Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

Duncan, Marilyn J.; Franklin, Kathleen M.

doi:10.1016/j.brainres.2007.01.044

Cited by 26 publications

(19 citation statements)

References 63 publications

(91 reference statements)

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“…CB immunoreactivity was abundant throughout the BNST, with an enrichment of cells in medial portions of the BNST in accordance with previous studies in mice (Frantz & Tobin, ). Prominent CB expression has also been noted in the medial BNST of hamsters (Duncan & Franklin, ), rats (Kemppainen & Pitkanen, ; Sequier, Hunziker, Andressen, & Celio, ), primates (Côté, Sadikot, & Parent, ; Fudge & Tucker, ), and humans (Walter, Mai, Lanta, & Görcs, ), suggesting conservation of CB expression in the BNST across multiple species. Approximately 25% of RXFP3+ neurons co‐localized with CB, and 16% of RXFP3+ cells were both GABA+/CB+.…”

Section: Discussionmentioning

confidence: 95%

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Ch’ng

Brown

et al. 2019

J of Comparative Neurology

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The bed nucleus of the stria terminalis (BNST) is a critical node involved in stress and reward‐related behaviors. Relaxin family peptide receptor 3 (RXFP3) signaling in the BNST has been implicated in stress‐induced alcohol seeking behavior. However, the neurochemical phenotype and connectivity of BNST RXFP3‐expressing (RXFP3+) cells have yet to be elucidated. We interrogated the molecular signature and electrophysiological properties of BNST RXFP3+ neurons using a RXFP3‐Cre reporter mouse line. BNST RXFP3+ cells are circumscribed to the dorsal BNST (dBNST) and are neurochemically heterogeneous, comprising a mix of inhibitory and excitatory neurons. Immunohistochemistry revealed that ~48% of BNST RXFP3+ neurons are GABAergic, and a quarter of these co‐express the calcium‐binding protein, calbindin. A subset of BNST RXFP3+ cells (~41%) co‐express CaMKIIα, suggesting this subpopulation of BNST RXFP3+ neurons are excitatory. Corroborating this, RNAscope® revealed that ~35% of BNST RXFP3+ cells express vVGluT2 mRNA, indicating a subpopulation of RXFP3+ neurons are glutamatergic. RXFP3+ neurons show direct hyperpolarization to bath application of a selective RXFP3 agonist, RXFP3‐A2, while around 50% of cells were depolarised by exogenous corticotrophin releasing factor. In behaviorally naive mice the majority of RXFP3+ neurons were Type II cells exhibiting Ih and T type calcium mediated currents. However, chronic swim stress caused persistent plasticity, decreasing the proportion of neurons that express these channels. These studies are the first to characterize the BNST RXFP3 system in mouse and lay the foundation for future functional studies appraising the role of the murine BNST RXFP3 system in more complex behaviors.

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Section: Discussionmentioning

confidence: 95%

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Ch’ng

Brown

et al. 2019

J of Comparative Neurology

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“…The agonist 8-OH-DPAT can act on both the 5HT 1A and 5HT 7 subtype. While age-related changes in response to serotonin agonists have been reported, it is possible that this is not mediated by changes in the 5HT 1A and 5HT 7 receptor subtypes within the SCN, as work has shown that there are no age-related changes in the expression of mRNA for either the 5HT 1A or 5HT 7 receptor with age in the hamster SCN (Duncan et al 1999;Duncan and Franklin 2007). Further work should investigate not only serotonin receptor numbers but also function within the mouse SCN.…”

Section: Discussionmentioning

confidence: 98%

Circadian clock resetting in the mouse changes with age

Biello

2009

AGE

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The most widely recognised consequence of normal age-related changes in biological timing is the sleep disruption that appears in old age and diminishes the quality of life. These sleep disorders are part of the normal ageing process and consist primarily of increased amounts of wakefulness and reduced amounts of deep sleep. Changes in the amplitude and timing of the sleep-wake cycle appear to represent, at least in part, a loss of effective circadian regulation of sleep. Understanding alterations in the characteristics of stimuli that help to consolidate internal rhythms will lead to recommendations to improve synchronisation in old age. Converging evidence from both human and animal studies indicate that senescence is associated with alterations in the neural structure thought to be primarily responsible for the generation of the circadian oscillation, the suprachiasmatic nuclei (SCN). Work has shown that there are changes in the anatomy, physiology and ability of the clock to reset in response to stimuli with age. Therefore it is possible that at least some of the observed age-related changes in sleep and circadian timing could be mediated at the level of the SCN. The SCN contain a circadian clock whose activity can be recorded in vitro for several days. We have tested the response of the circadian clock to a number of neurochemicals that reset the clock in a manner similar to light, including glutamate, N-methyl-D-aspartate (NMDA), gastrin-releasing peptide (GRP) and histamine (HA). In addition, we have also tested agents which phase shift in a pattern similar to behavioural 'non-photic' signals, including neuropeptide Y (NPY), serotonin (5HT) and gamma-aminobutyric acid (GABA). These were tested on the circadian clock in young and older mice (approximately 4 and 15 months old). We found deficits in the response to specific neurochemicals but not to others in our older mice. These results indicate that some changes seen in the responsiveness of the circadian clock to light with age may be mediated at the level of the SCN. Further, the responsiveness of the circadian clock with age is attenuated to some, but not all stimuli. This suggests that not all clock stimuli loose their effectiveness with age, and that it may be possible to compensate for deficits in clock performance by enhancing the strength of those stimulus pathways which are intact.

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“…The present study extended previous reports of age-related attenuation of SCN expression of VIP mRNA (Krajnak et al, 1998a;Duncan et al, 2001) by demonstrating that aging also decreases SCN expression of mRNA for GRP. It should be noted that aging appears to selectively suppress GRP mRNA and VIP mRNA in the hamster SCN, because no effect of aging has been detected for several other mRNAs expressed in the hamster SCN, including those coding for vasopressin, somatostatin, calbindin-D28 and GAD67 (Duncan & Wheeler, 1999;Duncan et al, 2001;Duncan & Franklin, 2007). Both VIP and GRP are expressed in the ventral SCN (although their distributions are not identical; Moore & Silver, 1998;Morin et al, 2006), which is the region of the SCN that first exhibits changes in expression of the immediate-early gene Fos and circadian clock genes Per1 and Per2, after phase-resetting light pulses (Earnest & Olschowka, 1993;Hamada et al, 2001Hamada et al, , 2004Dardente et al, 2002;Yan & Silver, 2002), and both peptides are involved in mediating light-induced circadian phase shifts.…”

Section: Discussionmentioning

confidence: 99%

The effects of aging and chronic fluoxetine treatment on circadian rhythms and suprachiasmatic nucleus expression of neuropeptide genes and 5‐HT_1B receptors

Duncan

Hester

Hopper

et al. 2010

Eur J of Neuroscience

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Age-related changes in circadian rhythms, including attenuation of photic phase shifts, are associated with changes in the central pacemaker in the suprachiasmatic nucleus (SCN). Aging decreases expression of mRNA for vasoactive intestinal peptide (VIP), a key neuropeptide for rhythm generation and photic phase shifts, and increases expression of serotonin transporters and 5-HT1B receptors, whose activation inhibits these phase shifts. Here we describe studies in hamsters showing that aging decreases SCN expression of mRNA for gastrin-releasing peptide, which also modulates photic phase resetting. Because serotonin innervation trophically supports SCN VIP mRNA expression, and serotonin transporters decrease extracellular serotonin, we predicted that chronic administration of the serotonin-selective reuptake inhibitor, fluoxetine, would attenuate the age-related changes in SCN VIP mRNA expression and 5-HT1B receptors. In situ hybridization studies showed that fluoxetine treatment does not alter SCN VIP mRNA expression, in either age group, at zeitgeber time (ZT)6 or 13 (ZT12 corresponds to lights off). However, receptor autoradiographic studies showed that fluoxetine prevents the age-related increase in SCN 5-HT1B receptors at ZT6, and decreases SCN 5-HT1B receptors in both ages at ZT13. Therefore, aging effects on SCN VIP mRNA and SCN 5-HT1B receptors are differentially regulated; the age-related increase in serotonin transporter sites mediates the latter but not the former. The studies also showed that aging and chronic fluoxetine treatment decrease total daily wheel running without altering the phase of the circadian wheel running rhythm, in contrast to previous reports of phase resetting by acute fluoxetine treatment.

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Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

Cited by 26 publications

References 63 publications

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Circadian clock resetting in the mouse changes with age

The effects of aging and chronic fluoxetine treatment on circadian rhythms and suprachiasmatic nucleus expression of neuropeptide genes and 5‐HT_1B receptors

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Expression of 5-HT7 receptor mRNA in the hamster brain: Effect of aging and association with calbindin-D28K expression

Cited by 26 publications

References 63 publications

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Characterization of the relaxin family peptide receptor 3 system in the mouse bed nucleus of the stria terminalis

Circadian clock resetting in the mouse changes with age

The effects of aging and chronic fluoxetine treatment on circadian rhythms and suprachiasmatic nucleus expression of neuropeptide genes and 5‐HT1B receptors

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Product

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The effects of aging and chronic fluoxetine treatment on circadian rhythms and suprachiasmatic nucleus expression of neuropeptide genes and 5‐HT_1B receptors