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Medial Entorhinal Cortex (medial + entorhinal_cortex)
Selected AbstractsGlutamine induces epileptiform discharges in superficial layers of the medial entorhinal cortex from pilocarpine-treated chronic epileptic rats in vitroEPILEPSIA, Issue 4 2009Nora Sandow Summary Purpose:, Glutamine (GLN) is a precursor for synthesis of glutamate and ,-aminobutyric acid (GABA) and has been found in the cerebrospinal fluid (CSF) at mean concentrations of 0.6 mM. Experiments on slices are usually performed in artificial CSF (aCSF) kept free of amino acids. Therefore, the role of glutamine, particularly in tissue of epileptic animals, remains elusive. Methods:, Using extracellular recordings we studied effects of GLN on field potentials and stimulus-evoked field responses in the medial entorhinal cortex (MEC) of combined entorhinal cortex hippocampal slices from pilocarpine-treated chronic epileptic rats and age-matched saline-injected control rats. Results:, In presence of GLN (0.5 and 2 mM) recurrent epileptiform discharges (REDs) were observed in slices from epileptic rats (64% and 80%, respectively), but not in slices from control rats. REDs were restricted to the superficial MEC, suppressed by the ,-Amino-3-hydroxy-5-methyl-4-isoxazol-propionate (AMPA)/kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (30 ,M), attenuated by the inhibitor of neuronal glutamine transporters methylamino-isobutyric acid (10 mM), and apparently augmented and prolonged by the GABAA receptor antagonist bicuculline-methiodide (5 ,M). In contrast, amplitudes of stimulus evoked nonsynaptic and synaptic field responses increased in slices from control rats (+23% and +12% of the reference values) and insignificantly less or not in those of epileptic rats (+6.5% and ,0.25%, respectively). Notably, stimulus-evoked slow negative transients confined to slices of epileptic animals were reduced in amplitude (,18%). Discussion:, In combined entorhinal hippocampal slices from chronic epileptic animals, GLN induces glutamatergic REDs via neuronal uptake in superficial layers of the MEC where inhibitory function seemed to be partially preserved. [source] Topographic distribution of direct and hippocampus- mediated entorhinal cortex activity evoked by olfactory tract stimulationEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 7 2004Vadym Gnatkovsky Abstract Olfactory information is central for memory-related functions, such as recognition and spatial orientation. To understand the role of olfaction in learning and memory, the distribution and propagation of olfactory tract-driven activity in the parahippocampal region needs to be characterized. We recently demonstrated that repetitive stimulation of the olfactory tract in the isolated guinea pig brain preparation induces an early direct activation of the rostrolateral entorhinal region followed by a delayed response in the medial entorhinal cortex (EC), preceded by the interposed activation of the hippocampus. In the present study we performed a detailed topographic analysis of both the early and the delayed entorhinal responses induced by patterned stimulation of the lateral olfactory tract in the isolated guinea pig brain. Bi-dimensional maps of EC activity recorded at 128 recording sites with 4 × 4 matrix electrodes (410 µm interlead separation) sequentially placed in eight different positions, showed (i) an early (onset at 16.09 ± 1.2 ms) low amplitude potential mediated by the monosynaptic LOT input, followed by (ii) an associative potential in the rostral EC which originates from the piriform cortex (onset at 33.2 ± 2.3 ms), and (iii) a delayed potential dependent on the previous activation of the hippocampus. The sharp component of the delayed response had an onset latency between 52 and 63 ms and was followed by a slow wave. Laminar profile analysis demonstrated that in the caudomedial EC the delayed response was associated with two distinct current sinks located in deep and in superficial layers, whereas in the rostrolateral EC a small-amplitude sink could be detected in the superficial layers exclusively. The present report demonstrates that the output generated by the hippocampal activation is unevenly distributed across different EC subregions and indicates that exclusively the medial and caudal divisions receive a deep-layer input from the hippocampus. In the rostrolateral EC, specific network interactions may be generated by the convergence of the direct olfactory input and the olfaction-driven hippocampal output. [source] Cholinergic suppression of excitatory synaptic responses in layer II of the medial entorhinal cortexHIPPOCAMPUS, Issue 2 2007Bassam N. Hamam Abstract Theta-frequency (4,12 Hz) electroencephalographic activity is thought to play a role in mechanisms mediating sensory and mnemonic processing in the entorhinal cortex and hippocampus, but the effects of acetylcholine on excitatory synaptic inputs to the entorhinal cortex are not well understood. Field excitatory postsynaptic potentials (fEPSPs) evoked by stimulation of the piriform (olfactory) cortex were recorded in the medial entorhinal cortex during behaviors associated with theta activity (active mobility) and were compared with those recorded during nontheta behaviors (awake immobility and slow wave sleep). Synaptic responses were smaller during behavioral activity than during awake immobility and sleep, and responses recorded during movement were largest during the negative phase of the theta rhythm. Systemic administration of cholinergic agonists reduced the amplitude of fEPSPs, and the muscarinic receptor blocker scopolamine strongly enhanced fEPSPs, suggesting that the theta-related suppression of fEPSPs is mediated in part by cholinergic inputs. The reduction in fEPSPs was investigated using in vitro intracellular recordings of EPSPs in Layer II neurons evoked by stimulation of Layer I afferents. Constant bath application of the muscarinic agonist carbachol depolarized membrane potential and suppressed EPSP amplitude in Layer II neurons. The suppression of EPSPs was not associated with a substantial change in input resistance, and could not be accounted for by a depolarization-induced reduction in driving force on the EPSP. The GABAA receptor-blocker bicuculline (50 ,M) did not prevent the cholinergic suppression of EPSPs, suggesting that the suppression is not dependent on inhibitory mechanisms. Paired-pulse facilitation of field and intracellular EPSPs were enhanced by carbachol, indicating that the suppression is likely due to inhibition of presynaptic glutamate release. These results indicate that, in addition to well known effects on postsynaptic conductances that increase cellular excitability, cholinergic activation in the entorhinal cortex results in a strong reduction in strength of excitatory synaptic inputs from the piriform cortex. © 2006 Wiley-Liss, Inc. [source] From grid cells to place cells: A mathematical modelHIPPOCAMPUS, Issue 12 2006Trygve Solstad Abstract Anatomical connectivity and recent neurophysiological results imply that grid cells in the medial entorhinal cortex are the principal cortical inputs to place cells in the hippocampus. The authors propose a model in which place fields of hippocampal pyramidal cells are formed by linear summation of appropriately weighted inputs from entorhinal grid cells. Single confined place fields could be formed by summing input from a modest number (10,50) of grid cells with relatively similar grid phases, diverse grid orientations, and a biologically plausible range of grid spacings. When the spatial phase variation in the grid-cell input was higher, multiple, and irregularly spaced firing fields were formed. These observations point to a number of possible constraints in the organization of functional connections between grid cells and place cells. © 2006 Wiley-Liss, Inc. [source] Enhancement of temporal and spatial synchronization of entorhinal gamma activity by phase resetHIPPOCAMPUS, Issue 4 2002Clayton T. Dickson Abstract The synchronization of cortical gamma oscillatory activity (25,80 Hz) is thought to coordinate neuronal assemblies in the processing and storage of information. The mechanism by which independently oscillating and distantly located cortical zones become synchronized is presumed to involve activity in corticocortical connections, although evidence supporting this conjecture has only been indirect. In the present study, we show that activation of synaptic inputs within and to the medial entorhinal cortex (mEC) of the in vitro isolated guinea pig brain preparation resets the phase of ongoing gamma activity induced by muscarinic receptor agonism with carbachol (frequency: 24 ± 2 Hz at 32°C). Phase reset was associated with a transient enhancement of the synchronization of gamma activity recorded at distant (>1 mm) mEC sites, across which low coherence (>0.75) was observed before stimulation. This increase in synchronization, as measured by cross-correlation analysis, was restricted to a maximal period of 200 ms after either local mEC or CA1 afferent stimulation. The results provide direct evidence that synaptic activation can enhance the rhythmic synchronization of spatially remote, independently oscillating neuronal assemblies in the mEC through a mechanism of synaptically evoked phase reset. Dynamic functional grouping of oscillatory discharges across long distances in the mEC may underlie coding processes involved in the integration and storage of incoming information and thus may be important for the role of this region in memory processes. Hippocampus 2002;12:447,456. © 2002 Wiley-Liss, Inc. [source] Cholinergic modulation of synaptic physiology in deep layer entorhinal cortex of the ratJOURNAL OF NEUROSCIENCE RESEARCH, Issue 1 2001Mi Young Cheong Abstract We have recently shown that cholinergic effects on synaptic transmission and plasticity in the superficial (II/III) layers of the rat medial entorhinal cortex (EC) are similar, but not identical, to those in the hippocampus (Yun et al. [2000] Neuroscience 97:671,676). Because the superficial and deep layers of the EC preferentially convey afferent and efferent hippocampal projections, respectively, it is of interest to compare cholinergic effects between the two regions. We therefore investigated the physiological effects of cholinergic agents in the layer V of medial EC slices under experimental conditions identical to those in the previous study. Bath application of carbachol (0.5 ,M) induced transient depression of field potential responses in all cases tested (30 of 30; 18.5% ± 2.3%) and rarely induced long-lasting potentiation (only 3 of 30; 20.4% ± 3.2% in successful cases). At 5 ,M, carbachol induced transient depression only (20 of 20, 48.9% ± 2.8%), which was blocked by atropine (10 ,M). Paired-pulse facilitation was enhanced during carbachol-induced depression, suggesting presynaptic action of carbachol. Long-term potentiation (LTP) could be induced in the presence of 10 ,M atropine by theta burst stimulation, but its magnitude was significantly lower (9.1% ± 4.7%, n = 15) compared to LTP in control slices (22.4% ± 3.9%, n = 20). These results, combined with our previous findings, demonstrate remarkably similar cholinergic modulation of synaptic transmission and plasticity across the superficial and deep layers of EC. J. Neurosci. Res. 66:117,121, 2001. © 2001 Wiley-Liss, Inc. [source] | ||||||||||