Effects of chronic substance P treatment and intracranial fetal grafts on learning after hippocampal kainic acid lesions

Sprick, Ulrich; Hasenöhrl, Rüdiger U.; Krauth, J.; Klapdor, Karin; Huston, Joseph P.

doi:10.1016/0196-9781(95)02105-1

Cited by 15 publications

(5 citation statements)

References 63 publications

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“…Notably, systemic SP treatment was able to improve long-term memory and reversal learning performances [20] , [24] , [52] , [53] , confirming the notion that SP easily crosses the blood-brain barrier [54] .…”

Section: Discussionsupporting

confidence: 59%

Systemic Administration of Substance P Recovers Beta Amyloid-Induced Cognitive Deficits in Rat: Involvement of Kv Potassium Channels

et al. 2013

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Reduced levels of Substance P (SP), an endogenous neuropeptide endowed with neuroprotective and anti-apoptotic properties, have been found in brain and spinal fluid of Alzheimer's disease (AD) patients. Potassium (K+) channel dysfunction is implicated in AD development and the amyloid-β (Aβ)-induced up-regulation of voltage-gated potassium channel subunits could be considered a significant step in Aβ brain toxicity. The aim of this study was to evaluate whether SP could reduce, in vivo, Aβ-induced overexpression of Kv subunits. Rats were intracerebroventricularly infused with amyloid-β 25–35 (Aβ25–35, 20 µg) peptide. SP (50 µg/Kg, i.p.) was daily administered, for 7 days starting from the day of the surgery. Here we demonstrate that the Aβ infused rats showed impairment in cognitive performances in the Morris water maze task 4 weeks after Aβ25–35 infusion and that this impairing effect was prevented by SP administration.Kv1.4, Kv2.1 and Kv4.2 subunit levels were quantified in hippocampus and in cerebral cortex by Western blot analysis and immunofluorescence. Interestingly, SP reduced Kv1.4 levels overexpressed by Aβ, both in hippocampus and cerebral cortex.Our findings provide in vivo evidence for a neuroprotective activity of systemic administration of SP in a rat model of AD and suggest a possible mechanism underlying this effect.

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Section: Discussionsupporting

confidence: 59%

Systemic Administration of Substance P Recovers Beta Amyloid-Induced Cognitive Deficits in Rat: Involvement of Kv Potassium Channels

et al. 2013

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“…1993). The role of SP in the hippocampus remains uncertain, although it has recently been suggested that the peptide can facilitate learning in the rat (Huston & Hasenohrl 1995;Sprick et al . 1996).…”

Section: Introductionmentioning

confidence: 99%

Modulation by substance P of synaptic transmission in the mouse hippocampal slice

Kouznetsova

Nistri

1998

Eur J of Neuroscience

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The modulatory action of substance P on synaptic transmission of CA1 neurons was studied using intra- or extracellular recording from the mouse hippocampal slice preparation. Bath-applied substance P (2-4 microM) or the selective NK1 receptor agonist substance P methylester (SPME, 10 nM-5 microM) depressed field potentials (recorded from stratum pyramidale) evoked by focal stimulation of Schaffer collaterals. This effect was apparently mediated via NK1 receptors since it was completely blocked by the selective NK1 antagonist SR 140333. The field potential depression by SPME was significantly reduced in the presence of bicuculline. Intracellular recording from CA1 pyramidal neurons showed that evoked excitatory postsynaptic potentials (EPSPs) and evoked inhibitory postsynaptic potentials (IPSPs) were similarly depressed by SPME, which at the same time increased the frequency of spontaneous GABAergic events and reduced that of spontaneous glutamatergic events. The effects of SPME on spontaneous and evoked IPSPs were prevented by the ionotropic glutamate receptor blocker kynurenic acid. In tetrodotoxin (TTX) solution, no change in either the frequency of spontaneous GABAergic and glutamatergic events or in the amplitude of responses of pyramidal neurons to 4 microM alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) or 10 microM N-methyl-D-aspartate (NMDA) was observed. On the same cells, SPME produced minimal changes in passive membrane properties unable to account for the main effects on synaptic transmission. The present data indicate that SPME exerted its action on CA1 pyramidal neurons via a complex network mechanism, which is hypothesized to involve facilitation of a subset of GABAergic neurons with widely distributed connections to excitatory and inhibitory cells in the CA1 area.

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“…2 (Flohr & Ltineburg, 1982;Igarashi et al, 1985;Mattioli et al, 1992;Antonawich et al, 1993;Bannon et al, 1995;Sprick et al, 1996). Such promotive effects might be due to their known neurotrophic effects (Jonsson & Hallman, 1982;Nyakas et al, 1985;van der Neut et al, 1988;Iwasaki et al, 1989;Kowall et al, 1991).…”

Section: Resultsmentioning

confidence: 99%

ACTH4 ‐10, Substance P, and Dizolcipine (Mk‐801) Accelerate Functional Recovery After Hemilabyrinthectomy in Goldfish

2000

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SUMMARYIn this study, we evaluated the goldfish model of hemilabyrinthectomy for investigating potential recovery-promoting drugs. In this lesion model, the unilateral removal of the labyrinth induces a postural imbalance in response to light (Dorsal Light Reflex), from which the animals can recover over time. The behavioral effects of two neuropeptides were testednamely, of substance P and ACTH4-10, both of which are known to promote functional recovery in several other lesion models. Furthermore, the effect of MK-801, an antagonist of the glutamatergic NMDAreceptor subtype, was tested because this substance has also been shown to exert a neuroprotective effect. After lesion of the right labyrinth, the animals (n=12) were treated intraperitoneally daily either with vehicle (n=12), substance P (n=ll),

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Effects of chronic substance P treatment and intracranial fetal grafts on learning after hippocampal kainic acid lesions

Cited by 15 publications

References 63 publications

Systemic Administration of Substance P Recovers Beta Amyloid-Induced Cognitive Deficits in Rat: Involvement of Kv Potassium Channels

Systemic Administration of Substance P Recovers Beta Amyloid-Induced Cognitive Deficits in Rat: Involvement of Kv Potassium Channels

Modulation by substance P of synaptic transmission in the mouse hippocampal slice

ACTH4 ‐10, Substance P, and Dizolcipine (Mk‐801) Accelerate Functional Recovery After Hemilabyrinthectomy in Goldfish

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