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At least 631 records · Page 35Linked to original sources
PubMed2004

Electrophysiological characterization of synaptic connections between layer VI cortical cells and neurons of the nucleus reticularis thalami in juvenile rats.

Corticothalamic (CT) feedback projections to the thalamus outnumber sensory inputs from the periphery by orders of magnitude. However, their functional role remains elusive. CT projections may directly excite thalamic relay cells or indirectly inhibit them via excitation of the nucleus reticularis thalami (nRT), a nuclear formation composed entirely of gamma-aminobutyric acidergic neurons. The relative strengths of these two pathways will ultimately control the effects of CT projections on the output of thalamic relay cells. However, corticoreticular synapses have not yet been fully physiologically characterized. Here, local stimulation of layer VI cells by focal application of K+ or AMPA elicited excitatory postsynaptic potentials in nRT neurons with a mean peak amplitude of 2.4 +/- 0.1 mV (n = 75, mean +/- SEM), a mean rise time (10-90%) of 0.74 +/- 0.03 ms and a weighted decay time constant of 11 +/- 0.3 ms. A pharmacological profile of responses was drawn in both current-clamp and voltage-clamp modes, showing the presence of a small N-methyl-d-aspartate receptor-dependent component at depolarized potentials. In two pairs of synaptically coupled layer VI cell-nRT neuron, moderate rates of transmission failures were observed while the latencies were above 5 ms in both cases. Our results indicate that the corticoreticular pathway fulfills the criteria for 'modulatory' inputs and is temporally restricted. We suggest that it may be involved in coincidence detection of convergent corticoreticular signals.

Animals↗
PubMed2005

Processes and components participating in the generation of intrinsic optical signal changes in vitro.

Imaging of intrinsic optical signals has become an important tool in the neurosciences. To better understand processes underlying changes in intrinsic optical signals, we studied electrical stimulation at varying strengths in hippocampal slices of adult Wistar rats. Following serial stimulation we observed an increase in light transmittance in all tested slices. During antidromic stimulation at minimum stimulation strength the increase in light transmittance was 75 +/- 8% (P < 0.05), and during orthodromic minimum stimulation 19.6 +/- 5.6% (P < 0.001) in the stratum pyramidale of the CA1-region. During orthodromic stimulation no significant difference between submaximum, maximum and supramaximum stimulation was found, indicating saturation. In contrast, submaximum antidromic stimulation yielded 56.2 +/- 12% (P < 0.05) of maximum stimulation strength, indicating recruitment. In a further set of experiments serial stimulation was carried out under glial blockade with fluoroacetate (FAC) or blockage of mitochondrial function. Amplitude and slope of the intrinsic optical signal significantly decreased in the presence of FAC (amplitude: 36 +/- 6%, P < 0.01; slope: 37 +/- 11% as compared with baseline conditions, P < 0.05). This suggests a glial participation in signal generation. Rotenone, an inhibitor of mitochondrial complex I, yielded decreased amplitudes of the intrinsic optical signal (27 +/- 7% after 40 min, P < 0.01). Our data indicate that the intrinsic optical signal change reflects type and strength of neuronal activation and point to glia and mitochondria as important participants in signal generation.

Action Potentials↗
PubMed2001

Simultaneous intracellular recordings from longitudinal and circular muscle during the peristaltic reflex in guinea-pig distal colon.

1. Simultaneous intracellular recordings were made from longitudinal muscle (LM) and circular muscle (CM) cells of guinea-pig distal colon during the peristaltic reflex. 2. Spontaneous rhythmical depolarizations with superimposed action potentials (mean amplitude: 19 +/- 2 mV) were regularly recorded from the LM (mean interval: 7 +/- 1 s). In contrast, in the CM layer, spontaneous action potentials occurred with an irregular frequency. Although spontaneous action potentials in LM were rarely correlated in time with those in CM, spontaneous inhibitory junction potentials (sIJPs) were found to occur synchronously in both muscles (5 out of 27 animals; 19 %). 3. Graded inflation of an intra-luminal balloon or mucosal stimulation oral to the recording electrodes elicited gradeable compound IJPs synchronously in both LM (mean amplitude: 6 +/- 1 mV) and CM (mean amplitude: 9 +/- 1 mV) (descending inhibitory reflex). Evoked IJPs were often followed by action potentials in both muscle layers. 4. Mucosal stimuli applied anal to the recording electrodes elicited compound excitatory junction potentials (EJPs) synchronously in both muscles layers that were often associated with the generation of action potentials. In the LM, evoked EJP amplitudes ranged from 3 mV (subthreshold) to 31 mV (including the action potential) and in the CM from 4 mV (subthreshold) to 44 mV (including the action potential). 5. Apamin (500 nM) reduced the evoked IJP in the CM by 55 % (from 11 +/- 2 to 5 +/- 1 mV), but caused no significant reduction in the LM layer (from 8 +/- 1 to 6 +/- 1 mV). Apamin-resistant IJPs in both muscle layers were likely to be due to nitric oxide, since they were abolished by L-NA (100 microM). 6. Atropine (1 microM) abolished the ascending excitatory reflex in both muscles. 7. Injection of neurobiotin into the LM and CM confirmed that simultaneous intracellular recordings were made from different muscle layers. 8. In conclusion, during the peristaltic reflex, the LM and CM layers receive synchronous inhibitory neuromuscular inputs during descending inhibition and synchronous excitatory neuromuscular inputs during ascending excitation. No evidence was found to support reciprocal innervation.

Action Potentials↗
PubMed1975

Specific and nonspecific multiple unit activities during the onset of pentylentetrazol seizures. I. Intact animals.

A quantitative evaluation of specific and nonspecific multiple unit activity (MUA) before and during pentylenetetrazol-induced EEG tonic-clonic discharges (OTCD) was made at four levels of the CNS: cortical, thalamic, mesencephalic, and pontine. In addition, MUA of sciatic nerve was recorded to detect possible spinal cord efferent discharges. At all levels, sustained increase in specific and nonspecific multiple unit activity preceded EEG and sciatic nerve discharges induced by pentylenetetrazol. Increments in nonspecific MUA occurred sooner and were larger than those of specific MUA, and increments in mesencephalic nonspecific MUA occurred sooner and were larger than those of other cortical, thalamic, and pontine nonspecific MUAs. This sequence of neuronal activation suggests that pentylenetetrazol seizures are initiated in nonspecific structures at the mesencephalic level.

Animals↗
PubMed1975

Effects of hippocampal afterdischarges on Purkinje cell activity.

Hippocampal afterdischarges can induce increased Purkinje cell activity that characteristically shows a pronounced acceleration during the period of the afterdischarges. Increased Purkinje cell activity may continue for many seconds after termination of the hippocampal activity. Typical frequency histograms are presented. A short period of hippocampal afterdischarges (under 25 sec) may occur with few if any alterations in cerebral activity and vice versa. However, such afterdischarges can produce changes in cerebellar activity as shown by enhanced Purkinje cell activity. These data support the view that the nucleus tegmenti pontis may be prominently involved in relaying hippocampal afterdischarges to the cerebellum whereas much of the neocortical seizure activity is relayed trough the pons, inferior olive, and lateral reticular nucleus, rather than through nucleus tegmenti pontis. EEG tracings taken from these areas illustrate the findings.

Action Potentials↗
PubMed1976

Specific and nonspecific multiple unit activities during the onset of pentylenetetrazol seizures. II. Acute lesions interrupting nonspecific system connections.

Nonspecific cortical, thalamic, mesencephalic, and pontine multiple unit activities (MUA) and changes in EEG and MUS of the sciatic nerve after threshold pentylenetetrazol activation were studied in three groups of animals in which neuronal connections were interrupted at three different levels of the central nervous system: spinal, mesencephalic, and prethalamic. Maximal increments of nonspecific MUA and maximal increments and maximal decrements of sciatic MUA after pentylenetetrazol from each group of lesioned animals were statistically compared with tose observed in intact animals. 1. Pentylenetetrazol threshold for producing cortical tonic-clonic EEG discharges was increased in animals with nesencephaic and prethalamic lesions but was not modified in animals with spinal transection. 2. Cortical MUA maximal increment was significantly decreased in mesencephalic and prethalamic lesioned animals, whereas thalamic MUA maximal increment was significantly decreased in mesencephalic and significantly increased in prethalamic lesioned animals. Pontine MUA maximal increment was significantly increased in spinal, mesencephalic, and prethalamic lesioned animals, and mesencephalic M-A maximal increment was not significantly modified in either prethalamic lesioned or in spinal transected animals. 3. Sciatic MUA maximal increment and maximal decrement were significatly decreased in spinal transected animals, whereas only maximal increment was significantly decreased in mesencephalic and only maximal decrement was significantly decreased in prethalamic lesioned animals. These results based on lesion experiments permit us to infer than under normal cinditions the development of generalized seizures induced by threshold pentylenetetrazol injection is highly dependent upon the neuronal interactions between nonspecific structures at different levels of the central nervous system. The possible nature of these neuronal interactions in the intact animals is discussed.

Animals↗
PubMed1990

Effects of vagal stimulation on experimentally induced seizures in rats.

Repetitive stimulation of the vagus nerve inhibits chemically induced seizures in dogs. We report here the results and conclusions from studies designed to answer some of the immediate questions raised by this finding. (1) Maximal stimulation of vagal C fibers at frequencies greater than 4 Hz prevents or reduces chemically and electrically induced seizures in young male rats. (2) Antiepileptic potency is directly related to the fraction of vagal C fibers stimulated. (3) Vagal stimulation shortens but does not shut down a chemical seizure once it has begun. (4) In rats, optimal stimulus frequency is approximately 10-20 Hz; duration of stimulus, 0.5-1 ms; and stimulus strength, 0.2-0.5 mA/mm2 of nerve cross-section. These results, when taken together with similar results obtained from dogs, monkeys, and humans, strongly suggest that periodic stimulation of the vagus nerve using appropriate stimulation parameters is a powerful method for preventing seizures. The data from the literature suggest that the antiepileptic actions of vagal stimulation are largely mediated by widespread release of GABA and glycine in the brainstem and cerebral cortex. The probable pathway is via projections from the nucleus of the solitary tract to the reticular formation and thence by diffuse projections to the cortex and other areas. Intermittent vagal stimulation has the potentiality of reducing the number and/or the intensity of seizures in patients with intractable epilepsy. These results indicate that feasibility studies in humans should be continued and expanded.

3-Mercaptopropionic Acid↗
PubMedDate not supplied

Comparison of 5 alpha-pregnan-3 alpha-ol-20-one and phenobarbital on cortical synaptic activation and inhibition studied in vitro.

The effects of 5 alpha-pregnan-3 alpha-ol-20-one (3 alpha-OH-DHP) and phenobarbital (PB) on synaptic excitation and inhibition in rat hippocampal slices in vitro were compared. Stimulations were made orthodromically and antidromically while we recorded extracellularly from the dendritic and the somatic layer of the CA1 region. Perfusion with 5 micrograms/ml of 3 alpha-OH-DHP for 30 min significantly increased the recurrent inhibition evoked by antidromic stimulation. The effect was most pronounced at short interstimulus intervals. The duration of the recurrent inhibition also was prolonged. There was no effect on the conditioned population spike after orthodromic paired-pulse stimulation. Furthermore, no effect was observed on the amplitude of the orthodromic fiber volley, the rate of increase in the field excitatory postsynaptic potential (EPSP) and the latency and amplitude of the CA1 population spike. Qualitative and quantitative similar findings were observed during perfusion with PB 0.1 mg/ml, (i.e., a concentration 20 times higher than that of 3 alpha-OH-DHP). Higher concentrations of PB also affected synaptic excitation. The findings suggest a similar effect of 3 alpha-OH-DHP and PB on recurrent GABA-ergic inhibition; however, 3 alpha-OH-DHP appears to be much more potent.

Animals↗
PubMed1996

Properties of a delayed rectifier potassium current in dentate granule cells isolated from the hippocampus of patients with chronic temporal lobe epilepsy.

PURPOSE: Properties of potassium outward currents were investigated in human hippocampal dentate gyrus granule cells from 11 hippocampal specimens obtained from patients with temporal lobe epilepsy (TLE) during resective surgery. METHODS: Dentate granule cells were isolated enzymatically and outward currents analyzed by using the whole-cell configuration of the patch-clamp method. Hippocampal specimens were classified neuropathologically with respect to severe segmental cell loss, gliosis, and axonal sprouting (Ammon's horn sclerosis, AHS), or the presence of a focal lesion in the adjacent temporal lobe. RESULTS: A delayed rectifier outward current (IK), but not an A-type potassium current (IA) or inwardly rectifying potassium currents, was observed in all cells. The average current density of IK, the time-dependent decay of IK, and the resting membrane characteristics were not significantly different between patients with and without AHS. The voltage of half-maximal activation V1/2(act) was 5.4 +/- 1.8 mV in AHS compared with -2.9 +/- 1.8 mV in lesion-associated epilepsy (NS). In contrast, V1/2(inact) was shifted in a hyperpolarizing direction in AHS (-67.7 +/- 0.6 mV) compared with that in hippocampi not showing AHS (-47.7 +/- 2.6 mV; p = 0.0017). CONCLUSIONS: The altered steady-state voltage-dependence of IK may result in abnormal excitability of dentate granule cells in AHS and exert a marked influence on input-output properties of the dentate gyrus.

Adult↗
PubMed1997

Basic mechanisms of epilepsy: targets for therapeutic intervention.

Although a wide variety of drugs are available for treatment of epilepsy, many patients with epilepsy still experience uncontrolled seizures. In addition, there is a need for new drugs that can halt epileptogenesis after brain injury. Mechanisms that underlie seizure processes constitute potential target areas for the development of new antiepileptic drugs (AEDs). An understanding of the underlying mechanisms of interictal spike discharge and seizure spread is critical for the development of AEDs for treatment of partial seizures. Suppression of specific forms of voltage-dependent calcium currents and inhibition of GABA(B) receptor-mediated inhibition are two key target areas for new AEDs to treat primary generalized seizures. As researchers gain more understanding of the cellular, molecular, and genetic mechanisms underlying seizure propagation, we should be better able to develop therapeutic agents designed to suppress seizure-provoking mechanisms and to enhance the brain's natural protective mechanisms.

Animals↗
PubMed1997

Identification and preclinical testing of novel antiepileptic compounds.

Procedures for identifying novel antiepileptic drugs (AEDs) are changing and need to change more. Widespread reliance on two primary screens has led to the identification of novel compounds that resemble either phenytoin (suppressing high-frequency repetitive firing in cultured neurons and prolonging inactivation of voltage-dependent sodium channels identified by the maximal electroshock test) or benzodiazepines (potentiating the inhibitory effect of gamma-aminobutyric acid (GABA), identified by the threshold pentylenetetrazol test). Advances in molecular neurobiology have identified specific molecular targets (subunits of ion channels, neurotransmitter receptors, and transporters) and have made them available in a form permitting high-throughput screening. AEDs can be designed to interact with specific sites on the target molecules. Alternatively, the molecular screens can be used to identify active components in natural products, including folk remedies. Preclinical in vivo screens can be improved by using animals with genetic or acquired epilepsies that have similar modifications in the properties of the target molecules as do human epilepsy syndromes. Future work is likely to define molecular targets for AEDs that will block or reverse chronic epileptogenesis.

Adenosine Triphosphatases↗
PubMed1999

Cortical malformations and epilepsy: new insights from animal models.

In the last decade, the recognition of the high frequency of cortical malformations among patients with epilepsy especially children, has led to a renewed interest in the study of the pathophysiology of cortical development. This field has also been spurred by the recent development of several experimental genetic and non-genetic, primarily rodent, models of cortical malformations. Epileptiform activity in these animals can appear as spontaneous seizure activity in vivo, in vitro hyperexcitability, or reduced seizure susceptibility in vitro and in vivo. In the neonatal freeze lesion model, that mimics human microgyria, hyperexcitability is caused by a reorganization of the network in the borders of the malformation. In the prenatal methylazoxymethanol model, that causes a diffuse cortical malformation, hyperexcitability is associated with alteration of firing properties of discrete neuronal subpopulations together with the formation of bridges between normally unconnected structures. In agreement with clinical evidence, these experimental data suggest that cortical malformations can both form epileptogenic foci and alter brain development in a manner that causes a diffuse hyperexcitability of the cortical network.

Abnormalities, Drug-Induced↗
PubMed2006

Benign course in multiple sclerosis: a review.

Since the 1950s, it has been recognized that a subgroup of multiple sclerosis (MS) patients exists that shows little or no progression in the severity of the disease over time. This group is referred to as 'benign' MS. Although a substantial amount of research in MS indicates a multifactorial background in disease severity, to date it is still difficult to predict whether the course will be benign at onset and it is difficult to find factors that influence the course of the disease over time. Maintaining or restoring neural conduction inside a central nervous system lesion seems to be the essence of staying 'benign'.

Axons↗
PubMed1994

A neural circuitry analysis of maternal behavior in the rat.

This article reviews work that shows that the medial preoptic area of the hypothalamus plays a crucial role in controlling the occurrence of maternal behavior in rats. A primary goal of this report is to fit the medial preoptic area into a larger neural circuitry, examining its critical inputs and outputs. Lesions of the medial preoptic area disrupt maternal behavior and estradiol and prolactin injections into this region activate maternal behavior. The medial amygdala, which is located in the limbic telencephalon, sends a neural projection to the preoptic region. Research indicates that this projection influences maternal behavior by relaying olfactory input to the medial preoptic area. The output of the preoptic area influences maternal behavior through descending projections to the brain stem. One of the influences of such projections might be to regulate neural circuits involved in controlling specific maternal responses, such as retrieval (carrying of pups) behavior.

Algorithms↗