Journal articles: 'Cortex entorhinal'

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Witter, Menno. "Entorhinal cortex." Scholarpedia 6, no. 10 (2011): 4380. http://dx.doi.org/10.4249/scholarpedia.4380.

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Caruana, Douglas A., and C. Andrew Chapman. "Stimulation of the Parasubiculum Modulates Entorhinal Cortex Responses to Piriform Cortex Inputs In Vivo." Journal of Neurophysiology 92, no. 2 (August 2004): 1226–35. http://dx.doi.org/10.1152/jn.00038.2004.

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Although a major output of the hippocampal formation is from the subiculum to the deep layers of the entorhinal cortex, the parasubiculum projects to the superficial layers of the entorhinal cortex and may therefore modulate how the entorhinal cortex responds to sensory inputs from other cortical regions. Recordings at multiple depths in the entorhinal cortex were first used to characterize field potentials evoked by stimulation of the parasubiculum in urethan-anesthetized rats. Current source density analysis showed that a prominent surface-negative field potential component is generated by synaptic activation in layer II. The surface-negative field potential was also observed in rats with chronically implanted electrodes. The response was maintained during short stimulation trains of ≤125 Hz, suggesting that it is generated by activation of monosynaptic inputs to the entorhinal cortex. The piriform cortex also projects to layer II of the entorhinal cortex, and interactions between parasubicular and piriform cortex inputs were investigated using double-site stimulation tests. Simultaneous activation of parasubicular and piriform cortex inputs with high-intensity pulses resulted in smaller synaptic potentials than were expected on the basis of summing the individual responses, consistent with the termination of both pathways onto a common population of neurons. Paired-pulse tests were then used to assess the effect of parasubicular stimulation on responses to piriform cortex stimulation. Responses of the entorhinal cortex to piriform cortex inputs were inhibited when the parasubiculum was stimulated 5 ms earlier and were enhanced when the parasubiculum was stimulated 20–150 ms earlier. These results indicate that excitatory inputs to the entorhinal cortex from the parasubiculum may enhance the propagation of neuronal activation patterns into the hippocampal circuit by increasing the responsiveness of the entorhinal cortex to appropriately timed inputs.

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van der Linden, Solange, Ferruccio Panzica, and Marco de Curtis. "Carbachol Induces Fast Oscillations in the Medial but not in the Lateral Entorhinal Cortex of the Isolated Guinea Pig Brain." Journal of Neurophysiology 82, no. 5 (November 1, 1999): 2441–50. http://dx.doi.org/10.1152/jn.1999.82.5.2441.

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Fast oscillations at 25–80 Hz (gamma activity) have been proposed to play a role in attention-related mechanisms and synaptic plasticity in cortical structures. Recently, it has been demonstrated that the preservation of the entorhinal cortex is necessary to maintain gamma oscillations in the hippocampus. Because gamma activity can be reproduced in vitro by cholinergic activation, this study examined the characteristics of gamma oscillations induced by arterial perfusion or local intracortical injections of carbachol in the entorhinal cortex of the in vitro isolated guinea pig brain preparation. Shortly after carbachol administration, fast oscillatory activity at 25.2–28.2 Hz was observed in the medial but not in the lateral entorhinal cortex. Such activity was transiently associated with oscillations in the theta range that showed a variable pattern of distribution in the entorhinal cortex. No oscillatory activity was observed when carbachol was injected in the lateral entorhinal cortex. Gamma activity in the medial entorhinal cortex showed a phase reversal at 200–400 μm, had maximal amplitude at 400–500 μm depth, and was abolished by arterial perfusion of atropine (5 μM). Local carbachol application in the medial entorhinal cortex induced gamma oscillations in the hippocampus, whereas no oscillations were observed in the amygdala and in the piriform, periamygdaloid, and perirhinal cortices ipsilateral and contralateral to the carbachol injection. Hippocampal oscillations had higher frequency than the gamma activity recorded in the entorhinal cortex, suggesting the presence of independent generators in the two structures. The selective ability of the medial but not the lateral entorhinal cortex to generate gamma activity in response to cholinergic activation suggests a differential mode of signal processing in entorhinal cortex subregions.

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Biella, Gerardo, Paolo Spaiardi, Mauro Toselli, Marco de Curtis, and Vadym Gnatkovsky. "Functional Interactions Within the Parahippocampal Region Revealed by Voltage-Sensitive Dye Imaging in the Isolated Guinea Pig Brain." Journal of Neurophysiology 103, no. 2 (February 2010): 725–32. http://dx.doi.org/10.1152/jn.00722.2009.

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The massive transfer of information from the neocortex to the entorhinal cortex (and vice versa) is hindered by a powerful inhibitory control generated in the perirhinal cortex. In vivo and in vitro experiments performed in rodents and cats support this conclusion, further extended in the present study to the analysis of the interaction between the entorhinal cortex and other parahippocampal areas, such as the postrhinal and the retrosplenial cortices. The experiments were performed in the in vitro isolated guinea pig brain by a combined approach based on electrophysiological recordings and fast imaging of optical signals generated by voltage-sensitive dyes applied to the entire brain by arterial perfusion. Local stimuli delivered in different portions of the perirhinal, postrhinal, and retrosplenial cortex evoked local responses that did not propagate to the entorhinal cortex. Neither high- and low-frequency-patterned stimulation nor paired associative stimuli facilitated the propagation of activity to the entorhinal region. Similar stimulations performed during cholinergic neuromodulation with carbachol were also ineffective in overcoming the inhibitory network that controls propagation to the entorhinal cortex. The pharmacological inactivation of GABAergic transmission by local application of bicuculline (1 mM) in area 36 of the perirhinal cortex facilitated the longitudinal (rostrocaudal) propagation of activity into the perirhinal/postrhinal cortices but did not cause propagation into the entorhinal cortex. Bicuculline injection in both area 35 and medial entorhinal cortex released the inhibitory control and allowed the propagation of the neural activity to the entorhinal cortex. These results demonstrate that, as for the perirhinal-entorhinal reciprocal interactions, also the connections between the postrhinal/retrosplenial cortices and the entorhinal region are subject to a powerful inhibitory control.

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Kajiwara, Riichi, Ichiro Takashima, Yuka Mimura, Menno P. Witter, and Toshio Iijima. "Amygdala Input Promotes Spread of Excitatory Neural Activity From Perirhinal Cortex to the Entorhinal–Hippocampal Circuit." Journal of Neurophysiology 89, no. 4 (April 1, 2003): 2176–84. http://dx.doi.org/10.1152/jn.01033.2002.

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A number of sensory modalities most likely converge in the rat perirhinal cortex. The perirhinal cortex also interconnects with the amygdala, which plays an important role in various motivational and emotional behaviors. The neural pathway from the perirhinal cortex to the entorhinal cortex is considered one of the main paths into the entorhinal–hippocampal network, which has a crucial role in memory processes. To investigate the potential associative function of the perirhinal cortex with respect to sensory and motivational stimuli and the influence of the association on the perirhinal–entorhinal–hippocampal neurocircuit, we prepared rat brain slices including the perirhinal cortex, entorhinal cortex, hippocampal formation, and amygdala. We used an optical imaging technique with a voltage-sensitive dye to analyze 1) the spatial and functional distribution of inputs from the lateral nucleus of the amygdala to the perirhinal cortex; 2) the spread of neural activity in the perirhinal cortex after layers II/III stimulation, which mimics sensory input to the perirhinal cortex; and 3) the effect of associative inputs to the perirhinal cortex from both the lateral amygdaloid nucleus and layers II/III of the perirhinal cortex on the perirhinal–entorhinal–hippocampal neurocircuit. Following stimulation in the superficial layers of the perirhinal cortex, electrical activity only propagated into the entorhinal cortex when sufficient activation occurred in the deep layers of perirhinal area 35. We observed that single stimulation of either the perirhinal cortex or amygdala did not result in sufficient neural activation of the deep layers of areas 35 to provoke activity propagation into the entorhinal cortex. However, the deep layers of area 35 were depolarized much more strongly when the two stimuli were applied simultaneously, resulting in spreading activation in the entorhinal cortex. Our observations suggest that a functional neural basis for the association of higher-order sensory inputs and emotion-related inputs exists in the perirhinal cortex and that transfer of sensory information to the entorhinal–hippocampal circuitry might be affected by the association of that information with incoming information from the amygdala.

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Coutureau, Etienne, and Georges Di Scala. "Entorhinal cortex and cognition." Progress in Neuro-Psychopharmacology and Biological Psychiatry 33, no. 5 (August 2009): 753–61. http://dx.doi.org/10.1016/j.pnpbp.2009.03.038.

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7

Biella, Gerardo, and Marco de Curtis. "Olfactory Inputs Activate the Medial Entorhinal Cortex Via the Hippocampus." Journal of Neurophysiology 83, no. 4 (April 1, 2000): 1924–31. http://dx.doi.org/10.1152/jn.2000.83.4.1924.

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The lateral and medial regions of the entorhinal cortex differ substantially in terms of connectivity and pattern of activation. With regard to olfactory input, a detailed and extensive physiological map of the olfactory projection to the entorhinal cortex is missing, even if anatomic studies suggest that the olfactory afferents are confined to the lateral and rostral entorhinal region. We studied the contribution of the medial and lateral entorhinal areas to olfactory processing by analyzing the responses induced by lateral olfactory tract stimulation in different entorhinal subfields of the in vitro isolated guinea pig brain. The pattern of synaptic activation of the medial and lateral entorhinal regions was reconstructed either by performing simultaneous multisite recordings or by applying current source density analysis on field potential laminar profiles obtained with 16-channel silicon probes. Current source density analysis demonstrated the existence of a direct monosynaptic olfactory input into the superficial 300 μm of the most rostral part of the lateral entorhinal cortex exclusively, whereas disynaptic sinks mediated by associative fibers arising from the piriform cortex were observed at 100–350 μm depth in the entire lateral aspect of the cortex. No local field responses were recorded in the medial entorhinal region unless a large population spike was generated in the hippocampus (dentate gyrus and CA1 region) by a stimulus 3–5× the intensity necessary to obtain a maximal monosynaptic response in the piriform cortex. In these conditions, a late sink was recorded at a depth of 600-1000 μm in the medial entorhinal area (layers III–V) 10.6 ± 0.9 (SD) msec after a population spike was simultaneously recorded in CA1. Diffuse activation of the medial entorhinal region was also obtained by repetitive low-intensity stimulation of the lateral olfactory tract at 2–8 Hz. Higher or lower stimulation frequencies did not induce hippocampal-medial entorhinal cortex activation. These results suggest that the medial and the lateral entorhinal regions have substantially different roles in processing olfactory sensory inputs.

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8

Bevilaqua, Lia R. M., Janine I. Rossato, Juliana S. Bonini, Jociane C. Myskiw, Julia R. Clarke, Siomara Monteiro, Ramón H. Lima, Jorge H. Medina, Martín Cammarota, and Iván Izquierdo. "The Role of the Entorhinal Cortex in Extinction: Influences of Aging." Neural Plasticity 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/595282.

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The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer's disease. It plays a key role in memory formation, retrieval, and extinction, as part of circuits that include the hippocampus, the amygdaloid nucleus, and several regions of the neocortex, in particular of the prefrontal cortex. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its effect may be in part mediated by the entorhinal cortex.

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9

Jacob, Pierre-Yves, Tiffany Van Cauter, Bruno Poucet, Francesca Sargolini, and Etienne Save. "Medial entorhinal cortex lesions induce degradation of CA1 place cell firing stability when self-motion information is used." Brain and Neuroscience Advances 4 (January 2020): 239821282095300. http://dx.doi.org/10.1177/2398212820953004.

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The entorhinal–hippocampus network plays a central role in navigation and episodic memory formation. To investigate these interactions, we examined the effect of medial entorhinal cortex lesions on hippocampal place cell activity. Since the medial entorhinal cortex is suggested to play a role in the processing of self-motion information, we hypothesised that such processing would be necessary for maintaining stable place fields in the absence of environmental cues. Place cells were recorded as medial entorhinal cortex–lesioned rats explored a circular arena during five 16-min sessions comprising a baseline session with all sensory inputs available followed by four sessions during which environmental (i.e. visual, olfactory, tactile) cues were progressively reduced to the point that animals could rely exclusively on self-motion cues to maintain stable place fields. We found that place field stability and a number of place cell firing properties were affected by medial entorhinal cortex lesions in the baseline session. When rats were forced to rely exclusively on self-motion cues, within-session place field stability was dramatically decreased in medial entorhinal cortex rats relative to SHAM rats. These results support a major role of the medial entorhinal cortex in processing self-motion cues, with this information being conveyed to the hippocampus to help anchor and maintain a stable spatial representation during movement.

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10

Sparks, Daniel W., and C. Andrew Chapman. "Heterosynaptic modulation of evoked synaptic potentials in layer II of the entorhinal cortex by activation of the parasubiculum." Journal of Neurophysiology 116, no. 2 (August 1, 2016): 658–70. http://dx.doi.org/10.1152/jn.00095.2016.

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The superficial layers of the entorhinal cortex receive sensory and associational cortical inputs and provide the hippocampus with the majority of its cortical sensory input. The parasubiculum, which receives input from multiple hippocampal subfields, sends its single major output projection to layer II of the entorhinal cortex, suggesting that it may modulate processing of synaptic inputs to the entorhinal cortex. Indeed, stimulation of the parasubiculum can enhance entorhinal responses to synaptic input from the piriform cortex in vivo. Theta EEG activity contributes to spatial and mnemonic processes in this region, and the current study assessed how stimulation of the parasubiculum with either single pulses or short, five-pulse, theta-frequency trains may modulate synaptic responses in layer II entorhinal stellate neurons evoked by stimulation of layer I afferents in vitro. Parasubicular stimulation pulses or trains suppressed responses to layer I stimulation at intervals of 5 ms, and parasubicular stimulation trains facilitated layer I responses at a train-pulse interval of 25 ms. This suggests that firing of parasubicular neurons during theta activity may heterosynaptically enhance incoming sensory inputs to the entorhinal cortex. Bath application of the hyperpolarization-activated cation current (Ih) blocker ZD7288 enhanced the facilitation effect, suggesting that cholinergic inhibition of Ih may contribute. In addition, repetitive pairing of parasubicular trains and layer I stimulation induced a lasting depression of entorhinal responses to layer I stimulation. These findings provide evidence that theta activity in the parasubiculum may promote heterosynaptic modulation effects that may alter sensory processing in the entorhinal cortex.

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Canto, Cathrin B., Floris G. Wouterlood, and Menno P. Witter. "What Does the Anatomical Organization of the Entorhinal Cortex Tell Us?" Neural Plasticity 2008 (2008): 1–18. http://dx.doi.org/10.1155/2008/381243.

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The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. The finding of the grid cells in all layers and reports on interactions between deep and superficial layers indicate that this rather simplistic perception may be at fault. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that layers in entorhinal cortex show different functional characteristics most likely not on the basis of strikingly different inputs or outputs, but much more likely on the basis of differences in intrinsic organization, combined with very specific sets of inputs. Here, we aim to summarize recent anatomical data supporting the notion that the traditional description of the entorhinal cortex as a layered input-output structure for the hippocampal formation does not give the deserved credit to what this structure might be contributing to the overall functions of cortico-hippocampal networks.

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Chapman, C. Andrew, and Ronald J. Racine. "Converging Inputs to the Entorhinal Cortex From the Piriform Cortex and Medial Septum: Facilitation and Current Source Density Analysis." Journal of Neurophysiology 78, no. 5 (November 1, 1997): 2602–15. http://dx.doi.org/10.1152/jn.1997.78.5.2602.

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Chapman, C. Andrew and Ronald J. Racine. Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis. J. Neurophysiol. 78: 2602–2615, 1997. The entorhinal cortex receives sensory inputs from the piriform cortex and modulatory inputs from the medial septum. To examine short-term synaptic facilitation effects in these pathways, current source density (CSD) analysis was used first to localize the entorhinal cortex membrane currents, which generate field potentials evoked by stimulation of these afferents. Field potentials were recorded at 50-μm intervals through the medial entorhinal cortex in urethan-anesthetized rats and the one-dimensional CSD was calculated. Piriform cortex stimulation evoked a surface-negative, deep-positive field potential component in the entorhinal cortex with mean onset and peak latencies of 10.4 and 18.4 ms. The component followed brief 100-Hz stimulation, consistent with a monosynaptic response. CSD analysis linked the component to a current sink, which often began in layer I before peaking in layer II. A later, surface-positive field potential component peaked at latencies near 45 ms and was associated with a current source in layer II. Medial septal stimulation evoked positive and negative field potential components which peaked at latencies near 7 and 16 ms, respectively. A weaker and more prolonged surface-negative, deep-positive component peaked at latencies near 25 ms. The early components were generated by currents in the hippocampal formation, and the late surface-negative component was generated by currents in layers II to IV of the entorhinal cortex. Short-term facilitation effects in conscious animals were examined using electrodes chronically implanted near layer II of the entorhinal cortex. Paired-pulse stimulation of the piriform cortex at interpulse intervals of 30 and 40 ms caused the largest facilitation (248%) of responses evoked by the second pulse. Responses evoked by medial septal stimulation also were facilitated maximally (59%) by a piriform cortex conditioning pulse delivered 30–40 ms earlier. Paired pulse stimulation of the medial septum caused the largest facilitation (149%) at intervals of 70 ms, but piriform cortex evoked responses were facilitated maximally (46%) by a septal conditioning pulse 100–200 ms earlier. Frequency potentiation effects were maximal during 12- to 18-Hz stimulation of either the piriform cortex or medial septum. Occlusion tests suggested that piriform cortex and medial septal efferents activate the same neurons. The CSD analysis results show that evoked field potential methods can be used effectively in chronically prepared animals to examine synaptic responses in the converging inputs from the piriform cortex and medial septum to the entorhinal cortex. The short-term potentiation phenomena observed here suggest that low-frequency activity in these pathways during endogenous oscillatory states may enhance entorhinal cortex responsivity to olfactory inputs.

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Stranahan, Alexis M., and Mark P. Mattson. "Selective Vulnerability of Neurons in Layer II of the Entorhinal Cortex during Aging and Alzheimer's Disease." Neural Plasticity 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/108190.

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All neurons are not created equal. Certain cell populations in specific brain regions are more susceptible to age-related changes that initiate regional and system-level dysfunction. In this respect, neurons in layer II of the entorhinal cortex are selectively vulnerable in aging and Alzheimer's disease (AD). This paper will cover several hypotheses that attempt to account for age-related alterations among this cell population. We consider whether specific developmental, anatomical, or biochemical features of neurons in layer II of the entorhinal cortex contribute to their particular sensitivity to aging and AD. The entorhinal cortex is a functionally heterogeneous environment, and we will also review data suggesting that, within the entorhinal cortex, there is subregional specificity for molecular alterations that may initiate cognitive decline. Taken together, the existing data point to a regional cascade in which entorhinal cortical alterations directly contribute to downstream changes in its primary afferent region, the hippocampus.

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Takehara-Nishiuchi, Kaori. "Entorhinal cortex and consolidated memory." Neuroscience Research 84 (July 2014): 27–33. http://dx.doi.org/10.1016/j.neures.2014.02.012.

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Beckmann, Helmut, and Helmut Heinsen. "Morphometry of the entorhinal cortex." Biological Psychiatry 25, no. 7 (April 1989): 977–78. http://dx.doi.org/10.1016/0006-3223(89)90281-3.

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Jung, Min Whan, Sung Hwan Yun, and Mi Young Cheong. "Synaptic plasticity in entorhinal cortex." International Congress Series 1250 (October 2003): 147–59. http://dx.doi.org/10.1016/s0531-5131(03)01009-4.

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Soininen, Hikka, and Mikko Laakso. "Entorhinal cortex atrophy and apoe." Neurobiology of Aging 21 (May 2000): 2–3. http://dx.doi.org/10.1016/s0197-4580(00)82684-6.

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HASSELMO, MICHAEL E., ERIK FRANSEN, CLAYTON DICKSON, and ANGEL A. ALONSO. "Computational Modeling of Entorhinal Cortex." Annals of the New York Academy of Sciences 911, no. 1 (January 25, 2006): 418–46. http://dx.doi.org/10.1111/j.1749-6632.2000.tb06741.x.

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Si, Bailu, Emilio Kropff, and Alessandro Treves. "Grid alignment in entorhinal cortex." Biological Cybernetics 106, no. 8-9 (August 15, 2012): 483–506. http://dx.doi.org/10.1007/s00422-012-0513-7.

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20

Ulfig, Norbert. "Ontogeny of the entorhinal cortex." Hippocampus 3, S1 (October 1993): 27–32. http://dx.doi.org/10.1002/hipo.1993.4500030706.

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Scharfman, H. E., J. H. Goodman, F. Du, and R. Schwarcz. "Chronic Changes in Synaptic Responses of Entorhinal and Hippocampal Neurons After Amino-Oxyacetic Acid (AOAA)–Induced Entorhinal Cortical Neuron Loss." Journal of Neurophysiology 80, no. 6 (December 1, 1998): 3031–46. http://dx.doi.org/10.1152/jn.1998.80.6.3031.

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Scharfman, H. E., J. H. Goodman, F. Du, and R. Schwarcz. Chronic changes in synaptic responses of entorhinal and hippocampal neurons after amino-oxyacetic acid (AOAA)–induced entorhinal neuron loss. J. Neurophysiol. 80: 3031–3046, 1998. Synaptic responses of entorhinal cortical and hippocampal neurons were examined in vivo and in vitro, 1 mo to 1.5 yr after a unilateral entorhinal lesion caused by a focal injection of amino-oxyacetic acid (AOAA). It has been shown previously that injection of AOAA into the medial entorhinal cortex produces cell loss in layer III preferentially. Although behavioral seizures stopped ∼2 h after AOAA treatment, abnormal evoked responses were recorded as long as 1.5 yr later in the entorhinal cortex and hippocampus. In the majority of slices from AOAA-treated rats, responses recorded in the superficial layers of the medial entorhinal cortex to white matter, presubiculum, or parasubiculum stimulation were abnormal. Extracellularly recorded responses to white matter stimulation were prolonged and repetitive in the superficial layers. Intracellular recordings showed that residual principal cells in superficial layers produced prolonged, repetitive excitatory postsynaptic potentials (EPSPs) and discharges in response to white matter stimulation compared with brief EPSPs and a single discharge in controls. Responses of deep layer neurons of AOAA-treated rats did not differ from controls in their initial synaptic response. However, in a some of these neurons, additional periods of excitatory activity occurred after a delay. Abnormal responses were recorded from slices ipsilateral as well as contralateral to the lesioned hemisphere. Recordings from the entorhinal cortex in vivo were abnormal also, as demonstrated by prolonged and repetitive responses to stimulation of the area CA1/subiculum border. Evoked responses of hippocampal neurons, recorded in vitro or in vivo, demonstrated abnormalities in selected pathways, such as responses of CA3 neurons to hilar stimulation in vitro. There was a deficit in the duration of potentiation of CA1 population spikes in response to repetitive CA3 stimulation in AOAA-treated rats. Theta activity was reduced in amplitude in area CA1 and the dentate gyrus of AOAA-treated rats, although evoked responses to angular bundle stimulation could not be distinguished from controls. The results demonstrate that a preferential lesion of layer III of the entorhinal cortex produces a long-lasting change in evoked and spontaneous activity in parts of the entorhinal cortex and hippocampus. Given the similarity of the lesion produced by AOAA and entorhinal lesions in temporal lobe epileptics, these data support the hypothesis that preferential damage to the entorhinal cortex contributes to long-lasting changes in excitability, which could be relevant to the etiology of temporal lobe epilepsy.

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Caruana, Douglas A., Robert E. Sorge, Jane Stewart, and C. Andrew Chapman. "Dopamine Has Bidirectional Effects on Synaptic Responses to Cortical Inputs in Layer II of the Lateral Entorhinal Cortex." Journal of Neurophysiology 96, no. 6 (December 2006): 3006–15. http://dx.doi.org/10.1152/jn.00572.2006.

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Dopaminergic modulation of neuronal function has been extensively studied in the prefrontal cortex, but much less is known about its effects on glutamate-mediated synaptic transmission in the entorhinal cortex. The mesocortical dopamine system innervates the superficial layers of the lateral entorhinal cortex and may therefore modulate sensory inputs to this area. In awake rats, systemic administration of the dopamine reuptake inhibitor GBR12909 (10 mg/kg, ip) enhanced extracellular dopamine levels in the entorhinal cortex and significantly facilitated field excitatory postsynaptic potentials (fEPSPs) in layer II evoked by piriform cortex stimulation. An analysis of the receptor subtypes involved in the facilitation of evoked fEPSPs was conducted using horizontal slices of lateral entorhinal cortex in vitro. The effects of 15-min bath application of dopamine on synaptic responses were bidirectional and concentration dependent. Synaptic responses were enhanced by 10 μM dopamine and suppressed by concentrations of 50 and 100 μM. The D1-receptor antagonist SCH23390 (50 μM) blocked the significant facilitation of synaptic responses induced by 10 μM dopamine and the D2-receptor antagonist sulpiride (50 μM) prevented the suppression of fEPSPs observed with higher concentrations of dopamine. We propose here that dopamine release in the lateral entorhinal cortex, acting through D1 receptors, can lead to an enhancement of the salience of sensory representations carried to this region from adjacent sensory cortices.

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Lipton, P. A., and H. Eichenbaum. "Complementary Roles of Hippocampus and Medial Entorhinal Cortex in Episodic Memory." Neural Plasticity 2008 (2008): 1–8. http://dx.doi.org/10.1155/2008/258467.

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Spatial mapping and navigation are figured prominently in the extant literature that describes hippocampal function. The medial entorhinal cortex is likewise attracting increasing interest, insofar as evidence accumulates that this area also contributes to spatial information processing. Here, we discuss recent electrophysiological findings that offer an alternate view of hippocampal and medial entorhinal function. These findings suggest complementary contributions of the hippocampus and medial entorhinal cortex in support of episodic memory, wherein hippocampal networks encode sequences of events that compose temporally and spatially extended episodes, whereas medial entorhinal networks disambiguate overlapping episodes by binding sequential events into distinct memories.

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Scharfman, H. E. "Hyperexcitability of entorhinal cortex and hippocampus after application of aminooxyacetic acid (AOAA) to layer III of the rat medial entorhinal cortex in vitro." Journal of Neurophysiology 76, no. 5 (November 1, 1996): 2986–3001. http://dx.doi.org/10.1152/jn.1996.76.5.2986.

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1. Injection of aminooxyacetic acid (AOAA) into the entorhinal cortex in vivo produces acute seizures and cell loss in medial entorhinal cortex. To understand these effects, AOAA was applied directly to the medial entorhinal cortex in slices containing both the entorhinal cortex and hippocampus. Extracellular and intracellular recordings were made in both the entorhinal cortex and hippocampus to study responses to angular bundle stimulation and spontaneous activity. 2. AOAA was applied focally by leak from a micropipette or by pressure ejection. Evoked potentials increased gradually within 5 min of application, particularly the late, negative components. Evoked potentials continued to increase for up to 1 h, and these changes persisted for the remainder of the experiment (up to 5 h after drug application). 3. Paired pulse facilitation (100-ms interval) was also enhanced after AOAA application. Increasing stimulus frequency to 1-10 Hz increased evoked potentials further, and after several seconds of such stimulation multiple field potentials occurred. When stimulation was stopped at this point, repetitive field potentials occurred spontaneously for 1-2 min. These recordings, and simultaneous extracellular recordings in different layers, indicated that spontaneous synchronous activity occurred in entorhinal neurons. Intracellularly labeled cortical pyramidal cells depolarized and discharged during spontaneous and evoked field potentials. 4. The effects of AOAA were blocked reversibly by bath application of the N-methyl-D-aspartate (NMDA) receptor antagonist D-amino-5-phosphonovalerate (D-APV; 25 microM) or focal application of D-APV to the medial entorhinal cortex. 5. Simultaneous extracellular recordings from the entorhinal cortex and hippocampus demonstrated that spontaneous synchronous activity in layer III was often followed within several milliseconds by negative field potentials in the terminal zones of the perforant path (stratum moleculare of the dentate gyrus and stratum lacunosum-moleculare of area CA1). The extracellular potentials recorded in the dentate gyrus corresponded to excitatory postsynaptic potentials and action potentials in dentate granule cells. However, extracellular potentials in area CA1 were small and rarely correlated with discharge in CA1 pyramidal cells. 6. The results demonstrate that AOAA application leads to an NMDA-receptor-dependent enhancement of evoked potentials in medial entorhinal cortical neurons, which appears to be irreversible. The potentials can be facilitated by repetitive stimulation, and lead to synchronized discharges of entorhinal neurons. The discharges invade other areas such as the hippocampus, indicating how seizure activity may spread after AOAA injection in vivo. These data suggest that AOAA may be a useful tool to study longlasting changes in NMDA receptor function that lead to epileptiform activity and neurodegeneration.

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Hasselmo, Michael E., and Mark P. Brandon. "Linking Cellular Mechanisms to Behavior: Entorhinal Persistent Spiking and Membrane Potential Oscillations May Underlie Path Integration, Grid Cell Firing, and Episodic Memory." Neural Plasticity 2008 (2008): 1–12. http://dx.doi.org/10.1155/2008/658323.

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The entorhinal cortex plays an important role in spatial memory and episodic memory functions. These functions may result from cellular mechanisms for integration of the afferent input to entorhinal cortex. This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration. The interaction of oscillations and persistent firing could contribute to encoding and retrieval of trajectories through space and time as a mechanism relevant to episodic memory.

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Bartesaghi, Renata, Tiziana Gessi, and Michele Migliore. "Input-output relations in the entorhinal-hippocampal-entorhinal loop: Entorhinal cortex and dentate gyrus." Hippocampus 5, no. 5 (1995): 440–51. http://dx.doi.org/10.1002/hipo.450050506.

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Canto, Cathrin B., and Menno P. Witter. "Cellular properties of principal neurons in the rat entorhinal cortex. II. The medial entorhinal cortex." Hippocampus 22, no. 6 (December 7, 2011): 1277–99. http://dx.doi.org/10.1002/hipo.20993.

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Canto, Cathrin B., and Menno P. Witter. "Cellular properties of principal neurons in the rat entorhinal cortex. I. The lateral entorhinal cortex." Hippocampus 22, no. 6 (December 7, 2011): 1256–76. http://dx.doi.org/10.1002/hipo.20997.

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Kinnavane, Lisa, Eman Amin, Cristian M. Olarte-Sánchez, and John P. Aggleton. "Medial temporal pathways for contextual learning: Network c-fos mapping in rats with or without perirhinal cortex lesions." Brain and Neuroscience Advances 1 (January 1, 2017): 239821281769416. http://dx.doi.org/10.1177/2398212817694167.

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Background: In the rat brain, context information is thought to engage network interactions between the postrhinal cortex, medial entorhinal cortex, and the hippocampus. In contrast, object information is thought to be more reliant on perirhinal cortex and lateral entorhinal cortex interactions with the hippocampus. Method: The ‘context network’ was explored by mapping expression of the immediate-early gene, c- fos, after exposure to a new spatial environment. Results: Structural equation modelling of Fos counts produced networks of good fit that closely matched prior predictions based on anatomically grounded functional models. These same models did not, however, fit the Fos data from home-cage controls nor did they fit the corresponding data from a previous study exploring object recognition. These additional analyses highlight the specificity of the context network. The home-cage controls, meanwhile, showed raised levels of inter-area Fos correlations between the many sites examined, that is, their changes in Fos levels lacked anatomical specificity. A total of two additional groups of rats received perirhinal cortex lesions. While the loss of perirhinal cortex reduced lateral entorhinal c- fos expression, it did not affect mean levels of hippocampal c- fos expression. Similarly, overall c- fos expression in the prelimbic cortex, retrosplenial cortex, and nucleus reuniens of the thalamus appeared unaffected by the perirhinal cortex lesions. Conclusion: The perirhinal cortex lesions disrupted network interactions involving the medial entorhinal cortex and the hippocampus, highlighting ways in which perirhinal cortex might affect specific aspects of context learning.

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Schmidt-Hieber, Christoph, and Michael Häusser. "How to build a grid cell." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1635 (February 5, 2014): 20120520. http://dx.doi.org/10.1098/rstb.2012.0520.

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Neurons in the medial entorhinal cortex fire action potentials at regular spatial intervals, creating a striking grid-like pattern of spike rates spanning the whole environment of a navigating animal. This remarkable spatial code may represent a neural map for path integration. Recent advances using patch-clamp recordings from entorhinal cortex neurons in vitro and in vivo have revealed how the microcircuitry in the medial entorhinal cortex may contribute to grid cell firing patterns, and how grid cells may transform synaptic inputs into spike output during firing field crossings. These new findings provide key insights into the ingredients necessary to build a grid cell.

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Kjelvik, Grete, Hallvard R. Evensmoen, Veronika Brezova, and Asta K. Håberg. "The human brain representation of odor identification." Journal of Neurophysiology 108, no. 2 (July 15, 2012): 645–57. http://dx.doi.org/10.1152/jn.01036.2010.

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Odor identification (OI) tests are increasingly used clinically as biomarkers for Alzheimer's disease and schizophrenia. The aim of this study was to directly compare the neuronal correlates to identified odors vs. nonidentified odors. Seventeen females with normal olfactory function underwent a functional magnetic resonance imaging (fMRI) experiment with postscanning assessment of spontaneous uncued OI. An event-related analysis was performed to compare within-subject activity to spontaneously identified vs. nonidentified odors at the whole brain level, and in anatomic and functional regions of interest (ROIs) in the medial temporal lobe (MTL). Parameter estimate values and blood oxygenated level—dependent (BOLD) signal curves for correctly identified and nonidentified odors were derived from functional ROIs in hippocampus, entorhinal, piriform, and orbitofrontal cortices. Number of activated voxels and max parameter estimate values were obtained from anatomic ROIs in the hippocampus and the entorhinal cortex. At the whole brain level the correct OI gave rise to increased activity in the left entorhinal cortex and secondary olfactory structures, including the orbitofrontal cortex. Increased activation was also observed in fusiform, primary visual, and auditory cortices, inferior frontal plus inferior temporal gyri. The anatomic MTL ROI analysis showed increased activation in the left entorhinal cortex, right hippocampus, and posterior parahippocampal gyri in correct OI. In the entorhinal cortex and hippocampus the BOLD signal increased specifically in response to identified odors and decreased for nonidentified odors. In orbitofrontal and piriform cortices both identified and nonidentified odors gave rise to an increased BOLD signal, but the response to identified odors was significantly greater than that for nonidentified odors. These results support a specific role for entorhinal cortex and hippocampus in OI, whereas piriform and orbitofrontal cortices are active in both smelling and OI. Moreover, episodic as well as semantic memory systems appeared to support OI.

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Bright, Ian M., Miriam L. R. Meister, Nathanael A. Cruzado, Zoran Tiganj, Elizabeth A. Buffalo, and Marc W. Howard. "A temporal record of the past with a spectrum of time constants in the monkey entorhinal cortex." Proceedings of the National Academy of Sciences 117, no. 33 (August 3, 2020): 20274–83. http://dx.doi.org/10.1073/pnas.1917197117.

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Episodic memory is believed to be intimately related to our experience of the passage of time. Indeed, neurons in the hippocampus and other brain regions critical to episodic memory code for the passage of time at a range of timescales. The origin of this temporal signal, however, remains unclear. Here, we examined temporal responses in the entorhinal cortex of macaque monkeys as they viewed complex images. Many neurons in the entorhinal cortex were responsive to image onset, showing large deviations from baseline firing shortly after image onset but relaxing back to baseline at different rates. This range of relaxation rates allowed for the time since image onset to be decoded on the scale of seconds. Further, these neurons carried information about image content, suggesting that neurons in the entorhinal cortex carry information about not only when an event took place but also, the identity of that event. Taken together, these findings suggest that the primate entorhinal cortex uses a spectrum of time constants to construct a temporal record of the past in support of episodic memory.

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BAIANO, M., C. PERLINI, G. RAMBALDELLI, R. CERINI, N. DUSI, M. BELLANI, G. SPEZZAPRIA, A. VERSACE, M. BALESTRIERI, and R. MUCELLI. "Decreased entorhinal cortex volumes in schizophrenia." Schizophrenia Research 102, no. 1-3 (July 2008): 171–80. http://dx.doi.org/10.1016/j.schres.2007.11.035.

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James, Adele, Tim J. von Oertzen, Ray Norbury, Hans-Juergen Huppertz, and Karen R. Brandt. "Left entorhinal cortex and object recognition." NeuroReport 29, no. 5 (March 2018): 363–67. http://dx.doi.org/10.1097/wnr.0000000000000974.

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MEGA, M. S. "The entorhinal cortex in Alzheimer's disease." Journal of Neurology, Neurosurgery & Psychiatry 71, no. 4 (October 1, 2001): 431a—432. http://dx.doi.org/10.1136/jnnp.71.4.431a.

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36

Welberg, Leonie. "Parietal entorhinal cortex cells in navigation." Nature Reviews Neuroscience 13, no. 4 (March 14, 2012): 223. http://dx.doi.org/10.1038/nrn3223.

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Dupret, David, and Jozsef Csicsvari. "The medial entorhinal cortex keeps Up." Nature Neuroscience 15, no. 11 (October 26, 2012): 1471–72. http://dx.doi.org/10.1038/nn.3245.

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Fyhn, M. "Spatial Representation in the Entorhinal Cortex." Science 305, no. 5688 (August 27, 2004): 1258–64. http://dx.doi.org/10.1126/science.1099901.

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Chapman, C. Andrew, Roland S. G. Jones, and Min Jung. "Neuronal Plasticity in the Entorhinal Cortex." Neural Plasticity 2008 (2008): 1–2. http://dx.doi.org/10.1155/2008/314785.

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van Hoesen, Gary W., Bradley T. Hyman, and Antonio R. Damasio. "Entorhinal cortex pathology in Alzheimer's disease." Hippocampus 1, no. 1 (January 1, 1991): 1–8. http://dx.doi.org/10.1002/hipo.450010102.

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Zdanovskis, Nauris, Ardis Platkājis, Andrejs Kostiks, and Guntis Karelis. "Structural Analysis of Brain Hub Region Volume and Cortical Thickness in Patients with Mild Cognitive Impairment and Dementia." Medicina 56, no. 10 (September 24, 2020): 497. http://dx.doi.org/10.3390/medicina56100497.

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Background and Objectives: A complex network of axonal pathways interlinks the human brain cortex. Brain networks are not distributed evenly, and brain regions making more connections with other parts are defined as brain hubs. Our objective was to analyze brain hub region volume and cortical thickness and determine the association with cognitive assessment scores in patients with mild cognitive impairment (MCI) and dementia. Materials and Methods: In this cross-sectional study, we included 11 patients (5 mild cognitive impairment; 6 dementia). All patients underwent neurological examination, and Montreal Cognitive Assessment (MoCA) test scores were recorded. Scans with a 3T MRI scanner were done, and cortical thickness and volumetric data were acquired using Freesurfer 7.1.0 software. Results: By analyzing differences between the MCI and dementia groups, MCI patients had higher hippocampal volumes (p < 0.05) and left entorhinal cortex thickness (p < 0.05). There was a significant positive correlation between MoCA test scores and left hippocampus volume (r = 0.767, p < 0.01), right hippocampus volume (r = 0.785, p < 0.01), right precuneus cortical thickness (r = 0.648, p < 0.05), left entorhinal cortex thickness (r = 0.767, p < 0.01), and right entorhinal cortex thickness (r = 0.612, p < 0.05). Conclusions: In our study, hippocampal volume and entorhinal cortex showed significant differences in the MCI and dementia patient groups. Additionally, we found a statistically significant positive correlation between MoCA scores, hippocampal volume, entorhinal cortex thickness, and right precuneus. Although other brain hub regions did not show statistically significant differences, there should be additional research to evaluate the brain hub region association with MCI and dementia.

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Rutecki, Paul A., Robert G. Grossman, Dawna Armstrong, and Susan Irish-Loewen. "Electrophysiological connections between the hippocampus and entorhinal cortex in patients with complex partial seizures." Journal of Neurosurgery 70, no. 5 (May 1989): 667–75. http://dx.doi.org/10.3171/jns.1989.70.5.0667.

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✓ The electrophysiological properties of the neural pathways between the hippocampus and the entorhinal cortex were studied intraoperatively in 31 patients undergoing anterior temporal lobectomy for medically intractable complex partial seizures. The hippocampus, removed en bloc, was studied histologically and the pathology was correlated with the electrophysiological findings. In 29 of the patients, entorhinal stimulation evoked a characteristic positive-negative potential in the hippocampus. The entorhinal-evoked hippocampal response closely resembled, or was identical to, the spontaneously occurring hippocampal interictal spike discharge. In patients with Ammon's horn sclerosis in whom there was a major loss of neurons in the hippocampal subfields CA1, CA3, and CA4, the evoked responses were of simple morphology and long latency(mean 21.9 msec to the peak of the first potential). In patients with a ganglioglioma in whom the hippocampus was histologically normal, the evoked responses were of greater complexity and shorter latency (mean 11.8 msec). Stimulation at a single entorhinal site evoked similar waveforms at different hippocampal recording sites. Conversely, stimulation at different entorhinal sites evoked similar responses at a single hippocampal recording site. Stimulation of the hippocampus evoked a potential in the entorhinal cortex and, in some instances, in the amygdala, insula, and lateral temporal cortex. These connections may produce a positive feedback loop that favors seizure generation.

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Hasselmo, Michael E. "Neuronal rebound spiking, resonance frequency and theta cycle skipping may contribute to grid cell firing in medial entorhinal cortex." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1635 (February 5, 2014): 20120523. http://dx.doi.org/10.1098/rstb.2012.0523.

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Data show a relationship of cellular resonance and network oscillations in the entorhinal cortex to the spatial periodicity of grid cells. This paper presents a model that simulates the resonance and rebound spiking properties of entorhinal neurons to generate spatial periodicity dependent upon phasic input from medial septum. The model shows that a difference in spatial periodicity can result from a difference in neuronal resonance frequency that replicates data from several experiments. The model also demonstrates a functional role for the phenomenon of theta cycle skipping in the medial entorhinal cortex.

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GUANELLA, ALEXIS, DANIEL KIPER, and PAUL VERSCHURE. "A MODEL OF GRID CELLS BASED ON A TWISTED TORUS TOPOLOGY." International Journal of Neural Systems 17, no. 04 (August 2007): 231–40. http://dx.doi.org/10.1142/s0129065707001093.

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The grid cells of the rat medial entorhinal cortex (MEC) show an increased firing frequency when the position of the animal correlates with multiple regions of the environment that are arranged in regular triangular grids. Here, we describe an artificial neural network based on a twisted torus topology, which allows for the generation of regular triangular grids. The association of the activity of pre-defined hippocampal place cells with entorhinal grid cells allows for a highly robust-to-noise calibration mechanism, suggesting a role for the hippocampal back-projections to the entorhinal cortex.

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Yeung, Lok-Kin, Rosanna K. Olsen, Bryan Hong, Valentina Mihajlovic, Maria C. D'Angelo, Arber Kacollja, Jennifer D. Ryan, and Morgan D. Barense. "Object-in-place Memory Predicted by Anterolateral Entorhinal Cortex and Parahippocampal Cortex Volume in Older Adults." Journal of Cognitive Neuroscience 31, no. 5 (May 2019): 711–29. http://dx.doi.org/10.1162/jocn_a_01385.

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The lateral portion of the entorhinal cortex is one of the first brain regions affected by tau pathology, an important biomarker for Alzheimer disease. Improving our understanding of this region's cognitive role may help identify better cognitive tests for early detection of Alzheimer disease. Based on its functional connections, we tested the idea that the human anterolateral entorhinal cortex (alERC) may play a role in integrating spatial information into object representations. We recently demonstrated that the volume of the alERC was related to processing the spatial relationships of the features within an object [Yeung, L. K., Olsen, R. K., Bild-Enkin, H. E. P., D'Angelo, M. C., Kacollja, A., McQuiggan, D. A., et al. Anterolateral entorhinal cortex volume predicted by altered intra-item configural processing. Journal of Neuroscience, 37, 5527–5538, 2017]. In this study, we investigated whether the human alERC might also play a role in processing the spatial relationships between an object and its environment using an eye-tracking task that assessed visual fixations to a critical object within a scene. Guided by rodent work, we measured both object-in-place memory, the association of an object with a given context [Wilson, D. I., Langston, R. F., Schlesiger, M. I., Wagner, M., Watanabe, S., & Ainge, J. A. Lateral entorhinal cortex is critical for novel object-context recognition. Hippocampus, 23, 352–366, 2013], and object-trace memory, the memory for the former location of objects [Tsao, A., Moser, M. B., & Moser, E. I. Traces of experience in the lateral entorhinal cortex. Current Biology, 23, 399–405, 2013]. In a group of older adults with varying stages of brain atrophy and cognitive decline, we found that the volume of the alERC and the volume of the parahippocampal cortex selectively predicted object-in-place memory, but not object-trace memory. These results provide support for the notion that the alERC may integrate spatial information into object representations.

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Kourrich, Saïd, Stephen D. Glasgow, Douglas A. Caruana, and C. Andrew Chapman. "Postsynaptic Signals Mediating Induction of Long-Term Synaptic Depression in the Entorhinal Cortex." Neural Plasticity 2008 (2008): 1–9. http://dx.doi.org/10.1155/2008/840374.

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The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. To induce LTD, pairs of pulses, using a 30-millisecond interval, were delivered at 1 Hz for 15 minutes. Induction of LTD was blocked by the NMDA receptor antagonist APV and by the calcium chelator BAPTA, consistent with a requirement for calcium influx via NMDA receptors. Induction of LTD was blocked when the FK506 was included in the intracellular solution to block the phosphatase calcineurin. Okadaic acid, which blocks activation of protein phosphatases 1 and 2a, also prevented LTD. Activation of protein phosphatases following calcium influx therefore contributes to induction of LTD in layer II of the entorhinal cortex.

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Suzuki, Wendy A., Earl K. Miller, and Robert Desimone. "Object and Place Memory in the Macaque Entorhinal Cortex." Journal of Neurophysiology 78, no. 2 (August 1, 1997): 1062–81. http://dx.doi.org/10.1152/jn.1997.78.2.1062.

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Suzuki, Wendy A., Earl K. Miller, and Robert Desimone. Object and place memory in the macaque entorhinal cortex. J. Neurophysiol. 78: 1062–1081, 1997. Lesions of the entorhinal cortex in humans, monkeys, and rats impair memory for a variety of kinds of information, including memory for objects and places. To begin to understand the contribution of entorhinal cells to different forms of memory, responses of entorhinal cells were recorded as monkeys performed either an object or place memory task. The object memory task was a variation of delayed matching to sample. A sample picture was presented at the start of the trial, followed by a variable sequence of zero to four test pictures, ending with a repetition of the sample (i.e., a match). The place memory task was a variation of delayed matching to place. In this task, a cue stimulus was presented at a variable sequence of one to four “places” on a computer screen, ending with a repetition of one of the previously shown places (i.e., a match). For both tasks, the animals were rewarded for releasing a bar to the match. To solve these tasks, the monkey must 1) discriminate the stimuli, 2) maintain a memory of the appropriate stimuli during the course of the trial, and 3) evaluate whether a test stimulus matches previously presented stimuli. The responses of entorhinal cortex neurons were consistent with a role in all three of these processes in both tasks. We found that 47% and 55% of the visually responsive entorhinal cells responded selectively to the different objects or places presented during the object or place task, respectively. Similar to previous findings in prefrontal but not perirhinal cortex on the object task, some entorhinal cells had sample-specific delay activity that was maintained throughout all of the delay intervals in the sequence. For the place task, some cells had location-specific maintained activity in the delay immediately following a specific cue location. In addition, 59% and 22% of the visually responsive cells recorded during the object and place task, respectively, responded differently to the test stimuli according to whether they were matching or nonmatching to the stimuli held in memory. Responses of some cells were enhanced to matching stimuli, whereas others were suppressed. This suppression or enhancement typically occurred well before the animals' behavioral response, suggesting that this information could be used to perform the task. These results indicate that entorhinal cells receive sensory information about both objects and spatial locations and that their activity carries information about objects and locations held in short-term memory.

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Stanger, Heather L., Rebekah Alford, David E. Jane, and Mark O. Cunningham. "The Role of -Containing Kainate Receptors in Entorhinal Cortex Gamma Frequency Oscillations." Neural Plasticity 2008 (2008): 1–12. http://dx.doi.org/10.1155/2008/401645.

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Using in vitro brain slices of hippocampus and cortex, neuronal oscillations in the frequency range of 30–80 Hz (gamma frequency oscillations) can be induced by a number of pharmacological manipulations. The most routinely used is the bath application of the broad-spectrum glutamate receptor agonist, kainic acid. In the hippocampus, work using transgenic kainate receptor knockout mice have revealed information about the specific subunit composition of the kainate receptor implicated in the generation and maintenance of the gamma frequency oscillation. However, there is a paucity of such detail regarding gamma frequency oscillation in the cortex. Using specific pharmacological agonists and antagonists for the kainate receptor, we have set out to examine the contribution of kainate receptor subtypes to gamma frequency oscillation in the entorhinal cortex. The findings presented demonstrate that in contrast to the hippocampus, kainate receptors containing the subunit are critically important for the generation and maintenance of gamma frequency oscillation in the entorhinal cortex. Future work will concentrate on determining the exact nature of the cellular expression of kainate receptors in the entorhinal cortex.

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Zhang, Sheng-Jia, Jing Ye, Jonathan J. Couey, Menno Witter, Edvard I. Moser, and May-Britt Moser. "Functional connectivity of the entorhinal–hippocampal space circuit." Philosophical Transactions of the Royal Society B: Biological Sciences 369, no. 1635 (February 5, 2014): 20120516. http://dx.doi.org/10.1098/rstb.2012.0516.

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The mammalian space circuit is known to contain several functionally specialized cell types, such as place cells in the hippocampus and grid cells, head-direction cells and border cells in the medial entorhinal cortex (MEC). The interaction between the entorhinal and hippocampal spatial representations is poorly understood, however. We have developed an optogenetic strategy to identify functionally defined cell types in the MEC that project directly to the hippocampus. By expressing channelrhodopsin-2 (ChR2) selectively in the hippocampus-projecting subset of entorhinal projection neurons, we were able to use light-evoked discharge as an instrument to determine whether specific entorhinal cell groups—such as grid cells, border cells and head-direction cells—have direct hippocampal projections. Photoinduced firing was observed at fixed minimal latencies in all functional cell categories, with grid cells as the most abundant hippocampus-projecting spatial cell type. We discuss how photoexcitation experiments can be used to distinguish the subset of hippocampus-projecting entorhinal neurons from neurons that are activated indirectly through the network. The functional breadth of entorhinal input implied by this analysis opens up the potential for rich dynamic interactions between place cells in the hippocampus and different functional cell types in the entorhinal cortex (EC).

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Butler, William N., Kiah Hardcastle, and Lisa M. Giocomo. "Remembered reward locations restructure entorhinal spatial maps." Science 363, no. 6434 (March 28, 2019): 1447–52. http://dx.doi.org/10.1126/science.aav5297.

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Ethologically relevant navigational strategies often incorporate remembered reward locations. Although neurons in the medial entorhinal cortex provide a maplike representation of the external spatial world, whether this map integrates information regarding learned reward locations remains unknown. We compared entorhinal coding in rats during a free-foraging task and a spatial memory task. Entorhinal spatial maps restructured to incorporate a learned reward location, which in turn improved positional decoding near this location. This finding indicates that different navigational strategies drive the emergence of discrete entorhinal maps of space and points to a role for entorhinal codes in a diverse range of navigational behaviors.

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Journal articles on the topic 'Cortex entorhinal'

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