc et a/. 1979;Obal et al 1985). Studies aimed at differentiating the noradrenergic and 5-HT-ergic components in the mechanism of actions on sleep of these drugs, however, are few (Justafre & Gaillard 1981;Kafi-de St. Hilaire et a/.…”

mentioning

confidence: 99%

“…1985) have been suggested to be involved in the regulation of wakefulness and sleep. Secondly, the sleep-wake cycle may result from a reciprocal interaction between slow wave sleep (SWS) and rapid eye movement sleep (REMS) (Borbely 1982) and changes in SWS are often mirrored by opposite alterations in wakefulness (Obal et al 1985). The use of adrenoceptor antagonists with different kinds of a-and P-adrenoceptor subtype selectivity makes it possible to study the mechanisms of the compensatory changes in the amounts of SWS and wakefulness occurring concurrently with the uptake-inhibitor induced REMS deprivation (Polc et al 1979;Reyes et al 1983;Obal et al 1985).…”

mentioning

confidence: 99%

Effects of Serotonin and Noradrenaline Uptake Blockers on Wakefulness and Sleep in Cats

Hilakivi

Kovala

Leppävuori

et al. 1987

Pharmacology & Toxicology

View full text Add to dashboard Cite

The aim of the study was to examine the role of serotonergic (5-HT) and noradrenergic mechanisms in the regulation of wakefulness and sleep. For this purpose, adult cats with implanted electrodes for EEG, EOG and EMG were exposed to the 5-HT uptake blocker citalopram (0.1, 0.5 and 5.0 mg/kg intraperitoneally) and the noradrenaline uptake blocker prindamine (5 mg/kg intraperitoneally) at the start of continuous 16-hour sleep-wake recordings. Citalopram increased deep slow wave sleep and decreased REMS. Also prindamine decreased REMS but initially increased the proportion of time spent in the state of active wakefulness. Furthermore, to examine the interactions between 5-HT-nergic and noradrenergic mechanisms in the regulation of sleep, the administration of citalopram was preceded by intraperitoneal injections of phentolamine (10 mg/kg), an alpha-antagonist, and propranolol (5 mg/kg), a beta-antagonist. Phentolamine was totally ineffective against citalopram whereas propranolol partially counteracted the effects of citalopram on sleep. Prindamine was combined with the alpha-antagonists yohimbine (1 mg/kg), phentolamine (10 mg/kg) and prazosin (1 mg/kg) or with the beta-antagonist propranolol (5 mg/kg). Yohimbine was without any effect on REMS, phentolamine partly antagonized prindamine-induced decrease in the percentage of REMS, and prazosin only prolonged REMS latency and reduced deep SWS as well. Propranolol partially antagonized the prindamine-induced initial increase in active wakefulness time.(ABSTRACT TRUNCATED AT 250 WORDS)

show abstract

Effects of acute and chronic treatment with amitryptyline on the sleep-wake activity of rats

Cited by 20 publications

References 23 publications

Primary Headache Disorders and Circadian Biology: A Clinical, Imaging, and Therapy Perspective

Primary Headache Disorders and Circadian Biology: A Clinical, Imaging, and Therapy Perspective

Acute administration of the novel serotonin and noradrenaline reuptake inhibitor, S33005, markedly modifies sleep–wake cycle architecture in the rat

Effects of Serotonin and Noradrenaline Uptake Blockers on Wakefulness and Sleep in Cats

Contact Info

Product

Resources

About