Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

Mantha, Anil K.; Moorthy, K.; Cowsik, Sudha M.; Baquer, Najma Zaheer

doi:10.1007/s10522-005-6044-z

Cited by 22 publications

(24 citation statements)

References 72 publications

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“…The activity of Na + -K + ATPase increased in all the age groups with an increase in the NKB peptide concentration, as compared with that of age matched control synaptosomes. This result supported the results of Mantha et al [28]. However incubation of synaptosomes of E2 treated rats with various concentration of NKB increased the activity of Na + -K + ATPase significantly.…”

Section: Discussionsupporting

confidence: 92%

“…Age related alterations of brain Na + -K + ATPase activity has been reported earlier [39] [40]. The activity of Na + -K + ATPase was measured using different concentrations of Aβ (25 -35), NKB and combined treatment of NKB and Aβ (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35) in different age groups of control (without E2 treated) and E2 treated rat brain synaptosomes. In different concentration of Aβ (25 -35) incubation, the enzyme Na + -K + ATPase inhibited in all the age groups when compared with age matched controls.…”

Section: Discussionmentioning

confidence: 89%

“…They are known to reduce oxidative stress in the brain [26]- [28], and to reverse the neurotoxic effects of Aβ in neurons and a role in neurodegenerative diseases [29] [30]. The SP or related tachykinins exert a neurotrophic action on central neurons and the loss of this input in selective areas results, in the expression of neurodegenerative disorders [31].…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic Potential of 17β Estradiol with Tachykinin Neuropeptide NKB and Aβ(25 - 35) on Na+ - K+ ATPase Activity in Aging Female Rat Brain

Jha¹,

Mishra²,

Kumar³

et al. 2015

AAR

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The Na + -K + ATPase is an enzyme responsible for the active transport of Na + and K + in most eukaryotic cells. The aim of the present study was to determine the effect of Tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 -35) on 17β estradiol (E2) treated aging female rat brain synaptosomes of different age groups, by assaying Na + -K + ATPase enzyme activity. An in vitro incubation of isolated synaptosomes with Aβ (25 -35) showed toxic effects while NKB showed stimulating effect on the Na + -K + ATPase activity, and the combined NKB + Aβ (25 -35) incubations showed a partial effect as compared to the Aβ (25 -35) alone. To understand whether E2 affects the expression of Na + -K + ATPase molecules, we examined the expression of Na + -K + ATPase subunit α1 and β2 in E2 treated aging female rat brain synaptosomes. The enzyme was quantified by SDS PAGE in control and E2 treated rat brain. We observed that the expression of α1 and β2 Na + -K + ATPase molecules increased and reversed to a normal level in E2 treated synaptosomes. These results confirmed that E2 increased turnover of Na + -K + ATPase molecules in aging rat brain. The present findings also suggest a possible role of NKB with E2 in the age related changes in the brain.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

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Therapeutic Potential of 17β Estradiol with Tachykinin Neuropeptide NKB and Aβ(25 - 35) on Na+ - K+ ATPase Activity in Aging Female Rat Brain

Jha¹,

Mishra²,

Kumar³

et al. 2015

AAR

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“…The aging-associated loss of cholinergic neurons can be prevented by the endogenous NK3-R agonist NK-B (37). NK-B stimulates AChE activity in the aged brain (38). Therefore, an attenuated increase in ACh level upon senktide administration in the inferior learners may have at least partially resulted from additional AChE activation.…”

Section: Discussionmentioning

confidence: 99%

Neurokinin3 receptor as a target to predict and improve learning and memory in the aged organism

Silva

Lenz

Rotter

et al. 2013

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

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Impaired learning and memory performance is often found in aging as an early sign of dementia. It is associated with neuronal loss and reduced functioning of cholinergic networks. Here we present evidence that the neurokinin3 receptors (NK3-R) and their influence on acetylcholine (ACh) release may represent a crucial mechanism that underlies age-related deficits in learning and memory. Repeated pharmacological stimulation of NK3-R in aged rats was found to improve learning in the water maze and in object-place recognition. This treatment also enhanced in vivo acetylcholinergic activity in the frontal cortex, hippocampus, and amygdala but reduced NK3-R mRNA expression in the hippocampus. Furthermore, NK3-R agonism incurred a significantly higher increase in ACh levels in aged animals that showed superior learning than in those that were most deficient in learning. Our findings suggest that the induced activation of ACh, rather than basal ACh activity, is associated with superior learning in the aged. To test whether natural variation in NK3-R function also determines learning and memory performance in aged humans, we investigated 209 elderly patients with cognitive impairments. We found that of the 15 analyzed single single-nucleotide ploymorphism (SNPs) of the NK3-R-coding gene, TACR3, the rs2765 SNP predicted the degree of impairment of learning and memory in these patients. This relationship could be partially explained by a reduced right hippocampus volume in a subsample of 111 tested dementia patients. These data indicate the NK3-R as an important target to predict and improve learning and memory performance in the aged organism. senktide | in vivo microdialysis H umans exhibit a decline in cognitive capacity with age, which may progressively lead to dementia (1). Age-dependent morphological and physiological changes within the cholinergic system of the brain have been described as a major mechanism underlying impairments of learning and memory (2, 3). Numerous studies in aged rats have revealed that a degeneration of cholinergic neurons in the basal forebrain is associated with learning and >memory deficits (4). Likewise, the consistent correlations found between cholinergic degeneration and cognitive impairments indicate a high correspondence between acetylcholinergic activity and the magnitude of cognitive decline (4-6). This relationship has also been shown in patients with Alzheimer's disease (7,8).The neuropeptide neurokinins (NKs) substance P, neurokinin A, neurokinin B (NK-B), neuropeptide K, neuropeptide γ, and hemokinin 1 bind to the three known NK-receptors (NK3-R) (NK1-, NK2-, and NK3-R) with different degrees of affinity, whereby NK-B is the preferred ligand to NK3-R (9). NK3-Rs are widespread in the brain, including areas that are implicated in processes governing learning and memory such as the hippocampus, frontal cortex (FC), and medial septum (10, 11). There is a close interaction between NK3-R and the cholinergic system. NK3-R are localized on cholinacetyltransferase-containing neurons in ...

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“…They are known to reduce oxidative stress in the brain [16][17][18]; to reverse the neurotoxic effects of Aβ in neurons and a role in neurodegenerative diseases [19,20].…”

Section: Introductionmentioning

confidence: 99%

Effects of tachykinin neuropeptide NKB and Aβ (25-35) on antioxidant enzymes status in 17β estradiol treated aging female rats

Jha¹,

Ali²,

Pandey³

et al. 2013

AAR

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Aging is the leading risk factor for neurodegenerative diseases and oxidative stress involved in the pathophysiology of these diseases. These changes increase during menopausal condition in females when the level of estradiol is decreased. The aim of the present study was to determine the effect of tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 -35) on 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. Aging brain functions were assayed by measuring the activities of antioxidant enzymes-superoxide dismutase (SOD) and monoamine oxidase (MAO) with neuropeptides. An in-vitro incubation of Aβ (25 -35) in E2 treated brain synaptosomes showed toxic effects on all the parameters. However, NKB and NKB combined with Aβ (25 -35) showed stimulating effects in E2 treated rat brain synaptosomes. In the present study, an increase in activity of SOD and decrease in the level of MAO, in the presence of NKB and combined NKB and Aβ in E2 treated brain synaptosomes of aging rats. This study elucidates that treatment of NKB and Aβ with E2 in combination exerts more protective influence than their individual application, against excitotoxicity in age related changes.

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Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

Cited by 22 publications

References 72 publications

Therapeutic Potential of 17<i>β</i> Estradiol with Tachykinin Neuropeptide NKB and A<i>β</i>(25 - 35) on Na<sup>+</sup> - K<sup>+</sup> ATPase Activity in Aging Female Rat Brain

Therapeutic Potential of 17<i>β</i> Estradiol with Tachykinin Neuropeptide NKB and A<i>β</i>(25 - 35) on Na<sup>+</sup> - K<sup>+</sup> ATPase Activity in Aging Female Rat Brain

Neurokinin3 receptor as a target to predict and improve learning and memory in the aged organism

Effects of tachykinin neuropeptide NKB and A<i>β</i> (25-35) on antioxidant enzymes status in 17<i>β</i> estradiol treated aging female rats

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Membrane Associated Functions of Neurokinin B (NKB) on Aβ (25–35) Induced Toxicity in Aging Rat Brain Synaptosomes

Cited by 22 publications

References 72 publications

Therapeutic Potential of 17&lt;i&gt;β&lt;/i&gt; Estradiol with Tachykinin Neuropeptide NKB and A&lt;i&gt;β&lt;/i&gt;(25 - 35) on Na&lt;sup&gt;+&lt;/sup&gt; - K&lt;sup&gt;+&lt;/sup&gt; ATPase Activity in Aging Female Rat Brain

Therapeutic Potential of 17&lt;i&gt;β&lt;/i&gt; Estradiol with Tachykinin Neuropeptide NKB and A&lt;i&gt;β&lt;/i&gt;(25 - 35) on Na&lt;sup&gt;+&lt;/sup&gt; - K&lt;sup&gt;+&lt;/sup&gt; ATPase Activity in Aging Female Rat Brain

Neurokinin3 receptor as a target to predict and improve learning and memory in the aged organism

Effects of tachykinin neuropeptide NKB and A&lt;i&gt;β&lt;/i&gt; (25-35) on antioxidant enzymes status in 17&lt;i&gt;β&lt;/i&gt; estradiol treated aging female rats

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Therapeutic Potential of 17<i>β</i> Estradiol with Tachykinin Neuropeptide NKB and A<i>β</i>(25 - 35) on Na<sup>+</sup> - K<sup>+</sup> ATPase Activity in Aging Female Rat Brain

Therapeutic Potential of 17<i>β</i> Estradiol with Tachykinin Neuropeptide NKB and A<i>β</i>(25 - 35) on Na<sup>+</sup> - K<sup>+</sup> ATPase Activity in Aging Female Rat Brain

Effects of tachykinin neuropeptide NKB and A<i>β</i> (25-35) on antioxidant enzymes status in 17<i>β</i> estradiol treated aging female rats