Activity Of Nerve Cells Research Articles

Protection of acanthopanax senticosus saponin on free radical injury induced aging of nerve cell

To study the effect of Acanthopanax senticosus saponin (ASS) on free radical injury induced neuron aging. On day 7 of fetal mice, cortical neuron primary passage cultures were divided into the normal control group, model group and ASS groups. The model group using free radical (FeSO4 plus H2O2) injury mode prepared in vivo cultured ICR mice cortical neuron aging model; ASS groups: 24 hrs before and after treated with H2O2 and FeSO4, different concentration of ASS was added, according to biochemical parameters such as lactate dehydrogenase (LDH), superoxide dismutase (SOD) and malondialdehyde (MDA) etc. and histomorphologic change to observe the protection of ASS on aging neurons. The LDH, SOD,MDA of the model group were compared with the normal group, < 0. 01; ASS groups added 1.25 mg/100 ml, 2.5 mg/100 ml, 5 mg/100 ml concentration of ASS, their LDH, SOD, MDA compared with the model group π.05-0.01, the difference was significant. In medicated groups the SOD activity of oxidization injured nerve cells obviously elevated, LDH activity and MDA content apparently lowered. Microscope and scanning electron microscopic observation showed that supplemented with ASS to protect the nerve cell injury abated, part of the cellular structure tended to normalize. ASS could act against free radical toxic effect, increase the anti-oxidase activity, strengthen the protection of neuron cells. It is assumed that the effect against nerve cell aging was possibly through scavenging oxygen free radical, strengthening the stability of cell membrane, thus delaying the development of aging.

Sex, stress and the hippocampus: allostasis, allostatic load and the aging process.

The adaptive responses of the body that maintain homeostasis in response to stressors can be called "allostasis", meaning "achieving stability through change". Mediators produced by the immune system, autonomic nervous system (ANS) and hypothalamo-pituitary-adrenal(HPA) axis produce allostasis. The brain also shows allostasis, involving the activation of nerve cell activity and the release of neurotransmitters. When the individual is challenged repeatedly or when the allostatic systems remain turned on when no longer needed, the mediators of allostasis can produce a wear and tear on the body and brain that has been termed "allostatic load". Examples of allostatic load include the accumulation of abdominal fat, the loss of bone minerals and the atrophy of nerve cells in the hippocampus. Studies of the hippocampus as a target of stress and sex hormones have revealed a considerable degree of structural plasticity and remodeling in the adult brain that differs between the sexes. Three forms of hippocampal structural plasticity are affected by circulating hormones: (1) repeated stress causes remodeling of dendrites in the CA3 region; (2) different modalities of stress suppress neurogenesis of dentate gyrus granule neurons; (3) ovarian steroids regulate synapse formation during the estrous cycle of female rats. All three forms of structural remodeling of the hippocampus are mediated by hormones working in concert with excitatory amino acids (EAA) and NMDA receptors. EAA and NMDA receptors are also involved in neuronal death that is caused in pyramidal neurons by seizures, by ischemia and by severe and prolonged psychosocial stress. The aging brain seems to be more vulnerable to such effects, although there are considerable individual differences in vulnerability that can be developmentally determined. Moreover, the brain retains considerable resilience in the face of stress, and estrogens appear to play a role in this resilience. "Resilience is an example of successful allostasis in which wear and tear is minimized, and estrogens exemplify the type of agent that works against the allostatic load associated with aging." This review discusses the current status of work on underlying mechanisms for protection and damage.

Effect of Bupivacaine application on cholinesterase activities, total protein- and albumin concentration in serum and cerebrospinal fluid

The rationale of this study was to determine whether Bupivacaine used for spinal anesthesia alters the specific secretory activity of nerve cells and/or the function of the blood/cerebrospinal fluid barrier. Four groups were assessed: (1) patients undergoing spinal anesthesia using Bupivacaine for lower limb surgery, (2) spinal Bupivacaine anesthesia without subsequent surgery, (3) local facet joint infiltration using Bupivacaine, and (4) general anesthesia for lower limb surgery without Bupivacaine application. Cholinesterase activities, total protein- and albumin concentrations in serum as well as in cerebrospinal fluid were significantly decreased after surgical intervention under spinal Bupivacaine anesthesia but remained unchanged following spinal Bupivacaine application without surgery. No significant correlation was found between Bupivacaine dosage and parameter alteration. There was no influence of intrathecal Bupivacaine application on the albumin ratio cerebrospinal fluid/serum, nor was there any significant alteration of total protein- or albumin concentrations and butyrylcholinesterase activity in the serum as a result of local injection of Bupivacaine to facet joints. These serum parameters were reduced after surgery under general anesthesia. Alterations of serum- and cerebrospinal fluid parameters investigated after surgery are not related to Bupivacaine application but to effects linked to operative treatment, i.e. suppressed secretory cell activity or protein depletion owing to blood loss. We conclude that the secretory function of cholinesterase-releasing nerve cells is not affected by spinal application of Bupivacaine. The blood/cerebrospinal fluid barrier remains intact.

The role of endogenous peptides in the development of long-term posttetanic potentiation

Using the model of long-term posttetanic potentiation (LTP) in slices of the olfactory cortex of rat brain, we have tested a hypothesis according to which activation of nerve cells results in a release of neuromodulatory factors into extracellular space; these factors, diffusing over significant distances, are capable of synchronously modifying the initial reactivity of neuronal populations. Using the technique of bioassay, i.e., transfer of perfusate from the tetanized donor slice to the recipient slice, in combination with pharmacological and neurochemical techniques, we found that in response to excitation, the cells of olfactory cortex slices secrete peptides. This observation confirms the above hypothesis. The spectrum of released peptides changes depending on the degree of cell excitation and, in addition, is frequency-dependent. It has been demonstrated that the key target of these peptides are N-methyl-D-aspartate and glutamate receptors. We propose that two peptide pools are involved in the initial and late phases of LTP. The possible significance of peptide cell regulation in mechanisms of neuronal plasticity is discussed.

Rapid lesioning of large numbers of identified vertebrate neurons: applications in zebrafish

Establishing a causal role between the activity of specific individual nerve cells and the behaviors they produce (or the neural computations they execute) is made difficult in vertebrate animals because of the large numbers of neurons involved. Traditional techniques for establishing causal roles, such as tract cutting and electrolytic lesions, are limited because they produce damage that affects a variety of different cell types, invariably intermingled, and often of uncertain identity. We propose here an alternative lesioning technique in which large numbers of neurons are lesioned, but the lesioned neurons are specifically identified by fluorescent labeling. We use the locomotor control system of the larval zebrafish to illustrate this approach. In this example, the technique involves injection of fluorescent dextrans into far-rostral spinal cord to label descending nerve fibers. Such injections appear to interrupt the descending nerve fibers, and therefore their accompanying locomotor control signals. This protocol is shown to produce significant behavioral deficits. Because the CNS of the larval zebrafish is transparent, the entire population of lesioned cells can be imaged in vivo and reconstructed using confocal microscopy. This large-scale lesioning technique is important, even in this relatively ‘simple’ vertebrate animal, because the ablation of smaller numbers of neurons, using more precise laser-ablation techniques, often fails to produce observable behavioral deficits. While this technique is most readily applied in simpler and transparent vertebrate animals, the approach is general in nature and might, in principle, be applied to any vertebrate nerve tract.

Current thinking about risks from currents

The production, transmission, distribution, and use of electricity generate electromagnetic fields having a frequency of 50–60 Hz, sometimes called power frequency. This range falls within the extremely low-frequency band (ELF-EMF). The hypothesis that exposure to such fields increases the risk of cancer has been controversial ever since a link was reported more than two decades ago. 1 Wertheimer N Leeper E Electrical wiring configurations and childhood cancer. Am J Epidemiol. 1979; 109: 273-384 Crossref PubMed Scopus (1372) Google Scholar The main reason for scepticism has been the low amount of energy that these fields transfer because of their low frequency; the wave-length corresponding to 50 Hz is similar to the radius of the earth. The only established mechanism for biological effects of ELF-EMF is induction of electrical currents in the tissue, but the fields to which a person is normally exposed in the environment are generally orders of magnitude too low to be of any significance in this context, in view of the endogenous electrical activity in nerve and muscle cells. These considerations have led physicists to claim that ELF-EMF cannot produce biological effects at the low levels of environmental exposure.

Blocker state dependence and trapping in hyperpolarization-activated cation channels: evidence for an intracellular activation gate.

Hyperpolarization-activated cation currents (I(h)) are key determinants of repetitive electrical activity in heart and nerve cells. The bradycardic agent ZD7288 is a selective blocker of these currents. We studied the mechanism for ZD7288 blockade of cloned I(h) channels in excised inside-out patches. ZD7288 blockade of the mammalian mHCN1 channel appeared to require opening of the channel, but strong hyperpolarization disfavored blockade. The steepness of this voltage-dependent effect (an apparent valence of approximately 4) makes it unlikely to arise solely from a direct effect of voltage on blocker binding. Instead, it probably indicates a differential affinity of the blocker for different channel conformations. Similar properties were seen for ZD7288 blockade of the sea urchin homologue of I(h) channels (SPIH), but some of the blockade was irreversible. To explore the molecular basis for the difference in reversibility, we constructed chimeric channels from mHCN1 and SPIH and localized the structural determinant for the reversibility to three residues in the S6 region likely to line the pore. Using a triple point mutant in S6, we also revealed the trapping of ZD7288 by the closing of the channel. Overall, the observations led us to hypothesize that the residues responsible for ZD7288 block of I(h) channels are located in the pore lining, and are guarded by an intracellular activation gate of the channel.

EFFECT OF NICARDIPINE TREATMENT ON THE EXPRESSION OF NEUROFILAMENT 200 KDa IMMUNOREACTIVITY IN THE BRAIN OF SPONTANEOUSLY HYPERTENSIVE RATS

Neurofilaments (NFP) are components of neuronal cytoskeleton involved primarily in axonal transport and in the regulation of dynamic activities of nerve cells. NFP consist of three subunits denominated high- (200 kDa, NFP–H), intermediate- (160 kDa, NFP-I), and low-molecular weight (68 kDa, NFP–L) neurofilament proteins. Their function and polymerization depends on phosphorylation status, and is regulated by Ca2+ influx. Ca2+ overload enhances degradation of NFP and may compromise axonal transport. An increased susceptibility to ischemia occurs in hypertension, which is also a cause of brain damage. In this study, the expression of phosphorylated NFP (P–NFP) was investigated in the brain of spontaneously hypertensive rats (SHR) using immunohistochemical techniques with antibodies against the phosphorylated epitope of NFP RT–97. Microanatomical analysis included frontal cortex, occipital cortex, hippocampus and cerebellar cortex. The effect of long-term treatment with the dihydropyridine-type Ca2+ antagonist nicardipine on the expression of P–NFP was investigated as well. In hypertension a decreased P–NFP immunoreactivity was observed in frontal and occipital cortex, in the CA1 subfield of hippocampus and in the dentate gyrus, but not in the CA3 subfield of hippocampus or in the cerebellar cortex. Treatment with a daily dose of 3 mg/kg of nicardipine and 10 mg/kg of hydralazine significantly reduced systolic pressure in SHR. The above dose of nicardipine and to a lesser extent a non-hypotensive dose of the compound (0.1 mg/kg/day), but not hydralazine, increased P–NFP immunoreactivity in the cerebral cortex and hippocampus, except the CA3 subfield. The possibility that rescued P–NFP immunoreactivity by treatment with nicardipine depends on improved brain perfusion caused by the compound and/or by countering neuronal Ca2+ overload is discussed.

Morphochemical features of plastic rearrangements of hippocampal neurons after rhythmic stimulation of the limbs in elderly rabbits.

The process of aging is accompanied by significant derangements to brain function, which are expressed particularly as the well-known phenomenon of memory disturbance [4,5]. Since memory functions are based on plastic rearrangements, in which the key role is played by metabolic processes, we elected to study the interactions between nerve cell activity and the state of protein biosynthesis during the formation of temporal associations in animals of different ages [3]. An interferometric method was considered appropriate in this regard as a method for estimating the dry weight of the cytoplasm and nucleus in neurons; this serves as a measure of their protein contents [1,2]. The aim of the present work was to identify the relationship between the process of impressing the assimilation trace of a rhythm during the acquisition of an analog of a conditioned reflex to time in hippocampal neurons and their morphochemical parameters in elderly rabbits.

Cochleotopic fos immunoreactivity in cochlea and cochlear nuclei evoked by bipolar cochlear electrical stimulation

Fos-like immunoreactivity evoked by basal, second or apical turn bipolar intracochlear electrical stimulation was evaluated in the spiral ganglion and cochlear nuclei. At stimulation levels of six times the electrically evoked auditory brain stem response thresholds, immunoreactive neurons were observed at appropriate discrete cochleotopic regions relative to stimulation site. The number of neurons increased with stimulus level and closely correlated to wave I amplitude. At 10 times thresholds, some spread in fos-like immunoreactivity to adjacent cochlear turns was found. However, fos-like immunoreactivity at this high level of stimulation still clearly showed a differential distribution in density of expression. These results indicated that the restricted topographic distribution of activity evoked by high levels of electrical stimulation is initiated at first order primary neurons of the system. For the profoundly deaf with cochlear implants, this indicates that place (channel) information can be maintained in the spiral ganglion and central nervous system even at very high levels of electrical stimulation. Together with our previous studies, these results indicate that fos provides a marker which can be used for evaluation of extent and pattern of cellular activation throughout the central auditory pathways, including activation of auditory nerve cells.

Temporal coupling between neuronal activity and blood flow in rat cerebellar cortex as indicated by field potential analysis.

1. Laser-Doppler flowmetry and extracellular recordings of field potentials were used to examine the temporal coupling between neuronal activity and increases in cerebellar blood flow (CeBF). 2. Climbing fibre-evoked increases in CeBF were dependent on stimulus duration, indicating that increases in CeBF reflected a time integral in neuronal activity. The simplest way to represent neuronal activity over time was to obtain a running summation of evoked field potential amplitudes (runSigmaFP). RunSigmaFP was calculated for each stimulus protocol and compared with the time course of the CeBF responses to demonstrate coupling between nerve cell activity and CeBF. 3. In the climbing fibre system, the amplitude and time course of CeBF were in agreement with the calculated postsynaptic runSigmaFP (2-20 Hz for 60 s). This suggested coupling between CeBF and neuronal activity in this excitatory, monosynaptic, afferent-input system under these conditions. There was no correlation between runSigmaFP and CeBF during prolonged stimulation. 4. Parallel fibre-evoked increases in CeBF correlated with runSigmaFP of pre- and postsynaptic potentials (2-15 Hz for 60 s). At higher stimulation frequencies and during longer-lasting stimulation the time course and amplitudes of CeBF responses correlated with runSigmaFP of presynaptic, but not postsynaptic potentials. This suggested a more complex relationship in this mixed inhibitory-excitatory, disynaptic, afferent-input system. 5. This study has demonstrated temporal coupling between neuronal activity and CeBF in the monosynaptic, excitatory climbing-fibre system. In the mixed mono- and disynaptic parallel fibre system, temporal coupling was most clearly observed at low stimulation frequencies. We propose that appropriate modelling of electrophysiological data is needed to document functional coupling of neuronal activity and blood flow.

Allostasis, allostatic load, and the aging nervous system: role of excitatory amino acids and excitotoxicity.

The adaptive responses of the body to challenges, often known as "stressors", consists of active responses that maintain homeostasis. This process of adaptation is known as "allostasis", meaning "achieving stability through change". Many systems of the body show allostasis, including the autonomic nervous system and hypothalamo-pituitary-adrenal (HPA) axis and they help to re-establish or maintain homeostasis through adaptation. The brain also shows allostasis, involving the activation of nerve cell activity and the release of neurotransmitters. When the individual is challenged repeatedly or when the allostatic systems remain turned on when no longer needed, the mediators of allostasis can produce a wear and tear on the body that has been termed "allostatic load". Examples of allostatic load include the accumulation of abdominal fat, the loss of bone minerals and the atrophy of nerve cells in the hippocampus. Circulating stress hormones play a key role, and, in the hippocampus, excitatory amino acids and NMDA receptors are important mediators of neuronal atrophy. The aging brain seems to be more vulnerable to such effects, although there are considerable individual differences in vulnerability that can be developmentally determined. Yet, at the same time, excitatory amino acids and NMDA receptors mediate important types of plasticity in the hippocampus. Moreover, the brain retains considerable resilience in the face of stress, and estrogens appear to play a role in this resilience. This review discusses the current status of work on underlying mechanisms for these effects.

In vitro biological activity and toxicity of tetanus and botulinum neurotoxins

Tetanus and botulinum neurotoxins are the most potent toxins known and cause tetanus and botulism, respectively. They are zinc-endopeptidases acting in the cytosol, where they cleave SNARE proteins. Here, we report on the assay of their metalloproteolytic activity in vitro on recombinant SNARE proteins. We also describe the assay of their activity in nerve cells in culture using antibodies specific for the SNARE proteins. Together with recent reports from other laboratories, these results show that the toxicity of these powerful neurotoxins can be appropriately assayed in vitro, thus reducing considerably the number of animals currently used in the evaluation of the toxicity of tetanus toxoid vaccine and of the botulinum neurotoxins to be used for human therapy.

Nonlinear dynamics and information processing in pacemaker neurons

The paper treats some nonlinear dynamic phenomena in oscillatory activity of a single nerve cell. Based on experiments with CNS bursting pacemaker neurons ofHelix pomatia snail, a mathematical model was studied. The model demonstrates the majority of experimentally observable phenomena and allows one to investigate the role of its separate components. The phenomena demonstrated by model neuron (chaotic behavior, bistability, and sensitivity to parameter variations, initial conditions, and stimuli) may be relevant to information processing in nerve cells. The complexity of [Ca2+]in−V phase diagrams of initial conditions depends on parameters. Transient synaptic impulse produces stable parameter-independent changes in activity of model neuron. These results indicate that a single bursting neuron can work in the neuronal ensemble as a dynamic switch. The sensitivity of this switch is regulated by a neurotransmitter.

Correlating structure and function in ATP-sensitive K + channels

ATP-sensitive K + channels couple cell metabolism to electrical activity in nerve, muscle and endocrine cells, and play important roles in these tissues under both physiological and pathological conditions. The K ATP channel is an octameric complex of two unrelated types of subunit: a pore-forming subunit (Kir6.2) and a regulatory subunit, the sulphonylurea receptor (SUR). This review focuses on the regulation of K ATP channel activity by nucleotides and cell metabolism and considers which regulatory mechanisms are intrinsic to Kir6.2 and which are conferred by association with SUR.

Activity-dependent regulation of dendritic BC1 RNA in hippocampal neurons in culture.

Several neuronal RNAs have been identified in dendrites, and it has been suggested that the dendritic location of these RNAs may be relevant to the spatiotemporal regulation of mosaic postsynaptic protein repertoires through transsynaptic activity. Such regulation would require that dendritic RNAs themselves, or at least some of them, be subject to physiological control. We have therefore examined the functional regulation of somatodendritic expression levels of dendritic BC1 RNA in hippocampal neurons in culture. BC1 RNA, an RNA polymerase III transcript that is a component of a ribonucleoprotein particle, became first detectable in somatodendritic domains of developing hippocampal neurons at times of initial synapse formation. BC1 RNA was identified only in such neurons that had established synapses on cell bodies and/or developing dendritic arbors. When synaptic contact formation was initiated later in low-density cultures, BC1 expression was coordinately delayed. Inhibition of neuronal activity in hippocampal neurons resulted in a substantial but reversible reduction of somatodendritic BC1 expression. We conclude that expression of BC1 RNA in somatic and dendritic domains of hippocampal neurons is regulated in development, and is dependent upon neuronal activity. These results establish (for the first time to our knowledge) that an RNA polymerase III transcript can be subject to control through physiological activity in nerve cells.

Illusions as neuro-signs

One of the reasons visual scientists find illusions fascinating is that their pictorial simplicity belies the complexity of visual processing. Illusions can direct us towards neurophysiological interpretations at many levels, which I have called ‘neuro-signs’. The most useful visual illusions are those that point to the simplest neural level possible, that is, those that provide signs of neural processing at early stages of the visual system, such as in the retina itself. The region of the retina that can change the activity of nerve cells throughout the visual system when light falls on it is called the ‘receptive field’ of those nerve cells. Primate retinal ganglion cells have receptive fields that are concentric and antagonistic — if the centre of a receptive field is excited by light the surround is inhibited (called ‘surround inhibition’), or vice versa. Are there any visual signs of such neural antagonism? There could be. In the black and white grid pattern shown below, a variety of illusory dots can be seen at the intersections of the black and white grid. In the upper half, dark grey dots appear at the white intersections between the black rectangles, although a light meter would not register such effects. This is called a Hermann grid; its reverse in the lower half, where illusory light grey dots are seen in the black intersections, is called a Hering grid. In both cases, the dots at an intersection disappear as soon as it is fixated, but they remain at those nearby. The dots are more difficult to see at the smallest intersections in both grids. Because of this effect, it is thought the illusory dots might be related to the distance from the centre of the retina (or ‘retinal eccentricity’); receptive fields have been found to be much smaller around the centre of the retina than more peripherally. Indeed, the optimal separation for producing the illusory dots increases with retinal eccentricity in a similar manner to the increase in receptive field size. But why do the illusory dots appear at all? One suggestion is that concentric receptive fields of the same dimensions will be stimulated differently when they fall at an intersection between four rectangles than when flanked by two rectangles — there would be more surround inhibition at an intersection than elsewhere. This would make a light intersection darker than its neighbours and a dark intersection lighter. Such an interpretation does not account for the dots that are visible between rectangles that are simply outlines, although these dots are not as compelling. When coloured rectangles are placed on a grey background (see above), the illusory dots at the intersections take on the colour of the rectangles: they appear to be light green in the grey intersections of the upper half, and reddish in the grey intersections of the lower half. This is because some receptive fields at the retinal ganglion cell level display colour opponency — the centre can be excited by, say, red and the surround inhibited by green; others operate on blue–yellow opponency. Hermann–Hering grids provide signs of a link between visual perception and neurophysiology. The link is made at an early stage of visual processing — the differences in the activity of the retinal ganglion cells — with the assumption that the neural signals for these differences are preserved in their transmission to the visual cortex of the brain. N Wade, Department of Psychology, University of Dundee, Dundee DD1 4HN, UK. This is the second in a short series of articles by Nicholas Wade, describing some common visual illusions.

Isolation of seven unique biogenic amine receptor clones from the honey bee by library scanning.

The biogenic amine receptor genes constitute an ancient and highly divergent family within the larger superfamily of G-protein-coupled receptors. These receptors play a central role in modulating nerve cell activity and thus behaviour. Because the honey bee offers numerous advantages for behavioural studies we endeavoured to isolate as many members of this gene family as possible from the bee. We compared numerous approaches to gene isolation and found that PCR amplification from small subfractions of cDNA or genomic DNA libraries enabled us to isolate clones that are otherwise undetectable. In total we isolated seven biogenic amine receptor clones and identified five additional related sequences by low-stringency Southern hybridization. Two clones, AmBAR4 and AmBAR6, are 84% and 72% identical to the Drosophila 5-HT2 and D1b receptors, respectively, and probably represent orthologous genes. Phylogenetic analysis indicates that AmBAR5 clusters loosely with a variety of tyramine and octopamine receptors with which it shares <66% identity. The other four clones, AmBAR1, AmBAR2, AmBAR3 and AmBAR7, are weakly to moderately related (28-45% identical) to Drosophila dopaminergic or mammalian adrenergic receptors and probably represent receptors of these classes whose orthologues have not previously been isolated from any insect. The honey bee clones expand the size of the known insect biogenic amine receptor gene family to sixteen members. Therefore the size of the biogenic amine receptor gene family of insects approaches that of vertebrates. This is true despite the reduced behavioural and genetic complexity of the insects relative to vertebrate animals.

The Effects of Allyl Chloride on Ca2+, Ca2+‐Free CaM, cAMP and Ca2+/CaM‐PK II Activity in Nerve Cells

The Effects of Allyl Chloride on Ca2+, Caz+‐Free CaM, cAMP and Ca24/CaM‐PK II Activity in Nerve Cells: Keqin Xie, et at. Institute of Toxicology, Shandong Medical University—Nerve cells in a culture from chicken embryo brain were used to study the allyl chloride‐induced effects on the contents of intracellular Ca2+, Ca2+‐free CaM, cAMP and the activity of Ca2+/CaM‐PK II. The results showed that with the increase in the concentration of allyl chloride there was a significant increase in the content of Ca2+and cAMP, and the activity of Ca2~/CaM‐PK II in the cells (P&lt;0.01), but a marked decrease in Ca2 + ‐free CaM (P&lt; 0.01). The results suggest that the neurotoxicity of allyl chloride might be related to the increase in intracellular Ca2+ and the activation of CaM and Ca2+/CaM‐PK II, eventually leading to the accumulation of degenerative MT in the nerve axon.

Use of artificial ion channels for quasi-intracellular recording of cerebral cortex neuron activity.

Action potentials and synaptic potentials were recorded in vivo from cortical neurons in baby rats aged 20-25 days using a new method based on the ionophore nystatin. Nystatin solution was used to fill a standard glass extracellular microelectrode, and became inserted into membranes. Spikes which were initially recorded as extracellular spikes showed increases in amplitude and were transformed into unipolar quasi-intracellular spikes at 0.5-5.0 min after formation of the high-conductance contact. This method allows stable recording of neuronal activity from cells for at least 1 h, and provides a good signal-to-noise ratio. The electrode does not puncture the neuron membrane, with the result that experiments do not require any isolation from vibration. Thus, the results obtained demonstrate that the method is highly efficient for recording the in vivo activity of small nerve cells.