Regional changes in neuropeptide levels after 5,7-dihydroxytryptamine-induced serotonin depletion in the rat brain

Kondo, Yoichi; Ogawa, Norio; Asanuma, Masato; Hirata, Hiroshi; Tanaka, Kazuhiko; Kawada, Yoshitaka; Mori, Akitane

doi:10.1007/bf01244874

Cited by 14 publications

(8 citation statements)

References 21 publications

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“…Whether this increase in SSLI reflects a decreased release, increased biosynthesis or decreased degradation of SSLI cannot be answered at this time. In agreement with the present results, a widespread increase in rat hippo¬ campal and cortical SSLI levels has been reported after intracerebroventricular injection of 5,7-DHT (Kakigi & Maeda 1992, Kondo et al 1993.…”

Section: Discussionsupporting

confidence: 94%

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Muñoz-Acedo

Alvaro-Alonso²,

Arilla³

1995

Journal of Endocrinology

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To date, it is unknown whether intrapancreatic serotonergic nerves can influence pancreatic somatostatin (SS) content and the SS receptor/effector system in the exocrine pancreas. In this study, the intrapancreatic serotonergic nerves were chemically ablated by injecting a specific serotonin (5-HT) neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), into the substance of the gland. Three days after the injection, the 5-HT-like immunoreactive levels in the pancreas were reduced by more than 85% whereas somatostatin-like immunoreactive levels had increased (86%). The number of SS receptors in the pancreatic acinar cell membranes of the 5,7-DHT-treated rats was also increased (72%). No significant differences were seen in basal or forskolin-stimulated adenylate cyclase (AC) enzyme activities in the control and the 5,7-DHT-treated groups. In spite of the increase in the number of SS receptors in the pancreatic acinar cell membranes of 5,7-DHT-treated rats, SS caused a significantly lower inhibition of AC activity in these membranes. This finding is related to the observed decrease of a 41 kD pertussis toxin-sensitive substrate, presumably the alpha i subunit of the guanine nucleotide inhibitory protein, in pancreatic acinar cell membranes 3 days after intrapancreatic 5,7-DHT administration when compared with the corresponding controls. The functions of pancreatic serotonergic nerves seem to be associated with enteropancreatic communication. These data together with the present results suggest that pancreatic SS content and the SS receptor/effector system in the exocrine pancreas may be regulated by enteropancreatic serotonergic nerve fibers and may participate in enteropancreatic reflexes.

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Section: Discussionsupporting

confidence: 94%

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Muñoz-Acedo

Alvaro-Alonso²,

Arilla³

1995

Journal of Endocrinology

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“…Messenger RNA for all three of these receptors is expressed in a large percentage of striatal neurons. The demonstration of substantial amounts of colocalization of these serotonin receptors with enkephalin, substance P and dynorphin provides an anatomical basis for earlier observations that alterations in serotonergic input can lead to changes in the levels of striatal neuropeptides (Walker et al, 1991;Kondo et al, 1993).…”

Section: The Striatal Serotonergic Systemmentioning

confidence: 84%

Colocalization of serotonin receptor subtypes 5-HT2A, 5-HT2C, and 5-HT6 with neuropeptides in rat striatum

1996

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There are two primary output pathways from the striatum: a projection to the globus pallidus, and projection to the substantia nigra. Certain striatally expressed neuropeptides are differentially distributed between these two pathways. Specifically, enkephalin is expressed in striatopallidal neurons, whereas substance P and dynorphin are expressed in striatonigral neurons. Several serotonin receptors are also prominently expressed in the striatum, but little is known about how they fit into the molecular neuroanatomy described above. We used double-label in situ hybridization to determine the striatal distribution of the mRNAs of the serotonin2A (5-HT2A), serotonin2C (5-HT2C), and serotonin6 (5-HT6) receptors in relation to enkephalin, substance P, and dynorphin expressing output neurons. Rat brain sections were simultaneously hybridized with an 35S riboprobe for one of the serotonin receptors and a digoxygenin labeled riboprobe for one of the neuropeptides. Sections were examined by using brightfield microscopy, and the degree of colocalization of the two mRNAs determined. All the serotonin receptors colocalized extensively with all three of the neuropeptides examined. None of the serotonin receptors showed preferential colocalization in striatopallidal (enkephalin containing), or striatonigral (substance P or dynorphin containing) cells. The 5-HT2A and 5-HT2C mRNAs displayed a differential distribution with regard to the scattered islands of strongly dynorphin mRNA positive cells, which are thought to reside in the striatal patch compartment. Within these islands, 5-HT2C mRNA expression was much higher than in surrounding areas. 5-HT2A mRNA showed the opposite pattern with decreased expression over dynorphin rich cell clusters.

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“…A key inhibitory pathway, noradrenergic fibers descending from the pons, sprout after peripheral nerve injury in mice and rats (Hayashida et al, 2008; Ma and Eisenach, 2003) and presence of this system may play an inhibitory role in glial activation in the spinal cord following peripheral nerve injury (Hayashida et al, 2012). On the other hand, a key facilitatory pathway from the nucleus raphe magnus releases serotonin into the spinal cord, resulting in increased synthesis of dynorphin (Hentall et al, 2006; Kondo et al, 1993). This endogenous opioid peptide paradoxically drives injury-induced hypersensitivity (Gardell et al, 2002; Wang et al, 2001) by actions on n-methyl-d-aspartate receptors (Laughlin et al, 1997).…”

Section: Introductionmentioning

confidence: 99%

The puerperium alters spinal cord plasticity following peripheral nerve injury

2013

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Tissue and nerve damage can result in chronic pain. Yet, chronic pain after cesarean delivery is remarkably rare in women and hypersensitivity from peripheral nerve injury in rats resolves rapidly if the injury occurs in the puerperium. Little is known regarding the mechanisms of this protection except for a reliance on central nervous system oxytocin signaling. Here we show that density of inhibitory noradrenergic fibers in the spinal cord is greater when nerve injury is performed in rats during the puerperium, whereas expression of the excitatory regulators dynorphin A and neuregulin-1 in the spinal cord is reduced. The puerperium did not alter spinal cord microgial and astrocyte activation. Astrocyte activation, as measured by GFAP expression, was not evident in female rats with injury, regardless of delivery status suggesting sex differences in spinal astrocyte activation after injury. These results suggest a change in the descending inhibitory/facilitating balance on spinal nociception neurotransmission during the puerperium, as mechanisms for its protective effect against injury-induced hypersensitivity.

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Regional changes in neuropeptide levels after 5,7-dihydroxytryptamine-induced serotonin depletion in the rat brain

Cited by 14 publications

References 21 publications

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Pancreatic changes in somatostatin content and receptor/effector system after intrapancreatic injection of 5,7-dihydroxytryptamine

Colocalization of serotonin receptor subtypes 5-HT2A, 5-HT2C, and 5-HT6 with neuropeptides in rat striatum

The puerperium alters spinal cord plasticity following peripheral nerve injury

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