Serotonergic dorsal raphe neurons from obese zucker rats are hyperexcitable

Ohliger-Frerking, Patricia; Horwitz, Barbara A; Horowitz, J. M.

doi:10.1016/s0306-4522(03)00360-9

Cited by 18 publications

(18 citation statements)

References 27 publications

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“…The latter effect declines with age [316] which would also be in line with ex vivo 5-HT measures [313]. A lower hypothalamic baseline concentration, although not being found in some studies, could be explained with an increased control via raphe somatodendritic 5-HT1A autoreceptors, although the physiological significance of intrinsically hyperexcitable dorsal raphe neurons in Zucker rats needs to be established [282]. Interestingly, the 5-HT1A agonist induced hypophagia in obese, but not in lean Zucker rats, where it expectedly stimulated feeding [313].…”

Section: Changes In the Brain Satiety In Different Nutritional Statessupporting

confidence: 52%

“…Decreased 5-HT transporter mRNA in neurons of the dorsal raphe nucleus in ob/ob mouse [278] seems to be in line with a rather direct 5-HT-leptin connection. In obese Zucker rats with a mutation in the leptin receptor [279][280][281] there is hyperexcitability of raphe neurons by leptin in an early developmental stage [282]. In normal rats, intracerebroventricular leptin aggravates the feeding-induced release of 5-HT in the LH [283].…”

Section: -Ht Interactions With Cck and Leptinmentioning

confidence: 99%

“…Changes in in the excitability of serotonergic raphe neurons in obese Zucker rats occur as early as between postnatal day 14 and 25 [282]. In addition to presynaptic feedback via autoreceptors, postsynaptic feedback in the control of 5-HT neurons has been suggested [323].…”

Section: Changes In the Brain Satiety In Different Nutritional Statesmentioning

confidence: 99%

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Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

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Serotonin has been implicated in the control of satiety for almost four decades. Historically, the insight that the appetite suppressant effect of fenfluramine is linked to serotonin has stimulated interest in and research into the role of this neurotransmitter in satiety. Various rodent models, including transgenic models, have been developed to identify the involved 5-HT receptor subtypes. This approach also required the availability of receptor ligands of different selectivity, and behavioural techniques had to be developed simultaneously which allow differentiating between unspecific pharmacological effects of these ligands and 'true' 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 3 IntroductionWhat are the behavioural and physiological mechanisms that promote satiety? How is satiety defined? Satiety can be seen as a behavioural state which arises from food consumption and suppresses the initiation of eating for a particular period of time [1]. This description alone suggests a high degree of complexity as peripheral post-ingestive and post-absorptive signals need to be relayed to the brain where they are integrated with other signals to produce (or not) the behavioural state called satiety. The state of satiety is brought about a process called satiation, where sensory, cognitive and early post-ingestive mechanisms bring feeding to a halt and thus stopping a meal. Promoting satiation alone must not necessarily lead to reduced total food intake as the frequency of meals could be increased subsequently. Many peripheral and brain mechanisms have been identified that are involved in the expression satiety and it has been suggested that serotonin accelerates satiation and prolongs satiety [2]. In the following, we will review the role of serotonin in satiety in more detail 1 . The reader will see that, despite immense progress made during the last years, the field is still far from being resolved.As serotonin (5-Hydroxytryptamine; 5-HT) is a phylogenetically old neurotransmitter, various functions had time to evolve in different phyla, but maybe also in different species. 5-HT receptors exist in animal cells for millions of years and they are as old as adrenoreceptors ore some peptide receptors, possibly even older [5,6]. Even in invertebrates such as molluscs (Aplysia californica) and annelids (Hirudo medicinalis), 5-HT might functionally be related to food intake [7]. 5-HT is involved in feeding even in the honeybee where it has separate effects in the gut and in the insect brain [8]. In general, however, 5-HT seems rather to be involved in appetitive behaviours in invertebrates whereas it has more of a satiating effect in vertebrates [9]. In general, 5-HT neurons seem to be more extensively distributed throughout the body in lower animals than in higher animals including mammals where 5-HT neurones...

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Section: Changes In the Brain Satiety In Different Nutritional Statessupporting

confidence: 52%

Section: -Ht Interactions With Cck and Leptinmentioning

confidence: 99%

See 1 more Smart Citation

Serotonin controlling feeding and satiety

Voigt

Fink

2015

Behavioural Brain Research

257

167

View full text Add to dashboard Cite

show abstract

“…Sustained hypoxia can result in decreased 5-HT cell expression in the DRN of rabbits [13] and Fos expression in the 5-HT neurons of the RMg and DRN in rats [14]. Ohliger-Frerking demonstrated that DRN 5-HT neurons are hyper-excitable in obese Zucker rats, which are often used as animal models of OSAS [15]. McNamara et al have observed that IH could result in a higher 5-HT concentration in DRN of adult rabbits [16].…”

Section: Introductionmentioning

confidence: 99%

Raphe serotonergic neurons modulate genioglossus corticomotor activity in intermittent hypoxic rats

Wang

Sun

et al. 2014

Respir Res

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Background Genioglossus activity is greater during wakefulness but decreases to a weaker state during sleep in obstructive sleep apnea syndrome (OSAS) patients, compared to healthy subjects. Previous studies suggested that the corticomotor control of the genioglossus was modified in OSAS patients. Intermittent hypoxia (IH), the typical pathophysiological change in OSAS, can induce genioglossus facilitation. The serotonergic neurons of the raphe dorsal (DRN) and magnus nuclei (RMg) are responsive to hypoxia and play important roles in the control of the genioglossus. However, it remains unknown whether DRN and RMg serotonergic neurons are responsible for the facilitated corticomotor activity of the genioglossus during IH. This study explored the influence of IH on the corticomotor activity of the genioglossus by transcranial magnetic stimulation (TMS), and the role of DRN and RMg serotonergic neurons in this effect. Methods Rats were exposed to IH and divided into two groups. In one group, anti-SERT-SAP was microinjected into the DRN and RMg respectively to kill serotonergic neurons. In the other group, artificial cerebrospinal fluid (ACSF) was injected. Comparisons were conducted between the two groups during four weeks of IH and four weeks after IH. Results Compared to the corresponding ACSF-injected group, the DRN lesion group and RMg lesion group showed longer TMS latencies and lower amplitudes during IH from the 1 st to the 28 th day. After 28 days of IH, longer latencies and lower amplitudes were seen only in the DRN lesion group. Conclusion These results indicate that DRN and RMg serotonergic neurons play different roles in the facilitation of genioglossus corticomotor activity induced by IH.

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“…Serotonin levels and serotonin turnover have been reported to be altered in the obese Zucker rat in different directions depending on the age of the animals (Ohliger-Frerking et al, 2003;Voigt et al, 2011). Anorectic agents, such as fenfluramine, release serotonin to decrease food intake and body weight (Weiss et al, 1990;Bello and Liang, 2011).…”

Section: Introductionmentioning

confidence: 99%