The Isolation of a New Hypotensive Peptide, Neurotensin, from Bovine Hypothalami

Carraway, Robert E.; Leeman, Susan E.

doi:10.1016/s0021-9258(19)43429-7

Cited by 1,424 publications

(194 citation statements)

References 18 publications

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“…NTS localization to specific brain regions suggested a link between NTS and the hypothalamic-anterior pituitary-ovarian axis. 12,13 Wellcontrolled studies showed that hypothalamic NTS is not involved in regulation of pituitary gonadotropin release, 12 but neural control of metabolism may directly or indirectly impact the reproductive endocrine axis. 60 A few reports implicate NTS in aspects of ovarian function, 61 oviductal transport, 62,63 implantation, 64 and sperm capacitation.…”

Section: Discussionmentioning

confidence: 99%

Neurotensin: A novel mediator of ovulation?

et al. 2021

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Section: Discussionmentioning

confidence: 99%

Neurotensin: A novel mediator of ovulation?

et al. 2021

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“…I) NEUROTENSIN. Neurotensin, a peptide of 13 amino acids, was originally isolated from bovine hypothalamus (288). The potential role of neurotensin in neuroendocrine regulation has been reviewed by Aronin et al (89) and more recently by Rostene and Alexander (1507).…”

Section: Neuropeptidesmentioning

confidence: 99%

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

et al. 2007

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Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin's signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

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“…Neurotensin, a tridecapeptide first isolated by Carraway and Leeman (1973) is found in brain and the periphery. Centrally it acts as both a neurotransmitter and neuromodulator involved in a wide range of physiological functions such as antinociception, hypothermia, stimulation of anterior pituitary hormone secretion, muscle relaxation and dopamine neurotransmission (Bissette, et al, 1976;Clineschmidt, et al, 1979;Rostene, et al, 1992;Kitabi, et al, 1992, Binder, et al, 2001.…”

Section: Introductionmentioning

confidence: 99%

Effects of chronic infusion of neurotensin and a neurotensin NT1 selective analogue PD149163 on amphetamine-induced hyperlocomotion

et al. 2008

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Neurotensin (NT) has been proposed as an endogenous antipsychotic based in part on the similarity in behavioural effects to antipsychotic drugs, for example, attenuation of both amphetamine-induced hyperlocomotion (AH) and amphetamine disrupted pre-pulse inhibition in the rat. However, there is some evidence that repeated administration of NT or an analogue produces behavioural tolerance to such effects. The present experiments sought to confirm and extend these findings by testing the effects on AH of 7 days central administration of NT and the NT1 selective analogue PD 149163 and the effects of 21 days central administration of NT. NT and PD149163 continuously administered for 7 days produced no effect on AH (in contrast to attenuation with a single injection here and previously reported), whereas 21 days of NT administration potentiated AH. Together, these studies report that the effects of NT or a NT analogue on AH depends on the duration of administration of peptide. The results are discussed in comparison with the reported antipsychotic properties of acute administration of NT and possible mechanisms involving NT1 receptors.

show abstract

The Isolation of a New Hypotensive Peptide, Neurotensin, from Bovine Hypothalami

Cited by 1,424 publications

References 18 publications

Neurotensin: A novel mediator of ovulation?

Neurotensin: A novel mediator of ovulation?

Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Effects of chronic infusion of neurotensin and a neurotensin NT1 selective analogue PD149163 on amphetamine-induced hyperlocomotion

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