Data set of CA1 pyramidal cell recordings using an intact whole hippocampus preparation, including recordings of rebound firing (V2)

<p>The frequency-current (f-I) profiles and an example of rebound firing of pyramidal cells are presented. Four .abf files contain the f-I curve data for the respective cell (as labelled PYR1, PYR2, PYR3 and PYR4 for Pyramidal cell 1, Pyramidal cell 2, Pyramidal cell 3 and Pyramidal cell 4).  That is, they contain the cell's response to the application of a series of depolarizing current steps of 1 s duration while the cells are held in current clamp, as well as the current clamp data itself.  Each recording is 2 s total.  Amplitudes of the input were increased incrementally with step sizes of 10 pA for PYR1, PYR3, and PYR4, and a step size of 25 pA for PYR 2.  PYR1 first spikes on the 5th of 30 steps with 38.7 pA of depolarizing input.  PYR2 first spikes on the 3rd of 13 steps with 1.2 pA of input.  PYR3 first spikes on the 7th of 34 steps with 62.0 pA of input, and PYR4 first spikes on the 7th of 30 steps with 12.1 pA of input.  In the .abf file labelled PYR5_rebound, an example of rebound firing of a pyramidal cell following hyperpolarizing input is given.  While the cell was held at -52 mV in current clamp, as series of 1 s hyperpolarizing steps (10 steps, 25 pA increments) were used to record the post- hyperpolarization rebound spiking.  For the figure showing this rebound spiking (Figure 1), the first two hyperpolarizing steps and the respective firing are shown.  For visualization purposes, the spike artifact in the current clamp input trace was removed and replaced with the mean current in the Figure. </p

Poly(3,4-ethylenedioxythiophene) (PEDOT) Coatings for High-Quality Electromyography Recording

Conducting polymer coatings on metal electrodes are an efficient solution to improve neural signal recording and stimulation, due to their mixed electronic-ionic conduction and biocompatibility. To date, only a few studies have been reported on conducting polymer coatings on metallic wire electrodes for muscle signal recording. Chronic muscle signal recording of freely moving animals can be challenging to acquire with coated electrodes, due to muscle movement around the electrode that can increase instances of coating delamination and device failure. The poor adhesion of conducting polymers to some inorganic substrates and the possible degradation of their electrochemical properties after harsh treatments, such as sterilization, or during implantation limits their use for biomedical applications. Here, we demonstrate the mechanical and electrochemical stability of the conducting polymer, poly(3,4-ethylenedioxythiophene) (PEDOT) doped with LiClO4, deposited on stainless steel multistranded wire electrodes for invasive muscle signal recording in mice. The mechanical and electrochemical stability was achieved by tuning the electropolymerization conditions. PEDOT-coated and bare stainless steel electrodes were implanted in the neck muscle of five mice for electromyographic (EMG) activity recording over a period of 6 weeks. The PEDOT coating improved the electrochemical properties of the stainless steel electrodes, lowering the impedance, resulting in an enhanced signal-to-noise ratio during in vivo EMG recording compared to bare electrodes

Phospholipase C activity increases in cerebrospinal fluid from migraineurs in proportion to the number of comorbid conditions: a case–control study

BACKGROUND: Migraineurs are more often afflicted by comorbid conditions than those without primary headache disorders, though the linking pathophysiological mechanism(s) is not known. We previously reported that phosphatidylcholine-specific phospholipase C (PC-PLC) activity in cerebrospinal fluid (CSF) increased during migraine compared to the same individual’s well state. Here, we examined whether PC-PLC activity from a larger group of well-state migraineurs is related to the number of their migraine comorbidities. METHODS: In a case–control study, migraineurs were diagnosed using International Headache Society criteria, and controls had no primary headache disorder or family history of migraine. Medication use, migraine frequency, and physician-diagnosed comorbidities were recorded for all participants. Lumbar CSF was collected between the hours of 1 and 5 pm, examined immediately for cells and total protein, and stored at −80°C. PC-PLC activity in thawed CSF was measured using a fluorometric enzyme assay. Multivariable logistic regression was used to evaluate age, gender, medication use, migraine frequency, personality scores, and comorbidities as potential predictors of PC-PLC activity in CSF. RESULTS: A total of 18 migraineurs-without-aura and 17 controls participated. In a multivariable analysis, only the number of comorbidities was related to PC-PLC activity in CSF, and only in migraineurs [parameter estimate (standard error) = 1.77, p = 0.009]. CONCLUSION: PC-PLC activity in CSF increases with increasing number of comorbidities in migraine-without-aura. These data support involvement of a common lipid signaling pathway in migraine and in the comorbid conditions

The absence of VGLUT3 predisposes to cocaine abuse by increasing dopamine and glutamate signaling in the nucleus accumbens

Tonically active cholinergic interneurons (TANs) from the nucleus accumbens (NAc) are centrally involved in reward behavior. TANs express a vesicular glutamate transporter referred to as VGLUT3 and thus use both acetylcholine and glutamate as neurotransmitters. The respective roles of each transmitter in the regulation of reward and addiction are still unknown. In this study, we showed that disruption of the gene that encodes VGLUT3 (Slc17a8) markedly increased cocaine self-administration in mice. Concomitantly, the amount of dopamine (DA) release was strongly augmented in the NAc of VGLUT3(-/-) mice because of a lack of signaling by metabotropic glutamate receptors. Furthermore, dendritic spines and glutamatergic synaptic transmission on medium spiny neurons were increased in the NAc of VGLUT3(-/-) mice. Increased DA and glutamate signaling in the NAc are hallmarks of addiction. Our study shows that TANs use glutamate to reduce DA release and decrease reinforcing properties of cocaine in mice. Interestingly, we also observed an increased frequency of rare variations in SLC17A8 in a cohort of severe drug abusers compared with controls. Our findings identify VGLUT3 as an unexpected regulator of drug abuse.This research was supported by funds from ANR (ANR-09-MNPS-033, ANR-13-SAMA-0005-01), Équipe FRM DEQ20130326486, FRC, Brain Canada Multi-Investigator Research Initiative, Djavad Mowafaghian Foundation, ERANET-Neuron Joint Transnational Call for "European Research Projects on Mental Disorders", INSERM, CNRS and UPMC. The research teams of SEM, SJ, MM, JC-PV, BG and FB are members of the Bio-Psy Laboratory of Excellence; this work was therefore supported by French state funds managed by the ANR within the Investissements d'Avenir program under reference ANR-11-IDEX-0004-02. DYS was funded by the École des Neurosciences de Paris. This work was also supported by the City of Paris and Inserm Atip-Avenir to MM. FV was supported by grants from the Mission Interministérielle de Lutte contre la Drogue et la Toxicomanie (MILDT, 2006); the Département de la Recherche Clinique et du Développement-Assistance Publique Hôpitaux de Paris (DRCD-APHP,OST07013); and from the Programme Hospitalier de Recherches Cliniques (PHRC program,AOM10165). The Cellular Imaging and Flow Cytometry Facility is supported by the Conseil Régional Ile-de-France