Modulation of memory retention by neuropeptide K

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

doi:10.1016/0006-8993(90)91717-u

Cited by 47 publications

(10 citation statements)

References 43 publications

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“…In these studies, the effects of SP were reversed by treatment with an NK1 receptor antagonist. Administration of SP has also been reported to improve passive and active avoidance performance (Pelleymounter et al 1986;Schlesinger et al 1983) and ICV administration of NKA enhances T-maze learning (Flood et al 1990). Systemic administration of SP has also been demonstrated to counteract age-related learning deficits (Hasenohrl et al 1990(Hasenohrl et al , 1994.…”

Section: Discussionmentioning

confidence: 97%

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

et al. 2007

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Section: Discussionmentioning

confidence: 97%

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

et al. 2007

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“…Tachykinins have been proposed to play a role in learning and memory possibly by a modulatory action in the hippocampus and amygdala (Flood et al , 1990; Nagel et al , 1993). The results from the present study have shown that senktide activated many limbic regions including the hippocampus and amygdala by acting on NK 3 tachykinin receptors, supporting the involvement of these receptors in learning and memory.…”

Section: Discussionmentioning

confidence: 99%

Localization of Fos‐like immunoreactivity induced by the NK₃ tachykinin receptor agonist, senktide, in the guinea‐pig brain

Yip

Chahl

1997

British J Pharmacology

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1 The e ects of intracerebroventricular (i.c.v.) administration of the NK 3 tachykinin receptor agonist, senktide (10 nmol each side), in guinea-pigs pretreated with the selective NK 3 tachykinin receptor antagonist, SR142801 (3 mg kg 71 subcutaneous, s.c., 30 min before senktide), or its less active enantiomer, SR142806 (3 mg kg 71 s.c. 30 min before senktide), on behaviour and on the distribution of Fos-like immunoreactivity (Fos-LI) in central neurones were investigated. Guinea-pigs were chosen for the study since they possess NK 3 tachykinin receptors with pharmacological characteristics similar to those in man. 2 Wet-dog shakes, but not locomotor activity, elicited by senktide i.c.v. were signi®cantly reduced by SR142801 but not by SR142806, con®rming the involvement of NK 3 tachykinin receptors in wet-dog shake behaviour. 3 Senktide induced increased numbers of Fos-LI neurones in the following brain areas: frontal, parietal and piriform cortex, the lateral septum, the CA1, CA2, subiculum and dentate gyrus of the hippocampus, most areas in the amygdala, thalamus and hypothalamus, medial geniculate nucleus and the ventral cochlear nucleus. Pretreatment with SR142801, but not with SR142806, before administration of senktide inhibited Fos-LI expression in the cingulate cortex, dentate gyrus of the hippocampus, some regions of the thalamus, hypothalamus and amygdala and the ventral cochlear nucleus. 4 The present results are the ®rst demonstration that senktide induces Fos-LI in widespread areas of the guinea-pig brain. It is proposed that NK 3 tachykinin receptors may play a more extensive role in the control of diverse brain functions, including cortical processing, learning and memory, neuroendocrine and behavioural regulation, than is currently recognized.

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“…Neuropeptide K has a similar distribution pattern as substance P in the hippocampus, and may be released together with substance P (Shults et al, 1987). Neuropeptide K improves memory when administered centrally or directly into the hippocampus (Flood et al, 1990). Thus, two peptides processed from ␤-preprotachykinin may occur in septohippocampal neurons and may modulate memory.…”

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confidence: 97%

GABAergic septohippocampal neurons are not necessary for spatial memory

et al. 2001

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The medial septum/vertical limb of the diagonal band of Broca (MSDB) provides a major input to the hippocampus and is important for spatial memory. Both cholinergic and GABAergic MSDB neurons project to the hippocampus, and nonselective lesions of the MSDB or transections of the septohippocampal pathway impair spatial memory. However, selective lesions of cholinergic MSDB neurons using 192-IgG saporin (SAP) do not impair or only mildly impair spatial memory. Previously, intraseptal kainic acid was found to reduce levels of glutamic acid decarboxylase, a marker of GABAergic neurons, but not to alter the levels of choline acetyltransferase, a marker of cholinergic neurons. The present study further characterized the effects of kainic acid on GABAergic MSDB neurons and examined the effects of intraseptal kainic acid on spatial memory. Saline, kainic acid, SAP, or the combination of kainic acid and SAP was administered into the MSDB of rats. Spatial memory was assessed in an eight-arm radial maze and a water maze. Kainic acid destroyed GABAergic septohippocampal neurons, but spared cholinergic neurons. SAP eliminated MSDB cholinergic neurons, sparing noncholinergic neurons. Coadministration of kainic acid and SAP destroyed GABAergic and cholinergic MSDB neurons. Acquisition of the radial maze task and performance on this task with 4-h delays were unimpaired by intraseptal kainic acid or SAP, but were impaired by coadministration of kainic acid and SAP. Acquisition of the water maze task was unaffected by intraseptal kainic acid, delayed slightly by SAP, and impaired severely by coadministration of kainic acid and SAP. These results provide evidence that kainic acid at appropriate concentrations effectively destroys GABAergic septohippocampal neurons, while sparing cholinergic MSDB neurons. Furthermore, lesions of the GABAergic septohippocampal neurons do not impair spatial memory. While lesions of cholinergic MSDB neurons may mildly impair spatial memory, the combined lesion of GABAergic and cholinergic septohippocampal neurons resulted in a memory impairment that was greater than that observed after a selective lesion to either population. Thus, damage of GABAergic or cholinergic MSDB neurons, which together comprise the majority of the septohippocampal pathway, cannot totally account for the spatial memory impairment that is observed after nonselective lesions of the MSDB.

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Modulation of memory retention by neuropeptide K

Cited by 47 publications

References 43 publications

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

Localization of Fos‐like immunoreactivity induced by the NK₃ tachykinin receptor agonist, senktide, in the guinea‐pig brain

GABAergic septohippocampal neurons are not necessary for spatial memory

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Modulation of memory retention by neuropeptide K

Cited by 47 publications

References 43 publications

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

Disruption of the neurokinin-3 receptor (NK3) in mice leads to cognitive deficits

Localization of Fos‐like immunoreactivity induced by the NK3 tachykinin receptor agonist, senktide, in the guinea‐pig brain

GABAergic septohippocampal neurons are not necessary for spatial memory

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Localization of Fos‐like immunoreactivity induced by the NK₃ tachykinin receptor agonist, senktide, in the guinea‐pig brain