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The Circuitry Mediating the Translation of Motivational Stimuli Into Adaptive Motor Responses
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Peter W. Kalivas, Lynn Churchill, Mark A. Klitenick
As outlined in Table 1, transmitter analogues mimicking accumbal afferents have been microinjected into the nucleus accumbens and evaluated for the capacity to modulate locomotor activity. Enhanced DA release produces motor activity which requires the stimulation of both D1 and D2 receptors.66–68 The blockade of GABAA receptors with Picrotoxin also elevates motor activity.69 Stimulation of either the AMP A or NMDA type of EAA receptors70,71 or stimulation of mu- or delta-opioid receptors,72–74 will also augment motor activity. Likewise, stimulation of nicotinic receptors elicits a motor response.67 An effect on motor activity by some transmitters is revealed only in animals whose motor activity has been augmented by DA. Thus, substance P enhances, while CCK and neurotensin inhibit DA-induced motor activity.75–77
Synaptic Modulation of Isolated Neurons of the Solitary Tract Nucleus
Published in I. Robin A. Barraco, Nucleus of the Solitary Tract, 2019
All of the cells studied also responded to GABA when applied to the soma. The reversal potential for the response in solutions that gave a calculated reversal for chloride of 0 mV was 0 mV and shifted to -80 mV with replacement of external chloride with methanesulfonic acid. This was indicative of activation of a GABAA type receptor, a chloride channel. The response was blocked by 100 μm picrotoxin.
P
Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Picrotoxin [Greek:pikros, bitter] Active principle of Anamirta cocculus, a plant native to the Malayan Islands, Ceylon and neighboring countries. Known as a poison to Arab physicians including Avicenna (980–1037) and used as a poison in England in 1597 to destroy vermin and fish. It was introduced into medicine by Italian physician Battista Condrochi who wrote De Baccis Orientalihus in the 16th century. The substance responsible for its poisonous properties was isolated by Boullay in 1812 and named.
Loss of mGluR1-LTD following cocaine exposure accumulates Ca2+-permeable AMPA receptors and facilitates synaptic potentiation in the prefrontal cortex
Published in Journal of Neurogenetics, 2021
The following drugs were used: cocaine (Sigma-Aldrich), (S)-3,5-Dihydroxyphenylglycine (DHPG, Tocris Bioscience), LY367385 (Tocris Bioscience), 3-((2-Methyl-1,3-thiazol-4-yl)ethynyl)pyridine hydrochloride (MTEP, Tocris Bioscience), 1-Naphthyl acetyl spermine trihydrochloride (Naspm, Sigma-Aldrich), picrotoxin (Sigma-Aldrich), PKI6-22 (Sigma-Aldrich), QX-314 (Sigma-Aldrich), rapamycin (Sigma-Aldrich), Ro67-7476 (Tocris Bioscience), SCH23390 (Tocris Bioscience), SKF81297 (Sigma-Aldrich), tetrodotoxin (Sigma-Aldrich), and U73122 (Tocris Bioscience). Picrotoxin was dissolved directly in the ACSF used for perfusion. LY367385 and MTEP were dissolved in DMSO with a 1:1000 ratio as stock solutions, which were added directly to ASCF to a desired final concentration during experiments. All other drugs were dissolved in distilled water with a 1:1000 ratio as stock solutions. Drugs were delivered to the recording chamber through a perfusion system (Harvard Apparatus).
Ultrastructural GABA immunogold labeling in the substantia nigra pars reticulata of kindled genetic absence epilepsy rats
Published in Ultrastructural Pathology, 2020
Serap Sirvanci, Dilek Akakin, Medine Gulcebi İdrizoglu, Ozlem Tugce Kaya, Tugba Karamahmutoglu, Zehra Nur Turgan Aşık, Filiz Onat
Mechanisms of stopping an absence seizure involve superficial and intermediate layers of superior colliculus, as well as the excitatory projections from the superior colliculus to the thalamus.26–28 Also, direct and indirect pathways from the basal ganglia generate disinhibition in the superior colliculus, resulting in the suppression of absence seizures.26–29 The nigro-thalamo-cortical pathway and the pedunculopontine tegmental nucleus are also involved in controlling absence seizures.14,26 In a previous study, GABA-releasing polymer matrices were grafted into the SN in the amygdala kindling model and the seizures were repressed.30 Transplantation of fetal GABAergic cells, immortalized GABAergic cells, or transgenic cell lines into the SN were reported to suppress the seizures in the kindling, pilocarpine, and kainic acid models.26,31–33 Decreasing the activity of the SNR leads to disinhibition of the output structures of the SNR, such as the superior colliculus and the ventromedial thalamus, resulting in the suppression of seizures.12,14 In contrast, application of picrotoxin, a GABAA receptor antagonist, to the SNR leads to the development of absence seizures.13
Effect of tadalafil and nitric oxide agonist sodium nitroprusside on penicillin-induced epileptiform activity
Published in Neurological Research, 2020
Many studies have been carried out to determine the role of NO in experimental epilepsies, and new studies are still being added [22–24]. Numerous studies using different experimental epilepsy models have reported that NO has an anticonvulsant effect. In a rat study, NMDA-induced seizures were found to increase with the administration of nitric oxide synthase (NOS) inhibitors [25,26]. In the PTZ-induced epileptiform activity, levosimendan increased seizure threshold and NO levels in hippocampus and temporal cortex [24]. In a picrotoxin-induced model, picrotoxin was found to decrease NOS activity and NO concentration, while L-arginine, a NO agonist, suppressed seizures by increasing NO concentration and NOS activity [27].In another study, it was found that L-arginine had a protective effect in the seizures caused by insulin-induced acute hypoglycemia of rats in a dose-dependent manner [28]. Anticonvulsant effect of NO agonist SNPon epileptiform activity in the present study was similar to what was reported in the literature. The present study also showed that use of SNP alone or in combination with tadalafil similarly reduced the epileptiform activity.