Modulation of memory processing by neuropeptide Y varies with brain injection site

Flood, James F.; Baker, Margaret; Hernandez, Ernesto N.; Morley, John E.

doi:10.1016/0006-8993(89)91706-x

Cited by 141 publications

(55 citation statements)

References 48 publications

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“…recently was assured by G. G. Glenner (personal communication) that it is not attributable to technical error in the original sequence determinations (10,11). Also tested were residues [12][13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28] …”

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confidence: 99%

“…The above peptides were dissolved appropriately for injection: [Gln'1]f-(1-28) and P- (18)(19)(20)(21)(22)(23)(24)(25)(26)(27)(28) were dissolved in dimethyl sulfoxide and diluted in physiological saline to a final concentration of 8% (vol/vol) dimethyl sulfoxide; p- (12)(13)(14)(15)(16)(17)(18)(19)(20) was dissolved in 0.01 M HCI followed by dilution and neutralization with 0.01 M NaOH; and p-(12-28) was dissolved directly in physiological saline. All solutions were prepared fresh daily and coded to eliminate experimenter bias.…”

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confidence: 99%

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Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease.

Flood

Morley

Roberts

1991

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

141

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Immediate post-training intracerebroventricular administration of a synthetic peptide homologous to IB protein of brain amyloid, [Gln"J].B-(1-28), caused amnesia for footshock active avoidance training in mice in a dose-dependent fashion. This effect was specific to memory processing since the peptide did not cause amnesia when injected 24 hr after training nor did it disturb storage or retrieval of older memories. Shorter fragments of the amyloid j3 protein consisting of residues 12-28, 18-28, and 12-20 also were amnestic when given intracerebroventricularly, residues 12-20 being least effective. The hippocampus, a brain structure importantly involved in learning and memory, consistently shows severe pathological changes and deposition ofamyloid in patients with Alzheimer disease. Immediate post-training bilateral intrahippocampal injection of [Gln"]fi-(1-28) produced amnesia at much lower doses than did [Gln"'],3-(1-28) injected intracerebroventricularly. Thus these experimental results suggest a possible direct role of amyloid .3 protein or fragments thereof in an aspect of the spectrum of cognitive deficit in Alzheimer disease.

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confidence: 99%

mentioning

confidence: 99%

Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease.

Flood

Morley

Roberts

1991

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

141

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“…NPY administered directly into the forebrain hippocampal memory (22, 31, 32). The DMTS paradigm developed for rats formation selectively enhances or impairs retention, depending in our laboratory is similar to others (5, 10, 11, 22), with the upon the location of injection within rostral or caudal portions important addition that reference memory is also measured on of the hippocampus (14). NPY has also been demonstrated each trial along with working memory (2,38).…”

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confidence: 75%

“…These data suggest that the effects may additionally be related to the specific anatomical loeffect of proactive interference resulting from NPY administracation of those receptors. In this regard, Flood et al (14) tion may only be revealed when there is weakened stimulus showed that injection of NPY into the rostral portion of the hipcontrol for the target stimulus for that trial.…”

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confidence: 99%

Neuropeptide-Y both improves and impairs delayed matching-to-sample performance in rats

Thomas

Ahlers

1991

Pharmacology Biochemistry and Behavior

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“…It is thought to be involved in a variety of physiological functions such as blood pressure regulation [2,3], memory processing and retention (4,5), and its most noticeable effect, that of stimulation of feeding [6,7]. It is a ubiquitous neuropeptide both in the central and peripheral nervous system.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

Gui-Hua¹,

Gardner²,

Westfall³

2007

Biochemical Pharmacology

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In rat pheochromocytoma (PC-12) cells the dopamine D 2 receptor agonists apomorphine (APO) and n-propylnorapomorphine (NPA) produced a concentration dependent inhibition of K + -evoked neuropeptide Y release (NPY-ir). The effect of APO was blocked by the dopamine D 2 -receptor antagonist, eticlopride, but not the D 1 /D 3 or the D 4 /D 2 antagonists, SCH23390 or clozapine, respectively. The D 1 /D 5 receptor agonist, SKF38393 or the D 3 agonists PD128907 and 7-OH DPAT had no effect. Selective N and L-type voltage gated Ca 2+ channel blockers, ω-Conotoxin GVIa (CtxGVIa) and nifedipine, respectively, produced a concentration dependent inhibition of NPY-ir release but were not additive with APO. The Ca 2+ /calmodulin-dependent protein kinase (CaM kinase) II inhibitor KN-62 produced a concentration-dependent inhibition of NPY-ir release but the combination of KN-62 and APO produced no further inhibition. PMA-mediated protein kinase C stimulation significantly increased both basal and K + -evoked release of NPY-ir, and in the presence of PMA APO had no inhibitory effect. The PKC antagonist, chelerythrine, inhibited K + -evoked NPYir release but was not additive with APO. Neither forskolin-mediated adenylate cyclase activation and the active cAMP analog Sp-cAMPS, nor the adenylate cyclase inhibitor SQ 22536, and the competitive inhibitor of cAMP-dependent protein kinases Rp-cAMPS, had any significant effect on K + -evoked NPY-ir release. This suggests the inhibitory effect of APO on K + -evoked release of NPYir from PC 12 cells is most likely mediated through activation of dopamine D 2 receptors leading to direct inhibition of N and L-type voltage gated Ca 2+ channels, or indirect inhibition of PKC, both of which would reduce [Ca 2+ ] i and inactivate CaM kinase.

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Modulation of memory processing by neuropeptide Y varies with brain injection site

Cited by 141 publications

References 48 publications

Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease.

Amnestic effects in mice of four synthetic peptides homologous to amyloid beta protein from patients with Alzheimer disease.

Neuropeptide-Y both improves and impairs delayed matching-to-sample performance in rats

Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells)

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