scholarly journals Electroacupuncture at ST36-ST37 and at Ear Ameliorates Hippocampal Mossy Fiber Sprouting in Kainic Acid-Induced Epileptic Seizure Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Chung-Hsiang Liu ◽  
Yi-Wen Lin ◽  
Hsin-Cheng Hsu ◽  
Hsu-Jan Liu ◽  
Wan-Jung Lin ◽  
...  
Keyword(s):  
Kainic Acid ◽  
Epileptic Seizure ◽  
Mossy Fiber ◽  
Intractable Epilepsy ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Mossy Fiber Sprouting ◽  
Parasympathetic Nerve ◽  
Treatment And Prevention ◽  
Sprague Dawley Rats

Our previous study showed that mossy fiber sprouting can occur in the hippocampus region in rats 6 wk after kainic acid-induced epileptic seizure, and this mossy fiber sprouting can facilitate epileptogenesis. Transcutaneous auricular vagal nerve stimulation (VNS), which is similar to cervical VNS, can reduce the occurrence of epileptic seizure in intractable epilepsy patients. Greater parasympathetic nerve activity can be caused by 2 Hz electroacupuncture (EA). Therefore, we investigated the effect of 2 Hz EA at ST-36-ST37 and at the ear on mossy fiber sprouting in kainic-treated Sprague-Dawley rats. The results indicated that applying 2 Hz EA at ST36-ST37 and at the ear for 3 d per week over 6 consecutive weeks can ameliorate mossy fiber sprouting in the hippocampus region of rats. These results indicated that applying 2 Hz EA at ST36-ST37 and at the ear might be beneficial for the treatment and prevention of epilepsy in humans.

scholarly journals The Role of 5-HTR6 in Mossy Fiber Sprouting: Activating Fyn and p-ERK1/2 in Pilocarpine-Induced Chronic Epileptic Rats

2017 ◽  
Vol 42 (1) ◽  
pp. 231-241 ◽  
Author(s):  
Wanhui Lin ◽  
Wenli Huang ◽  
Shenggen Chen ◽  
Mingxing Lin ◽  
Qingyu Huang ◽  
...  
Keyword(s):  
Mossy Fiber ◽  
Inhibitory Effect ◽  
Primary Objective ◽  
Control Group ◽  
Sprague Dawley ◽  
Mossy Fiber Sprouting ◽  
Male Adult ◽  
Sprague Dawley Rats ◽  
Two Stages

Objective: Our primary objective is to verify whether 5-HTR6 is involved in the development of mossy fiber sprouting (MFS), and to determine how the progression of MFS is affected by 5-HTR6. Methods: A total of 90 male adult Sprague-Dawley rats were allocated into either the control group (n=36) or the epileptic group (n=54). Status epilepticus (SE) of rats was induced by the intraperitoneal (i.p.) injection of LiCl-pilocarpine. We conducted our experiments in two stages. The first stage involves equally dividing 36 epileptic rats into three groups with treatments of none, 5-HTR6 antagonist SB-27104 (SB) and vehicle DMSO. Then behavior and electroencephalogram (EEG) of rats were monitored by video-EEG. The second stage involves dividing 126 epileptic rats into seven groups with treatments of none, 10% DMSO, SB (100 µg/kg), Fyn antagonist PP2 (50 µg/kg), p-ERK1/2 antagonist PD-98059 (30 µg/kg), SB (100 µg/ kg) + PP2 (50 µg/kg); SB (100 µg/kg) + PD-98059 (30 µg/kg). We also treated 18 rats in the control group of the first stage with 100 µg/kg 5-HTR6 agonist WAY-181187 (WAY). MFS of rats was detected through the approach of Timm’s staining. Finally, expressions of 5-HTR6, Fyn, p-ERK1/2 and GAP-3 were qualified and semi-quantified via western blotting or RT-PCR. Results: Induction of SE could stimulate formation of MFS and increased GAP-43 expressions. Expressions of 5-HTR6, Fyn and p-ERK1/2 were also up-regulated with increasing time after establishment of SE models. The development of MFS was remarkably inhibited by SB, PP2 and PD. Compared to the single antagonist, such an inhibitory effect was enhanced by SB+PD or SB+PP. Moreover, treatment of healthy rats with WAY would contribute to up-regulated Fyn and p-ERK1/2 expressions, as well as development of MFS (P < 0.05). Suppression of Fyn triggered a down-regulating trend of p-ERK1/2 (P < 0.05), however, suppressed p-ERK1/2 did not have such a significant effect on Fyn expression. Conclusion: HTR6 may affect the progression of MFS by activating both p-ERK1/2 and Fyn, which further modulate the expression of GAP-43.

scholarly journals The Discordance between Network Excitability and Cognitive Performance Following Vigabatrin Treatment during Epileptogenesis

Life ◽  
2021 ◽  
Vol 11 (11) ◽  
pp. 1213
Author(s):  
Ming-Chi Lai ◽  
Chin-Wei Huang
Keyword(s):  
Cognitive Performance ◽  
Mossy Fiber ◽  
Neuronal Damage ◽  
Intractable Epilepsy ◽  
Inhibitory Avoidance ◽  
Aminobutyric Acid ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Spontaneous Recurrent Seizures

Vigabatrin (VGB), a potent selective γ-aminobutyric acid transaminase (GABA-T) inhibitor, is an approved non-traditional anti-seizure drug for patients with intractable epilepsy. Nevertheless, its effect on epileptogenesis, and whether this effect is correlated with post-epileptogenic cognitive function remain unclear. Based on lithium-pilocarpine-induced seizure modeling, we evaluated the effect of VGB on epileptogenesis and neuronal damage following status epilepticus in Sprague–Dawley rats. Cognitive evaluations were performed with the aid of inhibitory avoidance testing. We found that VGB could interrupt epileptogenesis by reducing spontaneous recurrent seizures, hippocampal neuronal damage, and chronic mossy fiber sprouting. Nevertheless, VGB did not help with the retention of cognitive performance. Our findings suggest that further research into the role of VGB in epileptogenesis and the treatment of epilepsy in clinical practice is warranted.

scholarly journals Arcuate nucleus injection of an anti-insulin affibody prevents the sympathetic response to insulin

2013 ◽  
Vol 304 (11) ◽  
pp. H1538-H1546 ◽  
Author(s):  
Brittany S. Luckett ◽  
Jennifer L. Frielle ◽  
Lawrence Wolfgang ◽  
Sean D. Stocker
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arcuate Nucleus ◽  
Insulin Receptors ◽  
Ventromedial Hypothalamus ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sympathetic Response ◽  
Sprague Dawley Rats

Accumulating evidence suggests that insulin acts within the hypothalamus to alter sympathetic nerve activity (SNA) and baroreflex function. Although insulin receptors are widely expressed across the hypothalamus, recent evidence suggests that neurons of the arcuate nucleus (ARC) play an important role in the sympathoexcitatory response to insulin. The purpose of the present study was to determine whether circulating insulin acts directly in the ARC to elevate SNA. In anesthetized male Sprague-Dawley rats (275–425 g), the action of insulin was neutralized by microinjection of an anti-insulin affibody (1 ng/40 nl). To verify the efficacy of the affibody, ARC pretreatment with injection of the anti-insulin affibody completely prevented the increase in lumbar SNA produced by ARC injection of insulin. Next, ARC pretreatment with the anti-insulin affibody attenuated the lumbar sympathoexcitatory response to intracerebroventricular injection of insulin. Third, a hyperinsulinemic-euglycemic clamp increased lumbar, but not renal, SNA in animals that received ARC injection of a control affibody. However, this sympathoexcitatory response was absent in animals pretreated with the anti-insulin affibody in the ARC. Injection of the anti-insulin affibody in the adjacent ventromedial hypothalamus did not alter the sympathoexcitatory response to insulin. The ability of the anti-insulin affibody to prevent the sympathetic effects of insulin cannot be attributed to a general inactivation or nonspecific effect on ARC neurons as the affibody did not alter the sympathoexcitatory response to ARC disinhibition by gabazine. Collectively, these findings suggest that circulating insulin acts within the ARC to increase SNA.

scholarly journals Selected Contribution: Phrenic long-term facilitation requires 5-HT receptor activation during but not following episodic hypoxia

2001 ◽  
Vol 90 (5) ◽  
pp. 2001-2006 ◽  
Author(s):  
D. D. Fuller ◽  
A. G. Zabka ◽  
T. L. Baker ◽  
G. S. Mitchell
Keyword(s):  
Receptor Antagonist ◽  
Phrenic Nerve ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sprague Dawley Rats ◽  
Episodic Hypoxia ◽  
Baseline Levels ◽  
Long Term Facilitation

Episodic hypoxia evokes a sustained augmentation of respiratory motor output known as long-term facilitation (LTF). Phrenic LTF is prevented by pretreatment with the 5-hydroxytryptamine (5-HT) receptor antagonist ketanserin. We tested the hypothesis that 5-HT receptor activation is necessary for the induction but not maintenance of phrenic LTF. Peak integrated phrenic nerve activity (∫Phr) was monitored for 1 h after three 5-min episodes of isocapnic hypoxia (arterial Po 2 = 40 ± 2 Torr; 5-min hyperoxic intervals) in four groups of anesthetized, vagotomized, paralyzed, and ventilated Sprague-Dawley rats [ 1) control ( n = 11), 2) ketanserin pretreatment (2 mg/kg iv; n = 7), and ketanserin treatment 0 and 45 min after episodic hypoxia ( n = 7 each)]. Ketanserin transiently decreased ∫Phr, but it returned to baseline levels within 10 min. One hour after episodic hypoxia, ∫Phr was significantly elevated from baseline in control and in the 0- and 45-min posthypoxia ketanserin groups. Conversely, ketanserin pretreatment abolished phrenic LTF. We conclude that 5-HT receptor activation is necessary to initiate (during hypoxia) but not maintain (following hypoxia) phrenic LTF.

beta-Adrenoceptor modulation of renin response to short-term reductions in pressure in young SHR

1992 ◽  
Vol 263 (2) ◽  
pp. R405-R411
Author(s):  
J. P. Porter
Keyword(s):  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Short Term ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Beta Adrenoceptor ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Renal Nerve Activity

The increase in renin secretion in response to short-term (5 min) reductions in arterial pressure has recently been shown to be similar in young spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) animals. This was puzzling, since tonic renal nerve activity is thought to be elevated in the young SHR, and this has the potential to enhance the renin response. The purpose of the present investigation was to determine whether beta-adrenoceptor modulation of pressure-dependent renin release is diminished in the SHR. In conscious, age-matched SHR, WKY, and Sprague-Dawley rats, the effect on arterial plasma renin activity of 5-min reductions in renal perfusion pressure to 90 and 50 mmHg was determined before and during beta-adrenoceptor activation with isoproterenol or beta-adrenoceptor blockade with propranolol. Isoproterenol augmented the renin response at 50 mmHg in all three strains, with the greatest effect occurring in the Sprague-Dawley rats. The response at 90 mmHg was also enhanced in the SHR and Sprague-Dawley rats, but not the WKY rats. Propranolol had no effect in the SHR and WKY animals, but significantly reduced the renin response at 50 mmHg in the Sprague-Dawley rats. Thus, under the conditions of the present investigation (i.e., short-term reductions in pressure), tonic renal nerve activity does not affect pressure-dependent renin release through a beta-adrenergic receptor mechanism in either the SHR or WKY rats. However, under conditions of acute beta-adrenoceptor activation, the renin response is enhanced at a higher renal perfusion pressure in the SHR than in the WKY rat.

Kainic acid-induced mossy fiber sprouting and synapse formation in the dentate gyrus of rats

Hippocampus ◽  
2000 ◽  
Vol 10 (3) ◽  
pp. 244-260 ◽  
Author(s):  
H.J. Wenzel ◽  
C.S. Woolley ◽  
C.A. Robbins ◽  
P.A. Schwartzkroin
Keyword(s):  
Dentate Gyrus ◽  
Kainic Acid ◽  
Synapse Formation ◽  
Mossy Fiber ◽  
Mossy Fiber Sprouting

Nucleus Gracilis: An Integrator for Visceral and Somatic Information

1997 ◽  
Vol 78 (1) ◽  
pp. 521-527 ◽  
Author(s):  
Elie D. Al-Chaer ◽  
Karin N. Westlund ◽  
William D. Willis
Keyword(s):  
Kainic Acid ◽  
Visceral Pain ◽  
Neuronal Cell ◽  
Dorsal Column ◽  
Sprague Dawley ◽  
Nucleus Gracilis ◽  
Abdominal Organs ◽  
Neuronal Cell Bodies ◽  
Sprague Dawley Rats ◽  
Before And After

Al-Chaer, Elie D., Karin N. Westlund, and William D. Willis. Nucleus gracilis: an integrator for visceral and somatic information. J. Neurophysiol. 78: 521–527, 1997. The nucleus gracilis (NG) receives an abundance of visceral input from various abdominal organs and is proposed to play an important role in visceral pain processing. The purpose of this study was to investigate the necessity of the NG for colorectal input into the ventral posterolateral (VPL) nucleus of the thalamus. Single-cell recordings were made from nine VPL cells isolated in nine different male Sprague Dawley rats anesthetized with pentobarbital sodium. Responses of the VPL cells to colorectal distension (CRD) and to cutaneous stimuli were obtained before and after lesioning of the NG. Electrolytic ( n = 5) and chemical ( n = 4) lesions of the NG were made in different preparations. The chemical lesions were made by injecting a solution of kainic acid into the NG. Kainic acid presumably kills neuronal cell bodies and spares axons of passage. The results indicate that a lesion of the NG, regardless of its type, reduces dramatically the responses of VPL neurons to innocuous cutaneous stimuli, and, to a lesser extent, the responses to CRD. Attenuation of VPL neuronal responses to CRD as well as to innocuous cutaneous stimuli by the NG lesions emphasizes the role of the dorsal column in visceral nociception and suggests that the NG is an integration center for visceral and cutaneous information flowing into the VPL nucleus.

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