جستجوی مقالات مرتبط با کلیدواژه "low frequency stimulation" در نشریات گروه "پزشکی"

Applying deep brain stimulation at low-frequency has anticonvulsant effect on kindled seizures. In this study, the effect of low-frequency stimulation (LFS) on kindling-induced changes in the dendritic length of hippocampal CA1 neurons was investigated.

To administer LFS in the hippocampus, animals first underwent stereotactic surgery and a tripolar electrode were positioned in the CA1 region. Animals received intraperitoneal pentylenetetrazole (PTZ; 34 mg/kg) every other day until they showed three consecutive stage 4 or 5 seizures. LFS was administered to the dorsal hippocampal CA1 area in kindled+LFS group. Hippocampal samples were prepared for stereological assessment one week after termination of LFS application.

PTZ kindling was accompanied with a decrease in dendritic length in CA1 neurons. One week after application of LFS, the length of dendrites was restored to control group values, and there was a significant difference between kindled+LFS and kindled groups. Interestingly, the effect of administering LFS alone in control group, was similar to that of kindled group and a significant decrease was observed in dendritic length.

LFS had a restoring effect on morphological changes in CA1 neurons of kindled animals. This effect may be considered a mechanism for therapeutic action of deep brain stimulation in seizure.

low-frequency electrical stimulation (LFS) has been considered as a new treatment method for epilepsy patients resistant to drug treatment, but its mechanism of action is not fully understood. Gi protein-coupled receptors such as dopamine D2-like receptors may play a role in mediating the effects of LFS. In this study, the role of dopamine D2-like receptors in the effects of LFS on seizure-induced spontaneous synaptic activity in the hippocampal CA1 region of fully kindled rats has been investigated. Animals were kindled by semi-rapid kindling method (6 stimulations per day) by electrical stimulation of the hippocampal CA1 region. In LFS-treated groups, animals received 4 LFS packets at 5 minutes, 6 hours, 24 hours, and 30 hours after the last LFS stimulation.Each LFS package consisted of 4 series with an interval of 5 minutes, and each series consisted of 200 pulses, and the pulse duration was 0.1 ms with a frequency of 1 Hz. Haloperidol (D2 receptor antagonist, mµ2) or bromocriptine (D2 receptor agonist, g/µlitµ2) was injected into the lateral ventricle immediately after the last kindling stimulation, before applying LFS. The obtained results showed that the application of LFS in kindled animals did not affect the spontaneous excitatory currents in the hippocampus, but it caused a decrease in the spontaneous inhibitory currents in the hippocampus. D2 receptor agonist did not mimic the effects of LFS. The use of haloperidol did not affect the effects of LFS. Therefore, spontaneous excitatory and inhibitory potentials are not a suitable quantity to investigate the effectiveness of LFS.

Neurostimulation is one of the new therapeutic approaches in patients with drug-resistant epilepsy, and despite its high efficiency, its mechanism of action is still unclear. On the one hand, electrical stimulation in the human brain is immoral; on the other hand, the creation of the epilepsy model in laboratory animals affects the entire brain network. As a result, one of the ways to achieve the neurostimulation mechanism is to use epileptiform activity models In vitro. In vitro models, by accessing the local network from the whole brain, we can understand the mechanisms of action of neurostimulation.  

A literature search using scientific databases including PubMed, Google Scholar, and Scopus, using "Neurostimulation" and "epileptiform activity" combined with "high-frequency stimulation", " low-frequency stimulation ", and "brain slices” as keywords were conducted, related concepts to the topic gathered and are used in this paper.  

Electrical stimulation causes neuronal depolarization and the release of GABAA, which inhibits neuronal firing. Also, electrical stimulation inhibits the nervous tissue downstream of the stimulation site by preventing the passage of nervous activity from the upstream to the downstream of the axon.  

Neurostimulation techniques consisting of LFS and HFS have a potential role in treating epileptiform activity, with some studies having positive results. Further investigations with larger sample sizes and standardized outcome measures can be conducted to validate the results of previous studies.

In this study, the role of A1 adenosine receptors in improving the effect of Low-Frequency Electrical Stimulation (LFS) on seizure-induced hyperexcitability of hippocampal CA1 pyramidal neurons was investigated.

A semi-rapid hippocampal kindling model was used to induce seizures in male Wistar rats. Examination of the electrophysiological properties of CA1 pyramidal neurons of the hippocampus using whole-cell patch-clamp recording 48 h after the last kindling stimulation revealed that the application of LFS as two packages of stimulations at a time interval of 6 h for two consecutive days could significantly restore the excitability CA1 pyramidal neurons evidenced by a decreased in the of the number of evoked action potentials and enhancement of amplitude, maximum rise slope and decay slope of the first evoked action potential, rheobase, utilization time, adaptation index, first-spike latency, and post-AHP amplitude. Selective locked of A1 receptors by the administration of 8-Cyclopentyl-1,3-dimethylxanthine (1 μM, 1 μl, i.c.v.) before applying each LFS package, significantly reduced LFS effectiveness in recovering these parameters. 

On the other hand, selective activation of A1 receptors by an injection of N6-cyclohexyladenosine (10 μM, 1 μl, i.c.v.), instead of LFS application, could imitate LFS function in improving these parameters. 

It is suggested that LFS exerts its efficacy on reducing the neuronal excitability, partially by activating the adenosine system and activating its A1 receptors.

Epilepsy is a common neurological disorder that affects approximately 50 million people and about 30% of them have seizures despite antiepileptic-drug therapy. Even if 50% of these 600,000 or so patients benefit from surgical resection, many would still need new therapeutic approaches. Deep brain stimulation (DBS) has been suggested as an alternative to drug therapy. Low frequency stimulation (LFS) is an effective pattern of DBS that can decrease epileptic seizures. The incidence of epileptic seizures has been described by an imbalance between excitatory (glutamatergic) and inhibitory (GABAergic) neurotransmission. This phenomenon may be affected by other neurotransmitter systems, including serotonin (5-hydroxytryptamine, 5-HT). The Serotonergic system undergoes many alterations in the epileptic brain. The link between LFS and serotonin release has been studied and it is documented that 5- HT1A receptor antagonist reduces the anti-convulsant effects of LFS. Thus, considering the effects of the serotonergic system in neuronal activities in the epileptic brain, it may be involved in the anti-convulsant mechanism(s) of LFS. In this review, we introduce the effects of low frequency stimulation on seizure and its possible mechanisms. The role of some neuromodulators in mediating the anti-convulsive effects of LFS and the probable signaling changes will be discussed.