Role of dopamine D-1 and D-2 receptor subtypes in mediating dopamine agonist effects on food consumption in rats

Martin‐Iverson, Mathew T.; Dourish, C T

doi:10.1007/bf00216064

Cited by 60 publications

(17 citation statements)

References 34 publications

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“…6,7 Conversely, dopamine agents suppress feeding behavior in animal models. 32 This report, following up previous investigations, provides strong evidence that dopaminergic agents help treat, and are not the cause of NE. A review of the original SRED series noted that dopaminergic therapy resolved the dysfunctional eating in 7 of 8 patients in whom the treatment was attempted.…”

Section: Ne/sred In Rls Is Relieved By and Not Caused By Dopaminergicsupporting

confidence: 55%

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Howell

Schenck

2012

Journal of Clinical Sleep Medicine

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upon SRED. However, we have noticed subtler non-dysfunctional forms of NE, commonly in the setting of RLS. Also, we have noted that many cases of zolpidem-induced SRED had been originally misdiagnosed as having psychophysiological insomnia (INS), a condition for which a benzodiazepine receptor agonist was prescribed, but later noted to have underlying motor restlessness as the cause of their sleep diffi culties.To establish whether NE is common in RLS and whether NE is a product of frequent nocturnal awakenings, we compared the frequency of NE as well as SRED among patients presenting with RLS and INS, a distinct condition of cognitive hypervigilance that manifests with frequent nocturnal awaken- Measurements and Results:Patients presenting with RLS (n = 88) or INS (n = 42) were queried for the presence of NE and SRED. RLS patients described nocturnal eating (61%) and SRED (36%) more frequently than INS patients (12% and 0%; both p < 0.0001). These fi ndings were not due to arousal frequency, as INS patients were more likely to have prolonged nightly awakenings (93%) than RLS patients (64%; p = 0.003). Among patients on sedative-hypnotics, amnestic SRED and sleepwalking were more common in the setting of RLS (80%) than INS (8%; p < 0.0001). Further, NE and SRED in RLS were not secondary to dopaminergic therapy, as RLS patients demonstrated a substantial drop (68% to 34%; p = 0.0026) in the frequency of NE after dopamine agents were initiated, and there were no cases of dopaminergic agents inducing novel NE or SRED. Conclusion: NE is common in RLS and not due to frequent nocturnal awakenings or dopaminergic agents. Amnestic SRED occurs predominantly in the setting of RLS mistreatment with sedating agents. In light of previous reports, these fi ndings suggest that nocturnal eating is a non-motor manifestation of RLS with several clinical implications discussed here. S C I E N T I F I C I N V E S T I g A T I O N SR estless legs syndrome, or Willis-Ekbom Syndrome (labeled RLS), is characterized by an underlying discomfort, primarily in the lower extremities that compels the affl icted to move. These symptoms are relieved, although only momentarily, with movement and may interfere with sleep initiation or maintenance. 1 RLS has been associated with non-motor phenomena. In particular, patients with RLS often describe other comorbidities such as mood and anxiety disorders, 2 as well as other nocturnal compulsions such as nocturnal smoking that interfere with sleep.3 Further, patients with these non-motor manifestations of RLS have more severe motor restlessness as measured by the International RLS Rating Scale. Recently, an investigation demonstrated a high frequency of dysfunctional nocturnal eating (SRED) in patients with RLS. This community-based case-control study found that 33 of 100 RLS patients met criteria for SRED compared to only 1% of normal population controls. 4 The authors pondered whether SRED was related to underlying RLS brain pathology or whether it was merely "killing time" during prolonged nocturn...

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Section: Ne/sred In Rls Is Relieved By and Not Caused By Dopaminergicsupporting

confidence: 55%

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Howell

Schenck

2012

Journal of Clinical Sleep Medicine

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“…However, through the preponderance of evidence, it is suggested that dopamine agents are not the cause of SRED. First, dopamine agents suppress feeding behavior in animal models [100]. Second, a review of the original SRED series noted that dopaminergic therapy resolved the dysfunctional eating in 7 of 8 patients in whom the treatment was attempted [72].…”

Section: Nocturnal Eating (Ne) Is Pervasive Among Patients With Restlessmentioning

confidence: 99%

Parasomnias: An Updated Review

2012

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Parasomnias are abnormal behaviors emanating from or associated with sleep. Sleepwalking and related disorders result from an incomplete dissociation of wakefulness from nonrapid eye movement (NREM) sleep. Conditions that provoke repeated cortical arousals, or promote sleep inertia lead to NREM parasomnias by impairing normal arousal mechanisms. Changes in the cyclic alternating pattern, a biomarker of arousal instability in NREM sleep, are noted in sleepwalking disorders. Sleep-related eating disorder (SRED) is characterized by a disruption of the nocturnal fast with episodes of feeding after an arousal from sleep. SRED is often associated with the use of sedative-hypnotic medications; in particular, the widely prescribed benzodiazepine receptor agonists. Recently, compelling evidence suggests that nocturnal eating may in some cases be a nonmotor manifestation of Restless Legs Syndrome (RLS). rapid eye movement (REM) Sleep Behavior Disorder (RBD) is characterized by a loss of REM paralysis leading to potentially injurious dream enactment. The loss of atonia in RBD often predates the development of Parkinson's disease and other disorders of synuclein pathology. Parasomnia behaviors are related to an activation (in NREM parasomnias) or a disinhibition (in RBD) of central pattern generators (CPGs). Initial management should focus on decreasing the potential for sleep-related injury followed by treating comorbid sleep disorders. Clonazepam and melatonin appear to be effective therapies in RBD, whereas paroxetine has been reported effective in some cases of sleep terrors. At this point, pharmacotherapy for other parasomnias is less certain, and further investigations are necessary.Keywords Parasomnia . Sleepwalking . Sleep terrors . REM sleep behavior disorder . Restless legs syndrome Classification of ParasomniasParasomnias are typically classified by the sleep state from which they arise: non-rapid eye movement sleep (NREM) and rapid eye movement sleep (REM) (see Table 1 NREM parasomnias include: confusional arousals, sleepwalking disorder, and sleep terrors. These behaviors arise when the cortex incompletely arouses from deep NREM sleep, often due to comorbid conditions that provoke repeated arousal or promote sleep inertia. Changes in the cyclic alternating pattern, a biomarker of arousal instability in NREM sleep, are noted in sleepwalking and related disorders [3].Sleep-related eating disorder (SRED) is currently classified in the International Classification of Sleep Disorders, 2nd edition (ICSD-2) under "Other Parasomnia" [1]. However the vast majority of SRED cases emanate from NREM [4], and the complex amnestic behaviors with ambulation are striking similar to sleepwalking [5]. Furthermore, both SRED and sleepwalking are frequently triggered by sedating agents in the setting of underlying motor restlessness [6]. Thus, considering these similarities, SRED will be reviewed immediately after NREM parasomnias.REM sleep behavior disorder is the most clinically relevant REM parasomnia. The loss of atoni...

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“…Treit and Berridge (1990) have shown that the anorectic effect is not due to an enhancement of aversive palatability. Finally, the effect is measurable not only in non-deprived rats given access to a highly palatable diet, or in deprived rats with limited daily food availability, but is also detectable in free-feeding rats (Martin-Iverson and Dourish 1988).…”

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confidence: 99%

Differential antagonism of the effects of dopamine D1-receptor agonists on feeding behavior in the rat

Terry¹,

Katz²

1992

Psychopharmacology

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Abstract.A series of experiments was conducted to examine the effects of dopamine D 1 receptor agonists on food intake in rats. In the first experiment, the D 1 agonist SKF 38393 (3.0 30.0mg/kg) dose-dependently suppressed feeding during a 40 min food-access period, both in fooddeprived rats and in non-deprived rats fed a highly palatable diet. Non-deprived rats were more sensitive to these effects of SKF 38393. Using the limited-access, fooddeprivation procedure, a comparison was made between the anorectic effects of three D 1 agonists with differing intrinsic efficacies and receptor selectivities. Rank order of potencies for reducing food intake was SKF 82958 > SKF 77434 > SKF 38393 (EDs0 values: 0.7, 3.6 and 15.7 mg/kg, respectively). Dose-related, surmountable antagonism by the D 1 antagonist SCH 23390 (0.01 and 0.03mg/kg) was only obtained with SKF 82958 (0.1-10.0 mg/kg). In contrast to the other compounds, the effects of SKF 38393 were not appreciably altered by the D1 antagonist. The effects of SKF 82958 were also antagonized by the D 2 receptor antagonist spiperone (0.05 and 0.1 mg/kg), although not in a dose-dependent manner. The present results support a role for DI receptors in central feeding mechanisms. They also suggest that the effects of SKF 38393 on feeding may not be mediated exclusively by the D 1 receptor and, further, that SKF 38393 may not serve well in behavioral studies as a prototypical D~ agonist. The results also demonstrate the need for comparisons among several compounds in studies of D 1 mediated behavioral effects.

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Role of dopamine D-1 and D-2 receptor subtypes in mediating dopamine agonist effects on food consumption in rats

Cited by 60 publications

References 34 publications

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Restless Nocturnal Eating: A Common Feature of Willis-Ekbom Syndrome (RLS)

Parasomnias: An Updated Review

Differential antagonism of the effects of dopamine D1-receptor agonists on feeding behavior in the rat

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