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Neuronal Networks in Convulsant Drug-Induced Seizures
Published in Carl L. Faingold, Gerhard H. Fromm, Drugs for Control of Epilepsy:, 2019
Before convulsant drug administration most MRF and medullary RF neurons were not detectably responsive to repeated sensory stimuli. However, RF neurons became strikingly responsive to the sensory stimuli after subseizural doses of bicuculline, strychnine, PTZ, and seven other convulsants. The minority of RF neurons that displayed detectable responses prior to convulsant drug treatment became much more responsive to the sensory stimuli after drug administration (see Figure 4). The neuronal response enhancement accompanied the onset of enhancement of sensory-evoked field potentials.6 RF neuronal response enhancement occurred with each of the sensory modalities tested, and most RF neurons became responsive to stimuli in more than one modality. This effect of convulsants was reversible, and neuronal responsiveness reverted to predrug levels by 30 min after termination of drug administration. This sensory response enhancement occurred in the vast majority of the over 750 RF neurons examined after administration of the convulsant drug. The percentages of neurons affected in each brain locus and the mean degree of response increase is shown in Figure 3. The finding that the convulsant-induced RF neuronal response enhancement precedes the ability of these sensory stimuli to trigger generalized seizures, implicates this phenomenon in seizure initiation.
Functional Characteristics of Nucleus Accumbens Neurons: Evidence Obtained From In Vivo Electrophysiological Recordings
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Steven J. Henriksen, Jeannie Giacchino
Systemically administered heroin and morphine most commonly (55%) depress the discharge rates of spontaneously active nucleus accumbens cells in a naloxone-reversible fashion.23,24 However, evoked field responses and stimulation-evoked single cell activity are consistently unaltered by these drugs. We have as yet observed only depressant effects of electrophoretically applied morphine on spontaneously active nucleus accumbens neurons.24 We have also investigated the potential role of DA systems projecting to the nucleus accumbens from the VTA on the actions of systemic morphine on nucleus accumbens neurons.24,83 Microinfusions (1 microliter) of morphine into the ipsilateral VTA produces short latency, mostly inhibitory effects on spontaneously active nucleus accumbens neurons that are naloxone-reversible. However, the inhibition of nucleus accumbens neurons by VTA morphine infusions have been observed to be DA-dependent as well as DA-independent. We have been able to reverse some but not all VTA morphine-induced nucleus accumbens depressions by subsequent systemic administration of the DA receptor antagonist alpha-flupenthixol (0.5 mg/kg s.c). These data suggest that nucleus accumbens neurons have complex responses to systemically administered morphine that may involve both direct and indirect actions.83
Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
Physiol., 424, 513, 1990. Hsu F.-C. and Smith, S.S., Progesterone withdrawal reduces paired-pulse inhibition in rat hippocampus: dependence on GABA-A receptor alpha-4 upregulation, J. Neu-rophysiol., 89, 186, 2003.Karnup, S. and Stelzer, A., Temporal overlap of excitatory and inhibitory afferent input in guinea-pig CA1 pyramidal cells, J. Physiol., 516, 485, 1999.Rogers, C.J. and Hunter, B.E., Chronic ethanol treatment reduces inhibition in CA1 neurons of the rat hippocampus, Brain Res. Bull., 28, 587, 1992.Turner, D.A., Feed-forward inhibitory potentials and excitatory interactions in guinea-pig hippocampal pyramidal cells, J. Physiol., 422, 333, 1990.Kamphuis, W., Gorter, J.A., Wadman, W.J., and Lopes da Silva, F.H., Hippocampal kindling leads to different changes in paired-pulse depression of local evoked field potentials in CA1 area and in fascia dentata, Neurosci. Lett., 141, 101, 1992.Sloviter, R.S., Decreased hippocampal inhibition and a selective loss of interneurons in experimental epilepsy, Science, 235, 73, 1987.Zhao, D. and Leung, L.S., Effects of hippocampal kindling on paired-pulse response
Vanillic acid attenuates amyloid β1-40-induced long-term potentiation deficit in male rats: an in vivo investigation
Published in Neurological Research, 2021
Nesa Ahmadi, Naser Mirazi, Alireza Komaki, Samaneh Safari, Abdolkarim Hosseini
In the DG, field excitatory postsynaptic potential (fEPSP) and PS were the two components of the evoked field potentials. During the electrophysiological recordings, fEPSP slopes and alterations in the PS amplitudes were assessed. The slope functions of fEPSP were measured as the slope of the line which connects the beginning of the evoked potential’s initial positive deflection with the peak of the deflection in the second positive evoked potential. We measured the PS amplitudes from the first deflection’s peak which was positive in the evoked potential to the peak of the next potential which was negative [22,23]. The slope measurements of fEPSP were taken between 20% and 80% of the peak amplitude. In the current study, in order to evoke potentials, the adjustment of the stimulation intensity was implemented which included 40% of the maximum PS amplitude, specified by a curve of input/output [18].
The enigma of headaches associated with electromagnetic hyperfrequencies: Hypotheses supporting non-psychogenic algogenic processes
Published in Electromagnetic Biology and Medicine, 2020
Tattersall et al. demonstrated dose-dependent (SAR of 1.6 to 4.4 mW/kg; 5–15 min of exposure to a continuous 700 MHz HF in a stripline waveguide) perturbations of the recorded potential in the CA1 and CA3 areas of rats (Tattersall et al. 2001). At low field intensities, authors mainly reported a potentiation of the spike amplitudes by up to 20% on the electrically evoked field potential in CA1; however, higher intensity fields could produce either increases or decreases of up to 120% and 80%, respectively, in the amplitude of the population spikes. These findings suggest hyperexcitability at low intensities but hazardous consequences on excitability for higher irradiation rates. Disruption of motor activity (Van Eeghem et al. 2017) or disturbances in higher brain performance (Deshmukh et al. 2016, 2015; Hassanshahi et al. 2017) had also been reported. In the study of Van Eeghem, mice were exposed to 10 GHz HF (SAR of 0,3 W/Kg; amplitude modulation of 2 Hz and 8 Hz; brain temperature increasing of 0.23°C) for 6 d (Van Eeghem et al. 2017). For the 8 Hz exposure, significant locomotor activity reduction was observed immediately, with a normalization after 4 weeks. In contrast, there was no effect with 2 Hz modulation. For the study of Hassanshahi and al., authors investigate the effects of 2.4 GHz Wi-Fi radiation on multisensory integration in 80 male Wistar rats (sham group and exposed groups for 30 d, 12 h/day) (Hassanshahi et al. 2017). Their results showed that chronic exposure to 2,45 GHz HF can impair both unimodal and cross-modal encoding of information.
β-amyloid inhibits hippocampal LTP through TNFR/IKK/NF-κB pathway
Published in Neurological Research, 2018
Manikandan Samidurai, Vijay S. Ramasamy, Jihoon Jo
After 1–2 h of stabilization, hippocampal slices were transferred to the recording chamber, in which they were submerged in aCSF (28–30 °C) flowing at 2 ml/min. To record extracellular field excitatory postsynaptic potentials (fEPSP), two stimulating bipolar electrodes (66 μm twisted nichrome wire) were positioned on Schaffer collateral pathway (for LTP input) and subiculum region (for control input), respectively. fEPSP was recorded with a glass microelectrode prepared using a micropipette puller (Sutter Instrument, P-1000) and filled with 3 M NaCl (3–5 MΩ) placed on the CA1 region of the hippocampi. Stable baseline recordings of responses to low-frequency stimulation (single pulses delivered at 0.016 Hz with stimulation intensity were adjusted to 50–60% of the maximum spike-free fEPSP) were collected for at least 30 min prior to pharmacological manipulation or the induction of LTP. LTP was evoked by two trains of tetanus stimuli (100 Hz for 1 second with 30 seconds inter-tetanus interval). The stimulus intensity during tetanus stimuli was identical to that of the test pulse. After established the stable baseline for 30mins, fEPSP was further recorded for at least 60 min. The slope of the evoked field potential responses was measured and expressed relative to the normalized preconditioning baseline and expressed as a percentage of baselines. Data were collected by NI USB-6251 (National instruments) and amplified by Axopatch 200B (Axon instruments). Data were captured and analyzed using WinLTP software (www.winltp.com).