Neuropeptide-Y immunoreactivity in the pilocarpine model of temporal lobe epilepsy

Lurton, Dominique; Cavalheiro, Ésper A.

doi:10.1007/pl00005739

Cited by 43 publications

(28 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Third, immunostaining in the outer part of the molecular layer was less distinct, consistent with the loss of HIPP cells. These findings replicate previous reports (Lurton and Cavalheiro, 1997;Vezzani et al, 1999a;Scharfman et al, 2000) and confirm that recurrent mossy fibers expressed NPY at the time our electrophysiological studies were performed.…”

Section: Long-lasting Expression Of Npy In Mossy Fibers After Pilocarsupporting

confidence: 93%

See 1 more Smart Citation

Spontaneous Release of Neuropeptide Y Tonically Inhibits Recurrent Mossy Fiber Synaptic Transmission in Epileptic Brain

Tu¹,

Timofeeva²,

Jiao³

et al. 2005

J. Neurosci.

View full text Add to dashboard Cite

These results suggest that even the spontaneous release of NPY (or an active metabolite) from recurrent mossy fibers is sufficient to depress glutamate release from this pathway. Tonic release of NPY accounts at least partially for the low probability of glutamate release from recurrent mossy fiber terminals, impedes the ability of these fibers to synchronize granule cell discharge, and may protect the hippocampus from seizures that involve the entorhinal cortex. This pathway may synchronize granule cell discharge more effectively in human brain than in rat because of its lower expression of NPY.

show abstract

Section: Long-lasting Expression Of Npy In Mossy Fibers After Pilocarsupporting

confidence: 93%

“…Seizures dramatically alter the expression of neuropeptide Y (NPY) in the dentate gyrus (Schwarzer et al, 1995;Lurton and Cavalheiro, 1997;Makiura et al, 1999;Vezzani et al, 1999a). NPY, a 36-amino acid polypeptide, is one of the most abundant and widely distributed neuroactive peptides in the brain (Hökfelt et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Spontaneous Release of Neuropeptide Y Tonically Inhibits Recurrent Mossy Fiber Synaptic Transmission in Epileptic Brain

Tu¹,

Timofeeva²,

Jiao³

et al. 2005

J. Neurosci.

View full text Add to dashboard Cite

show abstract

“…NPY expression was found markedly increased in hilar GABAergic interneurons, granule cells and sprouted mossy fibers (Bellmann et al, 1991;Chafetz et al, 1995;Lurton and Cavalheiro, 1997;Scharfman et al, 1999Scharfman et al, , 2002Sperk et al, 1992;Takahashi et al, 2000;Vezzani et al, 1996). NPY in the dentate gyrus can influence synaptic transmission and neurogenesis, demonstrates remarkable plasticity after seizures (Scharfman and Gray, 2006), and may have an anticonvulsive action (Furtinger et al, 2001;Klapstein and Colmers, 1997;Vezzani et al, 1999).…”

Section: Discussionmentioning

confidence: 99%

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

Kharlamov

Kelly

2007

Brain Research

View full text Add to dashboard Cite

This study characterized morphological changes in the cortex and hippocampus of Sprague-Dawley rats following photothrombotic infarction and epileptogenesis with emphasis on the distribution of neuropeptide Y (NPY) expression. Animals were lesioned in the left sensorimotor cortex and compared with age-matched naïve and sham-operated controls by immunohistochemical techniques at 1, 3, 7, and 180 days post-lesioning (DPL). NPY immunostaining was assessed by light microscopy and quantified by the optical fractionator technique using unbiased stereological methods. At 1, 3, and 7 DPL, the number of NPY-positive somata in the lesioned cortex was increased significantly compared to controls and the contralateral cortex. At 180 DPL, lesioned epileptic animals with frequent seizure activity demonstrated significant increases of NPY expression in the cortex, CA1, CA3, hilar interneurons, and granule cells of the dentate gyrus. In addition to NPY immunostaining, neuronal degeneration, cell death/cell loss, and astroglial response were assessed with cell-specific markers. Nissl and NeuN staining showed reproducible infarctions at each investigated time point. FJB-positive somata were most abundant in the infarct core at 1 DPL, decreased markedly at 3 DPL, and virtually absent by 7 DPL. Activated astroglia were detected in the cortex and hippocampus following lesioning and the development of seizure activity. In summary, NPY protein expression and morphological changes following cortical photothrombosis were time-, region-and pathologic state-dependent. Alterations in NPY expression may reflect reactive or compensatory responses of the rat brain to acute infarction and to the development and expression of epileptic seizures.

show abstract

“…High doses of MK-801 may be less effective because in addition to blocking NMDA receptors both MK-801 and ketamine also block sigma receptors (Bouchard et al, 1997). There is growing evidence that sigma receptors modulate release of neurotransmitters such as glutamate (Meyer et al, 2002), and acetylcholine (Lurton and Cavalheiro, 1997;Vallee et al, 1997). It is possible that the actions of MK-801 at sigma receptors contribute to its failure at high doses.…”

Section: Discussionmentioning

confidence: 99%

A comparison of three NMDA receptor antagonists in the treatment of prolonged status epilepticus

2004

View full text Add to dashboard Cite

Three different classes of NMDA receptor antagonists were compared for their effectiveness in terminating prolonged status epilepticus (SE), induced by continuous hippocampal stimulation. Animals were treated after 150 min of SE by intraperitoneal administration of increasing doses of 3-((R,S)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP), MK-801 (dizocilpine), ifenprodil, or saline. EEG recordings were used to determine seizure termination. The first experiment (n = 57 animals) determined the most effective anticonvulsant dose of each agent by determining its ability to terminate SE within the next 300 min. Five control rats treated with normal saline after 150 min of SE continued to exhibit continuous seizures for the next 300 min. All drugs were administered after 150 min of SE. CPP terminated seizures with an ED 50 of 6.4 mg/kg; the maximal effective dose was 15 mg/kg. MK-801 has an ED 50 of 1.4 mg/kg; the maximal effective dose was 2 mg/kg. Ifenprodil was maximally effective at 30 mg/kg. However, an ED 50 could not be calculated. In a subsequent experiment, the NMDA antagonists were compared for their ability to terminate prolonged SE within 60 min of their administration at the most effective dose. MK-801 (2.0 mg/kg) terminated SE in 6 of 10 animals within 60 min, CPP (15 mg/kg) terminated it in 1 of 9 animals; ifenprodil (30 mg/kg) did not terminate it in any of 9 animals treated. In the 300 min following administration, CPP (6/9) and MK-801 (6/10) were equally efficacious in terminating SE but ifenprodil (2/7) was less effective (P = 0.065, chi-square test). The results indicate that the non-competitive NMDA receptor antagonist MK-801 was superior to the competitive antagonist CPP and the pH-sensitive site antagonist ifenprodil, in terminating prolonged experimental SE.

show abstract

Neuropeptide-Y immunoreactivity in the pilocarpine model of temporal lobe epilepsy

Cited by 43 publications

References 31 publications

Spontaneous Release of Neuropeptide Y Tonically Inhibits Recurrent Mossy Fiber Synaptic Transmission in Epileptic Brain

Spontaneous Release of Neuropeptide Y Tonically Inhibits Recurrent Mossy Fiber Synaptic Transmission in Epileptic Brain

Changes in neuropeptide Y protein expression following photothrombotic brain infarction and epileptogenesis

A comparison of three NMDA receptor antagonists in the treatment of prolonged status epilepticus

Contact Info

Product

Resources

About