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Chronic Infusion (chronic + infusion)
Selected AbstractsNeuropeptide Y delays hippocampal kindling in the ratHIPPOCAMPUS, Issue 5 2003Sophie Reibel Abstract Chronic intrahippocampal infusion of the neurotrophin brain-derived neurotrophic factor (BDNF) has been shown to delay kindling epileptogenesis in the rat and several lines of evidence suggest that neuropeptide Y could mediate these inhibitory effects. Chronic infusion of BDNF leads to a sustained overexpression of neuropeptide Y in the hippocampus, which follows a time course similar to that of the suppressive effects of BDNF on kindling. In vivo, acute applications of neuropeptide Y or agonists of its receptors exert anticonvulsant properties, especially on seizures of hippocampal origin. In this study, we examined how chronic infusion of this neuropeptide in the hippocampus affected kindling epileptogenesis. A 7-day continuous infusion of neuropeptide Y in the hippocampus delayed the progression of hippocampal kindling in the rat, whereas anti-neuropeptide Y immunoglobulins had an aggravating effect. These results show that neuropeptide Y exerts anti-epileptogenic properties on seizures originating within the hippocampus and lend support to the hypothesis that BDNF delays kindling at least in part through upregulation of this neuropeptide. They also suggest that the seizure-induced upregulation of neuropeptide Y constitutes an endogenous mechanism counteracting excessive hippocampal excitability. Hippocampus 2003;13:557,560. © 2003 Wiley-Liss, Inc. [source] Delayed neurotrophin treatment following deafness rescues spiral ganglion cells from death and promotes regrowth of auditory nerve peripheral processes: Effects of brain-derived neurotrophic factor and fibroblast growth factorJOURNAL OF NEUROSCIENCE RESEARCH, Issue 9 2007Josef M. Miller Abstract The extent to which neurotrophic factors are able to not only rescue the auditory nerve from deafferentation-induced degeneration but also promote process regrowth is of basic and clinical interest, as regrowth may enhance the therapeutic efficacy of cochlear prostheses. The use of neurotrophic factors is also relevant to interventions to promote regrowth and repair at other sites of nerve trauma. Therefore, auditory nerve survival and peripheral process regrowth were assessed in the guinea pig cochlea following chronic infusion of BDNF + FGF1 into scala tympani, with treatment initiated 4 days, 3 weeks, or 6 weeks after deafferentation from deafening. Survival of auditory nerve somata (spiral ganglion neurons) was assessed from midmodiolar sections. Peripheral process regrowth was assessed using pan-Trk immunostaining to selectively label afferent fibers. Significantly enhanced survival was seen in each of the treatment groups compared to controls receiving artificial perilymph. A large increase in peripheral processes was found with BDNF + FGF1 treatment after a 3-week delay compared to the artificial perilymph controls and a smaller enhancement after a 6-week delay. Neurotrophic factor treatment therefore has the potential to improve the benefits of cochlear implants by maintaining a larger excitable population of neurons and inducing neural regrowth. © 2007 Wiley-Liss, Inc. [source] Antagonism of AT2 receptors augments Angiotensin II-induced abdominal aortic aneurysms and atherosclerosisBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Alan Daugherty We have recently demonstrated that chronic infusion of Angiotensin II into apoE,/, mice promotes the development of abdominal aortic aneurysms. To determine the involvement of specific Angiotensin II receptors in this response, we co-infused Angiotensin II (1000 ng kg,1 min,1 for 28 days) with losartan (30 mg kg,1 day,1) or PD123319 (3 mg kg,1 day,1) to antagonize AT1 and AT2 receptors, respectively. Infusion of Angiotensin II promoted the development of abdominal aortic aneurysms in 70% of mature female apoE,/, mice. The formation of aortic aneurysms was totally inhibited by co-infusion of Angiotensin II with losartan (30 mg kg,1 day,1; P=0.003). In contrast, the co-infusion of Angiotensin II with PD123319 resulted in a marked increase in the incidence and severity of aortic aneurysms. To determine whether AT2 antagonism also promoted Angiotensin II-induced atherosclerosis, Angiotensin II was infused into young female apoE,/, mice that had little spontaneous atherosclerosis. In these mice, co-infusion of PD123319 led to a dramatic increase in the extent of atherosclerosis. This increase was associated with no change in plasma lipid concentrations and only transient and modest increases in blood pressure during co-infusion with PD123319. While antagonism of AT1 receptors totally prevented the formation of aneurysms, antagonism of AT2 receptors promoted a large increase in the severity of Angiotensin II-induced vascular pathology. British Journal of Pharmacology (2001) 134, 865,870; doi:10.1038/sj.bjp.0704331 [source] COMPARISON OF ANGIOTENSIN II-INDUCED BLOOD PRESSURE AND STRUCTURAL CHANGES IN FISCHER 344 AND WISTAR KYOTO RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2004Jocelyne Blanc SUMMARY 1.,The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2.,Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3.,Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 ± 7 vs 299 ± 9 g; P < 0.05) and heart weight (0.80 ± 0.02 vs 0.98 ± 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 ± 1 vs 123 ± 5 mmHg; P < 0.001) and diastolic BP (98 ± 3 vs 89 ± 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 ± 9 vs 131 ± 6 nm/g; P < 0.05) and abdominal aorta (264 ± 13 vs 217 ± 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 ± 13 vs 275 ± 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 ± 5 and 132 ± 4 mmHg in F344 and WKY rats, respectively; Pstrain × treatment < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 ± 39 vs 956 ± 12 kPa (P < 0.001) and 1107 ± 42 vs 813 ± 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 ± 9 mmHg, +10 ± 2 mmHg and ,40 ± 17 b.p.m., respectively, in F344 rats vs+28 ± 4 mmHg, + 4 ± 2 mmHg and ,19 ± 10 b.p.m. in WKY rats, respectively; Pstrain < 0.05 for BP and PP). The startle response was not affected by AngII. 4.,These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction. [source] | |||||||||||||