Cellular localization of substance P‐ and neurokinin A‐encoding preprotachykinin mRna in the female rat brain

Harlan, Richard E.; Garcia, Meredith M.; Krause, James E.

doi:10.1002/cne.902870204

Cited by 104 publications

(57 citation statements)

References 113 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition, the majority were positive for dynorphin but negative for enkephalin. Previous studies have shown that the ICjM contains substance P (Beckstead and Kersey 1985;Gerfen and Young 1988;Harlan et al 1989). This suggests that ICjM neurons contain both dynorphin and substance P as is the case for some medium spiny neurons in the dorsal striatum.…”

Section: Phenotypes Of Clozapine-induced Fos-positive Neuronsmentioning

confidence: 99%

Phenotypic Characterization of Neuroleptic-Sensitive Neurons in the Forebrain Contrasting Targets of Haloperidol and Clozapine

Guo

Vincent

Fibiger

1998

Neuropsychopharmacology

View full text Add to dashboard Cite

The prototypical neuroleptic haloperidol and the atypical antipsychotic clozapine induce distinctly different patterns of c-fos expression in the forebrain. While haloperidol appears to increase c-fos expression via its D2 dopamineClozapine has been termed an "atypical" antipsychotic agent in part because at therapeutic doses it fails to produce the extrapyramidal, Parkinsonian-like side effects that are associated with the use of "typical" neuroleptics such as haloperidol and chlorpromazine. While the mechanisms by which clozapine generates its unique clinical profile are not established, recent studies from several laboratories have demonstrated that, compared to typical neuroleptics, clozapine produces a rather unique regional pattern of Fos-like immunoreactive From the Divison

show abstract

Section: Phenotypes Of Clozapine-induced Fos-positive Neuronsmentioning

confidence: 99%

Phenotypic Characterization of Neuroleptic-Sensitive Neurons in the Forebrain Contrasting Targets of Haloperidol and Clozapine

Guo

Vincent

Fibiger

1998

Neuropsychopharmacology

View full text Add to dashboard Cite

show abstract

“…SP, NKA and NKB bind preferentially to the NK1, NK2 and NK3 receptor, respectively [26], but each of these three neuropeptides is capable of eliciting responses from all three neurokinin receptors [27]. Our recent study showed that oral administration of an antagonist for all three neurokinin receptors (NK1, NK2 and NK3 receptors) has testicular toxicity through inhibition of gonadotropin secretion in dogs [28], suggesting that the reproductive toxicity of the antagonist might be associated with the mechanism of GnRH pulse generation.Tac1 (gene encoding SP, NKA, NPK and NPγ) and Tac2 (gene encoding NKB) mRNA-expressing neurons are located in several hypothalamic nuclei such as the medial preoptic area and ARC in rats [29,30]. SP or NPK neurons project their fibers to hypothalamic areas such as the medial preoptic area [31,32], paraventricular nucleus [33] and ARC in rats [34].…”

mentioning

confidence: 99%

“…Tac1 (gene encoding SP, NKA, NPK and NPγ) and Tac2 (gene encoding NKB) mRNA-expressing neurons are located in several hypothalamic nuclei such as the medial preoptic area and ARC in rats [29,30]. SP or NPK neurons project their fibers to hypothalamic areas such as the medial preoptic area [31,32], paraventricular nucleus [33] and ARC in rats [34].…”

mentioning

confidence: 99%

Involvement of Neurokinin Receptors in the Control of Pulsatile Luteinizing Hormone Secretion in Rats

et al. 2011

View full text Add to dashboard Cite

Abstract. It has recently been shown that neurokinin B, a tachykinin, is associated with GnRH pulse generation in sheep and goats. The aim of the present study was to clarify the role of tachykinin receptors in the control of LH secretion in rats. To this end, we evaluated the effect of CS-003, an antagonist for all three neurokinin receptors (NK1, NK2 and NK3 receptors), on pulsatile LH secretion in both sexes of rats with different routes of administration. Both oral and third ventricular administration of CS-003 suppressed LH secretion in both sexes of gonadectomized animals. Furthermore, intact male rats with oral administration of CS-003 showed decreased serum testosterone levels, which might be due to suppressed LH secretion. None of the three subtype-specific neurokinin receptor antagonists showed a significant effect on LH secretion in ovariectomized rats when each antagonist was singly administered. The present results suggest that neurokinins play a role in the control of pulsatile GnRH/LH secretion via multiple neurokinin receptors in both male and female rats. Key words: Luteinizing hormone, Neurokinin, Rat, Receptor (J. Reprod. Dev. 57: [409][410][411][412][413][414][415] 2011) ulsatile gonadotropin-releasing hormone (GnRH)/luteinizing hormone (LH) release is indispensable for regulation of gonadal functions, such as folliculogenesis, spermatogenesis and steroidogenesis, in rodents [1], ruminants [2,3] and primates [4]. The mechanism generating GnRH/LH pulses, called the GnRH pulse generator, has been suggested to be localized in the hypothalamus [5]. Recent studies have revealed that kisspeptin neurons located in the hypothalamus play a central role in regulating GnRH release [6,7]. Kisspeptin neurons have two populations in the hypothalamus [8]: One is located in the hypothalamic arcuate nucleus (ARC), and the other is located in the anteroventral periventricular nucleus (AVPV). Of these two populations, the AVPV kisspeptin neurons have been reported to be involved in the regulation of GnRH/LH surge [9,10]. On the other hand, the role of ARC kisspeptin neurons is still unclear, but several lines of evidence suggest that the population is associated with GnRH pulse generation [11].Recent studies have shown an interesting and essential aspect of the ARC kisspeptin neurons. Most kisspeptin neurons have neurokinin B (NKB) and dynorphin (Dyn) in sheep [12], goats [13] and rodents [14], and thus the neurons have been called KNDy neurons [15]. Colocalization of those three neuropeptides in the ARC neurons might be associated with GnRH pulse generation. It has recently been reported that mutations of genes encoding NKB and its receptor are associated with gonadotropin deficiency in humans [16], and central administration of a selective NKB receptor agonist stimulates LH secretion in sheep [17] and monkeys [18]. These reports indicate the significance of NKB/NK3 signaling in GnRH/gonadotropin release in these animal species. In addition to neurokinin B, nor-BNI, a κ-opioid receptor antagonist (KOR), rev...

show abstract

“…For example, substance P is synthesized in nociceptive primary sensory neurons, which send C-and A␦ fibers to dorsal horn projection neurons in lamina I and IV-V, and to nociceptionspecific interneurons in lamina II-III of the spinal cord. Axons of projection neurons terminate in many supraspinal nuclei that are involved in pain transmission (10,11). Nociceptive stimulation triggers the release of substance P from C-afferent terminals in the marginal layers of the spinal cord (12), evokes slow excitatory postsynaptic potentials in second-order sensory neurons in the dorsal horn, and facilitates their activation (13).…”

mentioning

confidence: 99%

Hypoalgesia in mice with a targeted deletion of the tachykinin 1 gene

Zimmer

Baffi

et al. 1998

Proc. Natl. Acad. Sci. U.S.A.

198

103

View full text Add to dashboard Cite

The tachykinin neuropeptides, substance P and substance K, are produced in nociceptive primary sensory neurons and in many brain regions involved in pain signaling. However, the precise role and importance of these neuropeptides in pain responses has been debated. We now show that mice that cannot produce these peptides display no significant pain responses following formalin injection and have an increased pain threshold in the hotplate test. On the other hand, the mutant mice react normally in the tail f lick assay and acetic acid-induced writhing tests. These results demonstrate that substance P and͞or substance K have essential functions in specific responses to pain.The tachykinins are a family of structurally related neuropeptides. In the mouse, they are encoded by the genes Tac1 and Tac2. Tac1 produces substance P, substance P (neurokinin A), neurokinin A (3-10), neuropeptide K, and neuropeptide ␥ as a result of differential splicing and posttranslational processing (1-4). Tac2 produces the peptide neurokinin B.The undecapeptide substance P was first detected by von Euler and Gaddum (5) in 1931. Its structure was revealed by Leeman and her coworkers (6, 7) in 1971. The Tac1 cDNA was cloned in 1983 by Nakanishi and his coworkers (2,8). The Tac1 gene is expressed in many regions in the central and peripheral nervous system, as well as in nonneuronal tissues. Substance P has been implicated in a variety of physiological processes including cardiovascular, respiratory, and gastrointestinal functions; inflammatory responses; and nociception. In addition, Hunt and coworkers have suggested that substance P may be involved in axon guidance during embryonic development (9).The precise role of substance P in these processes is unclear. For example, substance P is synthesized in nociceptive primary sensory neurons, which send C-and A␦ fibers to dorsal horn projection neurons in lamina I and IV-V, and to nociceptionspecific interneurons in lamina II-III of the spinal cord. Axons of projection neurons terminate in many supraspinal nuclei that are involved in pain transmission (10, 11). Nociceptive stimulation triggers the release of substance P from C-afferent terminals in the marginal layers of the spinal cord (12), evokes slow excitatory postsynaptic potentials in second-order sensory neurons in the dorsal horn, and facilitates their activation (13). These data, together with other functional evidence (11,14), indicated an important role for substance P in the processing of nociceptive signals.We have begun to use a genetic approach to study the functions of tachykinin peptides. As a first step, we have generated mice with a targeted mutation in the Tac1 gene. These mice are viable and fertile, but exhibit striking defects in nociceptive behaviors. MATERIALS AND METHODS Generation and Breeding of Tac1؊͞؊ Mice. Tac1 mutations were established by homologous recombination in MPI2 embryonic stem (ES) cells according to standard protocols (15). One mutant ES cell line was used to derive chimeras by morula aggrega...

show abstract

Cellular localization of substance P‐ and neurokinin A‐encoding preprotachykinin mRna in the female rat brain

Cited by 104 publications

References 113 publications

Phenotypic Characterization of Neuroleptic-Sensitive Neurons in the Forebrain Contrasting Targets of Haloperidol and Clozapine

Phenotypic Characterization of Neuroleptic-Sensitive Neurons in the Forebrain Contrasting Targets of Haloperidol and Clozapine

Involvement of Neurokinin Receptors in the Control of Pulsatile Luteinizing Hormone Secretion in Rats

Hypoalgesia in mice with a targeted deletion of the tachykinin 1 gene

Contact Info

Product

Resources

About