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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present here a study on the effects of inhibitory recurrent collaterals of Purkinje cell (PC) axons on the activity of the immature rat cerebellar cortex. Simultaneous extracellular recordings of pairs of PCs were performed in rat pups aged 5-8 days postnatal. Bicuculline was applied to the surface of the cortex in order to functionally antagonize PC recurrent collaterals. At this early developmental stage these are the only inhibitory links in the network. Dye marks from the microelectrode tips and 3D serial-section reconstruction of the structure allowed the exact determination of the distance separating recorded cells and of their respective orientation in the cortex. Standard statistical tests and an informational entropy index were used to calculate levels of cooperativity. By comparing PC activity under control conditions and after bicuculline superfusion it is shown that recurrent collateral inhibition has a structurating effect on the PC activity and that it increases the informational content of the network. Inhibition decreases the activity of the cells by 35% and drastically changes the interspike interval histograms. This leads to a more constrained state of the system. Three types of coupling via recurrent collaterals are present: symmetrical, asymmetrical or non existent. The exact type of coupling follows a simple vicinity rule and strongly influences the cooperativity level between the recorded cells. This cooperativity was also found to be spatially compartmentalized. Several pairs were driven by common inputs via climbing fibers or parallel fibers. Using the predictive value of a theoretical model of this immature structure we propose a complementary explanation of the role of the recurrent collaterals at this stage of development: that of a spatial and temporal filter, specific to each different microzone.
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PMID:Effects of recurrent collateral inhibition on Purkinje cell activity in the immature rat cerebellar cortex--an in vivo electrophysiological study. 828 34

Overexcitation of neuronal networks in some forebrain structures and pathological synchronization of neuronal activity play crucial role in epileptic seizures. Seizure activity can be elicited experimentally by different convulsants. Because of various distribution of excitatory and inhibitory connections in the neocortex there might be laminar differences in seizure sensitivity. Current source density (CSD) analysis or immunocytochemical c-Fos localization offer suitable tools to localize increased activation of neurons during seizure. In the present experiments, interictal epileptiform activity elicited by 4-aminopiridine, bicuculline or Mg(2+)-free solution was recorded with a 16-channel multielectrode assembly in different layers of the somatosensory cortex, and CSDs were calculated. Parallel c-Fos immunocytochemistry was applied. Each convulsant elicited characteristic activation pattern. 4-aminopiridine induced relatively short discharges, which were associated with a huge sink in layer V, the sink and source pattern was relatively simple. Mg(2+)-free solution elicited the longest discharges, sinks appeared typically in the supragranular layers II and III than quickly distributed toward layers V and VI. Bicuculline induced rather similar seizure pattern as Mg(2+)-free solution, but the amplitudes of field potentials were larger, while the durations shorter. The peak of c-Fos activation, however, was not parallel with the largest electrical activation. Larger amount of stained cells appeared in layers II and III in 4-aminopiridine and bicuculline, respectively. In Mg(2+)-free solution the highest c-Fos activity was detected in upper layer VI. Long-lasting cellular effects do not always correspond to the largest electrical responses, which are primarily determined by the activation of asymmetrical pyramidal neurons. Interneurons, which possess more symmetric process arborisation, play less important role in the generation of field potentials, although they may be intensively activated during seizure.
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PMID:Laminar analysis of initiation and spread of epileptiform discharges in three in vitro models. 1653 65

Spike timing dependent plasticity (STDP) has been demonstrated in various neural systems of many animals. It has been shown that STDP depends on the target and the location of the synapse and is dynamically regulated by the activity of adjacent synapses, the presence of postsynaptic calcium, presynaptic GABA inhibition or the action of neuromodulators. Recent experimental evidence has reported that the profile of STDP in the CA1 pyramidal neuron can be classified into two types depending on its dendritic location: (1) A symmetric STDP profile in the proximal to the soma dendrites, and (2) an asymmetric one in the distal dendrites. Bicuculline application revealed that GABA(A) is responsible for the symmetry of the STDP curve. We investigate via computer simulations how GABA(A) shapes the STDP profile in the CA1 pyramidal neuron dendrites when it is driven by excitatory spike pairs (doublets). The model constructed uses calcium as the postsynaptic signaling agent for STDP and is shown to be consistent with classical long-term potentiation (LTP) and long-term depression (LTD) induced by several doublet stimulation paradigms in the absence of inhibition. Overall, simulation results provide computational evidence for the first time that the switch between the symmetrical and the asymmetrical STDP operational modes is indeed due to GABA inhibition. Furthermore, gamma frequency inhibition and not theta one is responsible for the transition from asymmetry-to-symmetry. The resulted symmetrical STDP profile is centered at +10 ms with two distinct LTD tails at -10 and +40 ms. Finally, the asymmetry-to-symmetry transition is strongly dependent on the strength (conductance) of inhibition and its relative onset with respect to pre- and postsynaptic spike stimulation.
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PMID:GABA inhibition modulates NMDA-R mediated spike timing dependent plasticity (STDP) in a biophysical model. 2083 91