Single Neurons In Brain Research Articles

Temperatures and Voltages From the Electroconvulsive Therapy Stimulus.

Brain voltage and temperature during electroconvulsive therapy (ECT) are not widely understood but are commonly mischaracterized as resembling a blast. To better understand brain voltage and temperature during ECT, basic mathematical structural models were constructed and calculations were made. In addition, thermographic images were recorded before and after ECT stimuli were applied to a pork shoulder. A basic structural voltage model indicates that the voltage drop across single brain neurons is about 6 mV, with a gradient of 0.6 V/cm. This is an order of magnitude smaller than the action potential. Basic structural temperature models indicate that 100 joules raises skin temperature underneath ECT electrodes no more than 1°C, and within the brain by much less. The average temperature increase at each electrode was 0.70 to 0.94°C. Voltage gradients and temperatures in the brain during the ECT stimulus are well within the range of ordinary physiological functioning. These results are consistent with previous reports that only a small fraction of the electrical stimulus enters the brain.

Effects of tipepidine on MK-801-induced cognitive impairment in mice

We previously reported that centrally acting non-narcotic antitussives, including tipepidine, inhibit G-protein-coupled inwardly rectifying potassium (GIRK) channel-activated currents of neurons. In addition, when administered at a cough suppressant dose, the drugs ameliorated the symptoms of various models of intractable brain disease in rodents. In the current study, we investigated whether tipepidine causes recovery from schizophrenia-like cognitive dysfunction, which was induced by MK-801 (0.2 mg/kg, i.p.) in mice. We also examined the effect of tipepidine and clozapine co-administration on the dysfunction. Moreover, we studied whether clozapine inhibits GIRK channel activated currents in single brain neurons using the patch-clamp technique. Tipepidine elicited recovery from MK-801-induced cognitive impairment in the novel objective recognition test and Y-maze test. Further, co-administration of tipepidine and clozapine, at subthreshold doses of each drug, improved MK-801-induced cognitive impairment in the novel objective recognition test. Clozapine (3 × 10−5 M) had a minor effect on baclofen-induced currents in dopamine neurons of the ventral tegmental area.

Glycine does not reverse the inhibitory actions of ethanol on NMDA receptor functions in cerebellar granule cells.

The effects of ethanol and/or glycine on NMDA-induced enhancement of cytoplasmic free Ca2+ concentrations ([Ca2+]i), 45Ca2+ influx, 4-b-[3H]phorbol-12,13-dibutyrate ([3H]PDBu) binding, and neuronal necrosis in cultured rat cortical and cerebellar granule neurons were examined. Using microfluorimetric techniques in combination with rapid perfusion of single brain neurons, we found that glycine (10 microM) was a necessary co-agonist for NMDA-induced depolarization in cerebellar granule cells. In contrast, depolarization with NMDA in cortical cells was observed even without the addition of exogenous glycine as well as in the absence or presence of 1 mM MgCl2. Ethanol (50 mM) inhibited the effects of NMDA in some, but not all, neurons indicative of the existence of ethanol-sensitive and ethanol-insensitive cortical and cerebellar granule neurons. In studies performed in monolayers of cortical and cerebellar granule cells, we observed that the presence of glycine (10 microM) was a necessary prerequisite to unmask inhibitory actions of ethanol on 45Ca2+ influx induced by NMDA. In another set of experiments, we noted that NMDA-induced stimulation of [3H]PDBu binding to monolayers of intact cerebellar granule cells was inhibited by ethanol (50 mM). Finally, we report that ethanol caused a concentration-dependent inhibition of NMDA-induced necrotic cell death, assessed by measuring the ability of cerebellar granule cells to transform 3-[4, 5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) into formazan. In none of the four assays used to demonstrate the inhibitory effects of ethanol on NMDA receptor activity, the ethanol-induced inhibition was reversed by glycine (up to 100 microM). Thus, in contrast to earlier reports, our data suggest that ethanol and glycine produce their effects by acting at different regulatory sites within the NMDA receptor system in brain neurons.

Australian funnel-web spider toxin, versutoxin, enhances spontaneous synaptic activity in single brain neurons in vitro

Neurotoxins isolated from the venoms of Australian funnel-web spiders increase spontaneous action potential activity in a variety of excitable cells. In the present study intracellular recordings were made with microelectrodes (30–60 MΩ, 2 M KCl) from locus coeruleus, mesencephalic nucleus of the trigeminal nerve and laterodorsal tegmental neurons in brain slices. Versutoxin, a polypeptide toxin isolated from the venom of Hadronyche versutus produced a profound increase in spontaneous synaptic activity impinging on neurons, which did not fully recover for up to 3 h after washout. The threshold concentration was 1.5 nM in locus coeruleus neurons, with increasing concentrations (up to 50 nM) producing larger effects. A modest increase in synaptic activity was observed in mesencephalic nucleus of the trigeminal nerve neurons during superfusion with 50 nM versutoxin. The increase in spontaneous synaptic activity was reversed by agents which block synaptic potentials impinging on locus coeruleus neurons, i.e., tetrodotoxin (100 nM), Co 2+ (3 nM) or the combination of 6-cyano-7-nitroquinoxaline-2,3-dione (10 μM) and bicuculline (30 μM). Threshold, peak amplitude, maximum rate of rise, duration, amplitude of afterhyperpolarisations and interspike intervals of action potentials in each type of neuron were unaffected by versutoxin. Voltage-current relationships were also unaffected. Calcium-dependent action potentials evoked in locus coeruleus neurons in the presence of tetrodotoxin were unaffected by versutoxin, as were depolarisations produced by exogenously applied glutamate. These results suggest that versutoxin increases spontaneous synaptic activity, but has no effect on the membrane properties of the soma of several types of rat brain neurons.

Cellular mechanisms of opioid tolerance: studies in single brain neurons.

Cellular mechanisms of opioid tolerance: studies in single brain neurons.

Role of motivational excitation in integrative activity of single brain neurons.

1. The dominant factor in the “tuning” of single brain neurons to special external environmental stimuli is the internal need and the dominant motivation arising on its basis. 2. Dominant motivation by means of ascending activating influences of hypothalamic centers on the cerebral cortex widens the convergent and discriminating properties of single cortical neurons and combines them functionally at the stage of afferent synthesis for the formation of behavior aimed at satisfying the dominant need. 3. Reinforcing excitation fixes a definite architecture of interconnected neurons on the canvas of brain neurons functionally combined by motivation, thereby fixing in the properties of those neurons all the parameters of the reinforcing stimulus and its dynamic spatiotemporal localization. This architecture of reinforcing excitation is extracted during each subsequent formation of the analogous need by the corresponding motivation and it is a controlling factor (the action result acceptor) of goal-directed activity.

Long-term recording' from single neurons in brain of unrestrained mammals.

Long-term recording' from single neurons in brain of unrestrained mammals.