A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.
Substances that act in the brain stem or spinal cord to produce tonic or clonic convulsions, often by removing normal inhibitory tone. They were formerly used to stimulate respiration or as antidotes to barbiturate overdose. They are now most commonly used as experimental tools.
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
Drugs used to prevent SEIZURES or reduce their severity.
The repeated weak excitation of brain structures, that progressively increases sensitivity to the same stimulation. Over time, this can lower the threshold required to trigger seizures.
A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.
Induction of a stress reaction in experimental subjects by means of an electrical shock; applies to either convulsive or non-convulsive states.
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The relationship between the dose of an administered drug and the response of the organism to the drug.

Involvement of tumor necrosis factor alpha and interleukin-1beta in enhancement of pentylenetetrazole-induced seizures caused by Shigella dysenteriae. (1/381)

Neurologic manifestations, mainly convulsions, are the most frequent extraintestinal complications of shigellosis. We used an animal model to study the roles of tumor necrosis factor alpha (TNF-alpha) and interleukin-1 beta (IL-1beta) in Shigella-related seizures. Administration of Shigella dysenteriae 60R sonicate enhanced the sensitivity of mice to the proconvulsant pentylenetetrazole (PTZ) within 7 h. This was indicated by a significantly higher mean convulsion score and an increased number of mice responding with clonic-tonic seizures in the Shigella-pretreated group. Preinjection of mice with anti-murine TNF-alpha (anti-mTNF-alpha) or anti-murine IL-1beta (anti-mIL-1beta) 30 min prior to administration of Shigella sonicate abolished their enhanced response to PTZ at 7 h. Mean convulsion scores were reduced by anti-mTNF-alpha from 1.2 to 0.8 (P = 0.017) and by anti-mIL-1beta from 1.3 to 0.7 (P = 0.008). Preinjection of anti-mTNF-alpha also reduced the percentage of mice responding with clonic-tonic seizures, from 48 to 29% (P = 0.002), and preinjection of anti-mIL-1beta reduced it from 53 to 21% (P = 0. 012). Neutralization of TNF-alpha or IL-1beta did not protect the mice from death due to S. dysenteriae 60R. These findings indicate that TNF-alpha and IL-1beta play a role in the very early sensitization of the central nervous system to convulsive activity after S. dysenteriae administration. Similar mechanisms may trigger neurologic disturbances in other infectious diseases.  (+info)

Determination of the lipophilicity of active anticonvulsant N-substituted amides of alpha-arylalkylamine-gamma-hydroxybutyric acid. (2/381)

The lipophilicities of fourteen anticonvulsant active N-substituted amides of alpha-arylalkylamine-gamma-hydroxybutyric acid [I-XIV] have been determined by reversed-phase thin-layer chromatography with a mixture of methanol, TRIS buffer, and acetic acid as the solvent system. The RM value of each compound decreased linearly with increasing concentration of methanol. The partition coefficients (log P) of the amides were calculated by use of the Prolog P module of the Pallas system. Comparison of RM and log P enabled clog P values to be calculated. It was found that the anticonvulsant activity of amides [I-XIV] can be explained on the basis of their lipophilicity.  (+info)

Synthesis and anticonvulsant activity of 1,2-aminoalkanol derivatives. (3/381)

A series of 1,2-aminoalkanol derivatives were prepared and evaluated for anticonvulsant activity in the maximal electroshock seizure (MES) and subcutaneous pentylenetetrazole seizure threshold (scMet) assays and for neurotoxicity (TOX). Most interesting were the anticonvulsant results of S-(+)-2-amino-1-butanol derivative VIII, which displayed anti-MES activity with a protective index (TD50/ED50) of 4.55 corresponding with that for phenytoin, carbamazepine and valproate.  (+info)

Acute pentylenetetrazol injection reduces rat GABAA receptor mRNA levels and GABA stimulation of benzodiazepine binding with No effect on benzodiazepine binding site density. (4/381)

The effects of a single convulsive dose of pentylenetetrazol (PTZ, 45 mg/kg i.p.) on rat brain gamma-aminobutyric acid type A (GABAA) receptors were studied. Selected GABAA receptor subunit mRNAs were measured by Northern blot analysis (with beta-actin mRNA as a standard). Four hours after PTZ, the GABAA receptor gamma2-mRNA was decreased in hippocampus, cerebral cortex, and cerebellum; alpha1-mRNA was decreased in cerebellum; and beta2 subunit mRNA was decreased in cortex and cerebellum. The alpha5 subunit mRNA level was not altered. Those mRNAs that had been reduced were increased in some brain regions at the 24-h time point, and these changes reverted to control levels by 48 h. PTZ effect on GABAA receptors was also studied by autoradiographic binding assay with the benzodiazepine agonist [3H]flunitrazepam (FNP), the GABAA agonist [3H]muscimol, and the benzodiazepine antagonist [3H]flumazenil. There was an overall decrease in [3H]FNP binding 12 but not 24 h after PTZ treatment. In contrast, [3H]muscimol binding was minimally affected, and [3H]flumazenil binding was unchanged after PTZ treatment. Additional binding studies were performed with well-washed cerebral cortical homogenates to minimize the amount of endogenous GABA. There was no PTZ effect on specific [3H]FNP binding. However, there was a significant reduction in the stimulation of [3H]FNP binding by GABA. The results showed that an acute injection of PTZ caused transient changes in GABAA receptor mRNA levels without altering receptor number but affected the coupling mechanism between the GABA and benzodiazepine sites of the GABAA receptor.  (+info)

Effects of novel 6-desfluoroquinolones and classic quinolones on pentylenetetrazole-induced seizures in mice. (5/381)

There have been several reports that convulsions, although rare, occur in patients who receive fluoroquinolones. In this study, the proconvulsant effects exhibited by a novel series of 6-desfluoroquinolones and some classic quinolones on pentylenetetrazole (PTZ)-induced seizures in mice were evaluated and compared. Animals were intraperitoneally injected with vehicle or quinolone derivatives (5 to 100 microg/g of body weight) 30 min before the subcutaneous (s.c.) administration of PTZ (40 microg/g). In each experiment, mice were then observed for 1 h to monitor for the incidence and onset of clonic seizures. The order of proconvulsant activity in our epileptic model was MF5184 > MF5187 > pefloxacin > MF5189 > ofloxacin > ciprofloxacin > MF5140 > MF5181 > MF5137 > rufloxacin > MF5143 > MF5158 > MF5191 > MF5128 > MF5138 > cinoxacin > MF5142 > norfloxacin > nalidixic acid. The relationship between the chemical structure and the proconvulsant activity of 6-desfluoroquinolone derivatives was studied. We observed that, in terms of toxicity to the central nervous system (CNS), besides the heterocyclic side chain (moiety) at the C-7 position, the C-6 substituent also appears to play an important role. In particular, a hydrogen at the C-6 position seemed to be responsible for major neurotoxic activity in comparison to an amino group located in the same position. The relationship between lipophilicity and proconvulsant activity was also investigated. We did not find any clear relationship between a higher level of lipophilicity and major proconvulsant properties. Although the principal mechanism by which quinolones induce potentiation of the proconvulsant effects of PTZ cannot be easily determined, it is possible that the convulsions are caused by drug interactions, because both PTZ and quinolones are believed to increase excitation of the CNS by inhibition of gamma-aminobutyric acid binding to receptors.  (+info)

Mapping loci for pentylenetetrazol-induced seizure susceptibility in mice. (6/381)

DBA/2J (D2) and C57BL/6J (B6) mice exhibit differential sensitivity to seizures induced by various chemical and physical methods, with D2 mice being relatively sensitive and B6 mice relatively resistant. We conducted studies in mature D2, B6, F1, and F2 intercross mice to investigate behavioral seizure responses to pentylenetetrazol (PTZ) and to map the location of genes that influence this trait. Mice were injected with PTZ and observed for 45 min. Seizure parameters included latencies to focal clonus, generalized clonus, and maximal seizure. Latencies were used to calculate a seizure score that was used for quantitative mapping. F2 mice (n = 511) exhibited a wide range of latencies with two-thirds of the group expressing maximal seizure. Complementary statistical analyses identified loci on proximal (near D1Mit11) and distal chromosome 1 (near D1Mit17) as having the strongest and most significant effects in this model. Another locus of significant effect was detected on chromosome 5 (near D5Mit398). Suggestive evidence for additional PTZ seizure-related loci was detected on chromosomes 3, 4, and 6. Of the seizure-related loci identified in this study, those on chromosomes 1 (distal), 4, and 5 map close to loci previously identified in a similar F2 population tested with kainic acid. Results document that the complex genetic influences controlling seizure response in B6 and D2 mice are partially independent of the nature of the chemoconvulsant stimulus with a locus on distal chromosome 1 being of fundamental importance.  (+info)

Resistance to excitotoxin-induced seizures and neuronal death in mice lacking the preprotachykinin A gene. (7/381)

Epileptic seizures are associated with increases in hippocampal excitability, but the mechanisms that render the hippocampus hyperexcitable chronically (in epilepsy) or acutely (in status epilepticus) are poorly understood. Recent evidence suggests that substance P (SP), a peptide that has been implicated in cardiovascular function, inflammatory responses, and nociception, also contributes to hippocampal excitability and status epilepticus, in part by enhancing glutamate release. Here we report that mice with disruption of the preprotachykinin A gene, which encodes SP and neurokinin A, are resistant to kainate excitoxicity. The mice show a reduction in the duration and severity of seizures induced by kainate or pentylenetetrazole, and both necrosis and apoptosis of hippocampal neurons are prevented. Although kainate induced the expression of bax and caspase 3 in the hippocampus of wild-type mice, these critical intracellular mediators of cell death pathways were not altered by kainate injection in the mutant mice. These results indicate that the reduction of seizure activity and the neuroprotection observed in preprotachykinin A null mice are caused by the extinction of a SP/neurokinin A-mediated signaling pathway that is activated by seizures. They suggest that these neurokinins are critical to the control of hippocampal excitability, hippocampal seizures, and hippocampal vulnerability.  (+info)

Sex differences in the pentylenetetrazol-like stimulus induced by ethanol withdrawal. (8/381)

This study investigated sex differences in responding to the pentylenetetrazol (PTZ, a gamma-aminobutyric acid A antagonist) discriminative stimulus and to substitution to PTZ during ethanol withdrawal. The PTZ stimulus has served as an anxiogenic stimulus in numerous studies. Adult male and female rats were trained to discriminate PTZ (16 mg/kg i.p.) from saline in a two-lever food-reinforced task. They were then gonadectomized or sham-operated. Ovariectomized (OVX) rats were also tested during 17beta-estradiol (2.5 mg, 21 days release, s.c.) replacement. The PTZ dose response (0-16 mg/kg i.p.) was tested in all groups. In general, fewer females than males responded to PTZ. Diazepam (DZP; 0-10 mg/kg i.p.) injected before PTZ (16 mg/kg) decreased the number of rats selecting the PTZ lever. This effect was greater in sham female and estradiol-replaced-OVX rats than in male or OVX rats. Rats then received chronic ethanol diet (6.5%) for 10 days. During ethanol withdrawal (12 h after termination of the ethanol diet), they were tested for PTZ lever selection. PTZ lever selection differed between groups: sham or castrated male rats > OVX > sham female or estradiol-replaced-OVX rats. In sham female rats, estradiol concentrations showed a cyclic pattern with an estradiol surge that did not influence their PTZ discrimination performance. After i.p. injection of ethanol (2 g/kg), blood ethanol concentrations were not different in male and female rats. These findings suggest that 1) female rats are less sensitive to the anxiogenic effects of PTZ; 2) female rats are less sensitive to the anxiogenic effects of ethanol withdrawal; and 3) estrogen plays some role in mediation of these sex differences.  (+info)

Pentylenetetrazole (PTZ) is not primarily considered a medical treatment, but rather a research compound used in neuroscience and neurology to study seizure activity and chemically induce seizures in animals for experimental purposes. It is classified as a proconvulsant agent. Medically, it has been used in the past as a medication to treat epilepsy, but its use is now largely historical due to the availability of safer and more effective anticonvulsant drugs.

In a medical or scientific context, Pentylenetetrazole can be defined as:

A chemical compound with the formula C6H5N5O2, which is used in research to investigate seizure activity and induce convulsions in animals. It acts as a non-competitive GABAA receptor antagonist and can lower the seizure threshold. Historically, it has been used as a medication to treat epilepsy, but its use for this purpose is now limited due to the development of safer and more effective anticonvulsant drugs.

Convulsants are substances or agents that can cause seizures or convulsions. These can be medications, toxins, or illnesses that lower the seizure threshold and lead to abnormal electrical activity in the brain, resulting in uncontrolled muscle contractions and relaxation. Examples of convulsants include bromides, strychnine, organophosphate pesticides, certain antibiotics (such as penicillin or cephalosporins), and alcohol withdrawal. It is important to note that some medications used to treat seizures can also have convulsant properties at higher doses or in overdose situations.

A seizure is an uncontrolled, abnormal firing of neurons (brain cells) that can cause various symptoms such as convulsions, loss of consciousness, altered awareness, or changes in behavior. Seizures can be caused by a variety of factors including epilepsy, brain injury, infection, toxic substances, or genetic disorders. They can also occur without any identifiable cause, known as idiopathic seizures. Seizures are a medical emergency and require immediate attention.

Anticonvulsants are a class of drugs used primarily to treat seizure disorders, also known as epilepsy. These medications work by reducing the abnormal electrical activity in the brain that leads to seizures. In addition to their use in treating epilepsy, anticonvulsants are sometimes also prescribed for other conditions, such as neuropathic pain, bipolar disorder, and migraine headaches.

Anticonvulsants can work in different ways to reduce seizure activity. Some medications, such as phenytoin and carbamazepine, work by blocking sodium channels in the brain, which helps to stabilize nerve cell membranes and prevent excessive electrical activity. Other medications, such as valproic acid and gabapentin, increase the levels of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which has a calming effect on nerve cells and helps to reduce seizure activity.

While anticonvulsants are generally effective at reducing seizure frequency and severity, they can also have side effects, such as dizziness, drowsiness, and gastrointestinal symptoms. In some cases, these side effects may be managed by adjusting the dosage or switching to a different medication. It is important for individuals taking anticonvulsants to work closely with their healthcare provider to monitor their response to the medication and make any necessary adjustments.

Kindling, in the context of neurology, refers to a process of neural sensitization where repeated exposure to sub-convulsive stimuli below the threshold for triggering a seizure can eventually lower this threshold, leading to an increased susceptibility to develop seizures. This concept is often applied in the study of epilepsy and other neuropsychiatric disorders.

The term "kindling" was first introduced by Racine in 1972 to describe the progressive increase in the severity and duration of behavioral responses following repeated electrical stimulation of the brain in animal models. The kindling process can occur in response to various types of stimuli, including electrical, chemical, or even environmental stimuli, leading to changes in neuronal excitability and synaptic plasticity in certain brain regions, particularly the limbic system.

Over time, repeated stimulation results in a permanent increase in neural hypersensitivity, making it easier to induce seizures with weaker stimuli. This phenomenon has been implicated in the development and progression of some forms of epilepsy, as well as in the underlying mechanisms of certain mood disorders and other neurological conditions.

Diazepam is a medication from the benzodiazepine class, which typically has calming, sedative, muscle relaxant, and anticonvulsant properties. Its medical uses include the treatment of anxiety disorders, alcohol withdrawal syndrome, end-of-life sedation, seizures, muscle spasms, and as a premedication for medical procedures. Diazepam is available in various forms, such as tablets, oral solution, rectal gel, and injectable solutions. It works by enhancing the effects of a neurotransmitter called gamma-aminobutyric acid (GABA) in the brain, which results in the modulation of nerve impulses in the brain, producing a sedative effect.

It is important to note that diazepam can be habit-forming and has several potential side effects, including drowsiness, dizziness, weakness, and impaired coordination. It should only be used under the supervision of a healthcare professional and according to the prescribed dosage to minimize the risk of adverse effects and dependence.

Electroshock, also known as electroconvulsive therapy (ECT), is a medical procedure in which electric currents are passed through the brain to treat certain mental health conditions. It is primarily used to treat severe forms of depression that have not responded to other treatments, and it may also be used to treat bipolar disorder and schizophrenia.

During an ECT procedure, electrodes are placed on the patient's head, and a carefully controlled electric current is passed through the brain, intentionally triggering a seizure. The patient is under general anesthesia and given muscle relaxants to prevent physical injury from the seizure.

ECT is typically administered in a series of treatments, usually two or three times a week for several weeks. While the exact mechanism of action is not fully understood, ECT is thought to affect brain chemistry and help regulate mood and other symptoms. It is generally considered a safe and effective treatment option for certain mental health conditions when other treatments have failed. However, it can have side effects, including short-term memory loss and confusion, and it may not be appropriate for everyone.

Epilepsy is a chronic neurological disorder characterized by recurrent, unprovoked seizures. These seizures are caused by abnormal electrical activity in the brain, which can result in a wide range of symptoms, including convulsions, loss of consciousness, and altered sensations or behaviors. Epilepsy can have many different causes, including genetic factors, brain injury, infection, or stroke. In some cases, the cause may be unknown.

There are many different types of seizures that can occur in people with epilepsy, and the specific type of seizure will depend on the location and extent of the abnormal electrical activity in the brain. Some people may experience only one type of seizure, while others may have several different types. Seizures can vary in frequency, from a few per year to dozens or even hundreds per day.

Epilepsy is typically diagnosed based on the patient's history of recurrent seizures and the results of an electroencephalogram (EEG), which measures the electrical activity in the brain. Imaging tests such as MRI or CT scans may also be used to help identify any structural abnormalities in the brain that may be contributing to the seizures.

While there is no cure for epilepsy, it can often be effectively managed with medication. In some cases, surgery may be recommended to remove the area of the brain responsible for the seizures. With proper treatment and management, many people with epilepsy are able to lead normal, productive lives.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Pentylenetetrazol, also known as pentylenetetrazole, leptazol, metrazol, pentetrazol (INN), pentamethylenetetrazol, Corazol, ... The mechanism of pentylenetetrazol is not well understood, and it may have multiple mechanisms of action. In 1984, Squires et ... Pentylenetetrazol is also a prototypical anxiogenic drug and has been extensively used in animal models of anxiety. ... In 1939, pentylenetetrazol was replaced by electroconvulsive therapy, which is easier to administer, as the preferred method ...
... ip administered 30 min followed by pentylenetetrazole induction measured for 30 min relative to control. ... Anticonvulsant activity in pentylenetetrazole-induced Mus musculus albino (mouse) seizure model assessed as survival at 220 mg/ ...
... assessed as protection against pentylenetetrazol-induced seizures administered 30 min prior to seizure induction measured for ...
Antiepileptic potential of Anisomeles indica (Linn.) Kuntze aerial parts in pentylenetetrazole-induced experimental convulsions ... model and pentylenetetrazole (PTZ) models at doses of 200, 400 mg/kg, po once. Phenytoin and diazepam (25 and 2 mg/kg, ip) were ...
Activation of the GABA(A)-receptor δ-subunit gene promoter following pentylenetetrazole-induced seizures in transgenic mice. In ... Activation of the GABA(A)-receptor δ-subunit gene promoter following pentylenetetrazole-induced seizures in transgenic mice. / ... Dive into the research topics of Activation of the GABA(A)-receptor δ-subunit gene promoter following pentylenetetrazole- ... Activation of the GABA(A)-receptor δ-subunit gene promoter following pentylenetetrazole-induced seizures in transgenic mice. ...
We investigate the expression of Kir channels in epileptic cardiac tissue by using pentylenetetrazole (PTZ)-kindling model in ... Expression of cardiac inwardly rectifying potassium channels in pentylenetetrazole kindling model of epilepsy in rats. ... We investigate the expression of Kir channels in epileptic cardiac tissue by using pentylenetetrazole (PTZ)-kindling model in ... Expression of cardiac inwardly rectifying potassium channels in pentylenetetrazole kindling model of epilepsy in rats-, ...
Electrode implantation and detection of pentylenetetrazol (PTZ)-induced seizure susceptibility in cohort 5. To monitor the ...
Dive into the research topics of Sex differences in the pentylenetetrazol-like stimulus induced by ethanol withdrawal. ...
Pentylenetetrazole Grants and funding * R21 MH106919/MH/NIMH NIH HHS/United States ...
... lacosamide and topiramate on epileptogenesis and related cognitive dysfunction in an experimental model of pentylenetetrazole ( ...
pentylenetetrazol-induced convulsions. positive modulation of GABAAR and antioxidant properties. Silva et al., 2009 [84]. ... 20] reported that pre-inhalation of the EO of Acorus gramineus markedly delayed the appearance of pentylenetetrazole-induced ... pentylenetetrazole-induced convulsion; sedative effect; CNS inhibitory effects. increased GABA level; decreased GABA ... Effects of isopulegol on pentylenetetrazol-induced convulsions in mice: possible involvement of GABAergic system and ...
Investigation of Compositional, Structural, and Dynamical Changes of Pentylenetetrazol-Induced Seizures on a Rat Brain by FT-IR ... Therefore, the current study determined molecular consequences of seizures induced by pentylenetetrazol (PTZ), which is a ... and Dynamical Changes of Pentylenetetrazol-Induced Seizures on a Rat Brain by FT-IR Spectroscopy," ANALYTICAL CHEMISTRY, pp. ...
Anticonvulsant potential of Grewia tiliaefolia in pentylenetetrazole induced epilepsy: ins Anticonvulsant potential of Grewia ... Hence, the methanol extract was further explored for its anticonvulsant potential in pentylenetetrazole (PTZ) induced acute ... tiliaefolia in pentylenetetrazole induced epilepsy: insights from in vivo and in silico studies. ...
Therefore, this study was designed to examine the effects of chronic administration of vitamin D3 on pentylenetetrazole (PTZ)- ... Inhibitory effects of chronic administration of vitamin D3 on pentylenetetrazole-induced seizures in mice ... pentylenetetrazole-induced seizure; priority journal; seizure threshold; tonic clonic seizure; vitamin supplementation; animal ... Inhibitory effects of chronic administration of vitamin D3 on pentylenetetrazole-induced seizures in mice. Epilepsy Research, ...
AGAINST SEIZURES INDUCED BY PENTYLENETETRAZOLE AND ELECTROCONVULSIVE SHOCK IN MICE EVALUATION OF ANTICONVULSANT ACTIVITY OF THE ... AGAINST SEIZURES INDUCED BY PENTYLENETETRAZOLE AND ELECTROCONVULSIVE SHOCK IN MICE. Abstract Nyctanthes arbortristis Linn. ( ... arbortristis protected mice against tonic convulsions induced by maximal electroshock and especially by pentylenetetrazole. ...
in maximal electroshock and pentylenetetrazole-induced rat models of epilepsy. In: Brain Injury. 2013 ; Vol. 27, No. 13-14. pp ... in maximal electroshock and pentylenetetrazole-induced rat models of epilepsy, Brain Injury, vol. 27, no. 13-14, pp. 1707-1714 ... in maximal electroshock and pentylenetetrazole-induced rat models of epilepsy. Brain Injury. 2013 Jan 1;27(13-14):1707-1714. ... in maximal electroshock and pentylenetetrazole-induced rat models of epilepsy. Adhikari Snehunsu, N. Mukunda, M. C. Satish ...
Effect of pentylenetetrazol-induced epileptic seizure on thiol redox state in the mouse cerebral cortex. Epilepsy Res. 2004;62( ... Gupta Y, Kumar MV, Srivastava A. Effect of Centella asiatica on pentylenetetrazole-induced kindling, cognition and oxidative ... Feng Y, LeBlanc MH, Regunathan S. Agmatine reduces extracellular glutamate during pentylenetetrazole-induced seizures in rat ... and learning in pentylenetetrazole-induced kindling rats Running title: Biarum carduchrum effects on seizure, oxidative stress ...
Results: Our results showed that the pentylenetetrazole-induced seizure threshold was 33.4 0.42 mg/kg in control group. In ... Comparison of the Effect of Verapamil, Nifedipine and Diltiazem on Pentylenetetrazole-Induced Clonic Seizure Threshold in Mice ... nifedipine and diltiazem on pentylenetetrazole-induced seizure threshold and to compare these effects in mice ... before intravenously the determination of the pentylenetetrazole-induced seizure threshold. ...
In contrast to studies where repeated pentylenetetrazole (PTZ) stimulation resulted in an increase in migrating neurons in ... Kindling status in Sprague-Dawley rats induced by pentylenetetrazole: involvement of a critical development period. Am J Pathol ...
Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling. مجله علوم اعصاب پایه و ... Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling ... Tavassoli M, Ardjmand A. Pentylenetetrazol and Morphine Interaction in a State-dependent Memory Model: Role of CREB Signaling. ... Several studies have reported that Pentylenetetrazole (PTZ) impairs memory in experimental animal models. Due to certain ...
We sought to determine whether tolerance occurs to the anticonvulsant activity of ganaxolone in the pentylenetetrazol seizure ...
pentylenetetrazole. QTAP. quantitative targeted absolute proteomics. SRM/MRM. selected/multiple reaction monitoring. ... Pentylenetetrazole (PTZ)-kindled and spontaneous model of epilepsy (EL) mice were used as models of chemically induced and ... Pentylenetetrazole (PTZ)-kindled mouse is a well-established chemically induced epilepsy model, but it is difficult to ... 1999) Enhanced susceptibility of pentylenetetrazole kindled mice to quinolone effects. Int J Antimicrob Agents 12:239-244. ...
Pentylenetetrazole (Metrazol) 7. Dopamine (Intropin) 8. 1- Methyl- 4- phenyl- 1,2,3,6- tetrahydropyridine (MPTP) ...
Pentylenetetrazole (Metrazol) Related Therapies and Procedures. 1. Intraperitoneal Injections 2. Injections 3. Aftercare (After ...
... inhibits pentylenetetrazole-induced epileptiform seizures. An electrophysiological study: Special issue related to kynurenine. ...
2017). P38 MAPK pathway mediates cognitive damage in pentylenetetrazole-induced epilepsy via apoptosis cascade. Epilepsy Res. ... The MAPK pathway also was reported to contributed to cognitive damage in pentylenetetrazole-induced epilepsy by downregulated ... It was demonstrated that the cognitive deficits in pentylenetetrazole (PTZ)-induced epilepsy was associated with the abnormal ... Effect of lamotrigine on epilepsy-induced cognitive impairment and hippocampal neuronal apoptosis in pentylenetetrazole-kindled ...
... did not prevent seizure induced by strychnine or pentylenetetrazol. ...
Idemudia SO, Bhadra S, Lal H (June 1989). "The pentylenetetrazol-like interoceptive stimulus produced by ethanol withdrawal is ...
  • Therefore, this study was designed to investigate the anti-epileptogenic and antioxidant activity of repeated administration of Lavandula officinalis extract on pentylenetetrazol (PTZ) kindling seizures in mice model. (nih.gov)
  • 5-HT(3) receptor mediates the dose-dependent effects of citalopram on pentylenetetrazole-induced clonic seizure in mice: involvement of nitric oxide. (ac.ir)
  • Inhibition of NMDA receptor/NO signaling blocked tolerance to the anti-convulsant effect of morphine on pentylenetetrazole-induced seizures in mice. (ac.ir)
  • Levetiracetam was devoid of anticonvulsant activity in the acute maximal electroshock seizure test and in the maximal pentylenetetrazol seizure test in mice (up to 540 mg/kg, i.p.) but exhibited potent protection against generalised epileptic seizures in electrically and pentylenetetrazol-kindled mice (ED50 values = 7 and 36 mg/kg, respectively, i.p. (nih.gov)
  • Krivanek J, McGaugh JL (1968) Effects of pentylenetetrazol on memory storage in mice. (springer.com)
  • The researchers used two epilepsy models: the PPS model of temporal lobe epilepsy (TLE) in rats and the pentylenetetrazol (PTZ) model in mice. (news-medical.net)
  • The extract exhibited dose-dependent prevention of tonic seizures induced by pentylenetetrazole (ED50 = 154.4 mg/kg). (ac.ir)
  • The pentylenetetrazol (PTZ) or Metrazol test detects the ability of a test compound to raise the chemoconvulsant-induced seizure threshold of an animal and thus protect it from exhibiting a clonic, forebrain seizure. (nih.gov)
  • Pentylenetetrazol produces a reliable discriminative stimulus, which is largely mediated by the GABAA receptor. (wikipedia.org)
  • Several classes of compounds can modulate the pentylenetetrazol discriminative stimulus, including 5-HT1A, 5-HT3, NMDA, glycine, and L-type calcium channel ligands. (wikipedia.org)
  • To investigate this hypothesis, we examined the expression of ATF3 and p53 in hippocampal tissues of rats kindled by pentylenetetrazole (PTZ) using immunofluorescence, immunohistochemistry and western blotting. (spandidos-publications.com)
  • A recent study by our group showed that TLRs modulate neurite outgrowth in the hippocampus of pentylenetetrazole (PTZ)-kindled rats ( 6 ). (spandidos-publications.com)
  • In the present study, the effects of tamoxifen on pentylenetetrazole (PTZ)-induced repeated seizures and hippocampal neuronal damage in ovariectomized rats were investigated. (en-journal.org)
  • In rats, 3-picoline induced a statistically significant increase in the length of time between pentylenetetrazole (PTZ)-induced myoclonic seizures, and decreased the severity of the seizures when compared to controls. (nih.gov)
  • However, after chemical-induction with pentylenetetrazole, there was a higher incidence of tonic-clonic seizures with APOE4 compared to APOE3 . (frontiersin.org)
  • Objectives The aim of this study was to investigate the potential effects of Sargassum oligocystum extract on the pentylenetetrazole (PTZ) seizure and the contribution of antioxidant capacity of this alga to its antiepileptic effect. (ac.ir)
  • Several studies have focused on the way pentylenetetrazol influences neuronal ion channels. (wikipedia.org)
  • Nonselective GABA antagonists, opioid antagonist naloxone (NLX) and pentylenetetrazole (PTZ), were employed to assess the potential role of GABAergic and opioidergic processes. (iasp-pain.org)
  • However, ethosuximide (pKi = 3.5 +/- 0.1), pentobarbital (pKi = 3.8 +/- 0.1), pentylenetetrazole (pKi = 4.1 +/- 0.1) and bemegride (pKi = 5.0 +/- 0.1) competed with [3H]levetiracetam with pKi values comparable to active drug concentrations observed in vivo. (nih.gov)
  • Because these effects were antagonized by calcium channel blockers, pentylenetetrazol apparently acts at calcium channels, and it causes them to lose selectivity and conduct sodium ions, as well. (wikipedia.org)
  • Picrotoxin and pentylenetetrazol had effects similar to, but greater than, was formed those of delta-9-THC. (erowid.org)
  • We investigated the feasibility of using low-intensity, pulsed radiation of focused ultrasound (FUS) to non-invasively suppress epileptic activity in an animal model (rat), which was induced by the intraperitonial injection of pentylenetetrazol (PTZ). (nih.gov)
  • Many GABA-A ligands, such as the sedatives diazepam and phenobarbital, are effective anticonvulsants, but presumably pentylenetetrazol has the opposite effect when it binds to the GABA-A receptor. (wikipedia.org)
  • Menzikov, S.A., Karpova, M.N. and Kalinina, M.V. (2012) Effect of Pentylenetetrazole on the GABAA-Coupled Cl - , HCO 3 - -Activated Mg 2+ -ATPase Activity of the Plasma Membrane from Rat Brain Both in Vitro and in Vivo Experiences. (scirp.org)
  • published a report analyzing pentylenetetrazol and several structurally related convulsant drugs. (wikipedia.org)
  • To test sensitivity, a 2.5 mM subconvulsant dose of pentylenetetrazole (PTZ) was used, which was not able to increase seizure events in larvae or adults exposed to ethanol during embryonic phase. (biorxiv.org)
  • A 1987 study found that pentylenetetrazol increases calcium influx and sodium influx, both of which depolarize the neuron. (wikipedia.org)
  • Pentylenetetrazol is also a prototypical anxiogenic drug and has been extensively used in animal models of anxiety. (wikipedia.org)
  • Pentylenetetrazol has been used experimentally to study seizure phenomena and to identify pharmaceuticals that may control seizure susceptibility. (wikipedia.org)
  • Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility. (bvsalud.org)

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