scholarly journals Heading direction with respect to a reference point modulates place-cell activity

2018 ◽  
Author(s):  
P.E. Jercog ◽  
Y. Ahmadian ◽  
C. Woodruff ◽  
R. Deb-Sen ◽  
L.F. Abbott ◽  
...  
Keyword(s):  
Reference Point ◽  
Dorsal Hippocampus ◽  
Cell Activity ◽  
Pyramidal Cells ◽  
Neural Responses ◽  
Neuronal Responses ◽  
Ca1 Pyramidal Cells ◽  
Electrophysiological Recordings ◽  
Heading Direction ◽  
Freely Moving

AbstractUtilizing electrophysiological recordings from CA1 pyramidal cells in freely moving mice, we find that a majority of neural responses are modulated by the heading-direction of the animal relative to a point within or outside their enclosure that we call a reference point. Our findings identify a novel representation in the neuronal responses in the dorsal hippocampus.

scholarly journals Heading direction with respect to a reference point modulates place-cell activity

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
P. E. Jercog ◽  
Y. Ahmadian ◽  
C. Woodruff ◽  
R. Deb-Sen ◽  
L. F. Abbott ◽  
...  
Keyword(s):  
Reference Point ◽  
Cell Activity ◽  
Place Cell ◽  
Heading Direction

scholarly journals Representation of Objects in Space by Two Classes of Hippocampal Pyramidal Cells

2004 ◽  
Vol 124 (1) ◽  
pp. 9-25 ◽  
Author(s):  
Bruno Rivard ◽  
Yu Li ◽  
Pierre-Pascal Lenck-Santini ◽  
Bruno Poucet ◽  
Robert U. Muller
Keyword(s):  
Cell Activity ◽  
Pyramidal Cells ◽  
Place Cell ◽  
Place Cells ◽  
Rat Hippocampus ◽  
Ca1 Pyramidal Cells ◽  
New Class ◽  
Familiar Environment ◽  
Current Arrangement ◽  
Number Of Cells

Humans can recognize and navigate in a room when its contents have been rearranged. Rats also adapt rapidly to movements of objects in a familiar environment. We therefore set out to investigate the neural machinery that underlies this capacity by further investigating the place cell–based map of the surroundings found in the rat hippocampus. We recorded from single CA1 pyramidal cells as rats foraged for food in a cylindrical arena (the room) containing a tall barrier (the furniture). Our main finding is a new class of cells that signal proximity to the barrier. If the barrier is fixed in position, these cells appear to be ordinary place cells. When, however, the barrier is moved, their activity moves equally and thereby conveys information about the barrier's position relative to the arena. When the barrier is removed, such cells stop firing, further suggesting they represent the barrier. Finally, if the barrier is put into a different arena where place cell activity is changed beyond recognition (“remapping”), these cells continue to discharge at the barrier. We also saw, in addition to barrier cells and place cells, a small number of cells whose activity seemed to require the barrier to be in a specific place in the environment. We conclude that barrier cells represent the location of the barrier in an environment-specific, place cell framework. The combined place + barrier cell activity thus mimics the current arrangement of the environment in an unexpectedly realistic fashion.

scholarly journals Most hippocampal CA1 pyramidal cells in rabbits increase firing during awake sharp-wave ripples and some do so in response to external stimulation and theta

2020 ◽  
Vol 123 (5) ◽  
pp. 1671-1681
Author(s):  
Miriam S. Nokia ◽  
Tomi Waselius ◽  
Joonas Sahramäki ◽  
Markku Penttonen
Keyword(s):  
Eyeblink Conditioning ◽  
Cell Activity ◽  
Pyramidal Cells ◽  
External Stimulation ◽  
Ca1 Pyramidal Cells ◽  
Sharp Wave ◽  
Hippocampal Ca1 ◽  
Trace Eyeblink Conditioning ◽  
Do So

We studied hippocampal sharp-wave ripples and theta and CA1 pyramidal cell activity during trace eyeblink conditioning in rabbits. Conditioning trials suppressed ripples while increasing theta for a period of several seconds. A quarter of the cells increased firing in response to the conditioned stimulus and fired extensively during endogenous theta as well as ripples. The role of endogenous theta epochs in off-line memory consolidation should be studied further.

Intracellular Correlates of Spatial Memory Acquisition in Hippocampal Slices: Long-Term Disinhibition of CA1 Pyramidal Cells

2001 ◽  
Vol 86 (2) ◽  
pp. 881-899 ◽  
Author(s):  
Pavel A. Gusev ◽  
Daniel L. Alkon
Keyword(s):  
Dorsal Hippocampus ◽  
Hippocampal Slices ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Membrane Properties ◽  
Postsynaptic Potentials ◽  
Ca1 Pyramidal Cells ◽  
The Mean ◽  
Reversal Potentials

Despite many advances in our understanding of synaptic models of memory such as long-term potentiation and depression, cellular mechanisms that correlate with and may underlie behavioral learning and memory have not yet been conclusively determined. We used multiple intracellular recordings to study learning-specific modifications of intrinsic membrane and synaptic responses of the CA1 pyramidal cells (PCs) in slices of the rat dorsal hippocampus prepared at different stages of the Morris water maze (WM) task acquisition. Schaffer collateral stimulation evoked complex postsynaptic potentials (PSP) consisting of the excitatory and inhibitory postsynaptic potentials (EPSP and IPSP, respectively). After rats had learned the WM task, our major learning-specific findings included reduction of the mean peak amplitude of the IPSPs, delays in the mean peak latencies of the EPSPs and IPSPs, and correlation of the depolarizing-shifted IPSP reversal potentials and reduced IPSP-evoked membrane conductance. In addition, detailed isochronal analyses revealed that amplitudes of both early and late IPSP phases were reduced in a subset of the CA1 PCs after WM training was completed. These reduced IPSPs were significantly correlated with decreased IPSP conductance and with depolarizing-shifted IPSP reversal potentials. Input-output relations and initial rising slopes of the EPSP phase did not indicate learning-related facilitation as compared with the swim and naı̈ve controls. Another subset of WM-trained CA1 PCs had enhanced amplitudes of action potentials but no learning-specific synaptic changes. There were no WM training-specific modifications of other intrinsic membrane properties. These data suggest that long-term disinhibition in a subset of CA1 PCs may facilitate cell discharges that represent and record the spatial location of a hidden platform in a Morris WM.

scholarly journals CRAC channels regulate astrocyte Ca2+ signaling and gliotransmitter release to modulate hippocampal GABAergic transmission

2019 ◽  
Vol 12 (582) ◽  
pp. eaaw5450 ◽  
Author(s):  
Anna B. Toth ◽  
Kotaro Hori ◽  
Michaela M. Novakovic ◽  
Natalie G. Bernstein ◽  
Laurie Lambot ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Pyramidal Cells ◽  
Protease Activated Receptors ◽  
Ca1 Pyramidal Cells ◽  
Crac Channels ◽  
Electrophysiological Recordings ◽  
Major Route ◽  
Vesicular Exocytosis ◽  
Influx Pathways ◽  
The Brain

Astrocytes are the major glial subtype in the brain and mediate numerous functions ranging from metabolic support to gliotransmitter release through signaling mechanisms controlled by Ca2+. Despite intense interest, the Ca2+ influx pathways in astrocytes remain obscure, hindering mechanistic insights into how Ca2+ signaling is coupled to downstream astrocyte-mediated effector functions. Here, we identified store-operated Ca2+ release–activated Ca2+ (CRAC) channels encoded by Orai1 and STIM1 as a major route of Ca2+ entry for driving sustained and oscillatory Ca2+ signals in astrocytes after stimulation of metabotropic purinergic and protease-activated receptors. Using synaptopHluorin as an optical reporter, we showed that the opening of astrocyte CRAC channels stimulated vesicular exocytosis to mediate the release of gliotransmitters, including ATP. Furthermore, slice electrophysiological recordings showed that activation of astrocytes by protease-activated receptors stimulated interneurons in the CA1 hippocampus to increase inhibitory postsynaptic currents on CA1 pyramidal cells. These results reveal a central role for CRAC channels as regulators of astrocyte Ca2+ signaling, gliotransmitter release, and astrocyte-mediated tonic inhibition of CA1 pyramidal neurons.

scholarly journals Theta-modulation drives the emergence of network-wide connectivity patterns underlying replay in a model of hippocampal place cells

2017 ◽  
Author(s):  
Panagiota Theodoni ◽  
Bernat Rovira ◽  
Yingxue Wang ◽  
Alex Roxin
Keyword(s):  
Cell Activity ◽  
Pyramidal Cells ◽  
Spatial Location ◽  
Medial Septum ◽  
Place Cell ◽  
Place Cells ◽  
Synaptic Connectivity ◽  
Pairwise Correlation ◽  
Ca1 Pyramidal Cells ◽  
Spatial Environment

SummaryPlace cells of the rodent hippocampus fire action potentials when the animal traverses a particular spatial location in a given environment. Therefore, for any given trajectory one will observe a repeatable sequence of place cell activations as the animal explores. Interestingly, when the animal is quiescent or sleeping, one can observe similar sequences of activation, although at a highly compressed rate, known as “replays”. It is hypothesized that this replay underlies the process of memory consolidation whereby memories are “transferred” from hippocampus to cortex. However, it remains unclear how the memory of a particular environment is actually encoded in the place cell activity and what the mechanism for replay is. Here we study how plasticity during spatial exploration shapes the patterns of synaptic connectivity in model networks of place cells. Specifically, we show how plasticity leads to the emergence of patterns of activity which represent the spatial environment learned. These states become spontaneously active when the animal is quiescent, reproducing the phenomenology of replays. Interestingly, replay emerges most rapidly when place cell activity is modulated by an ongoing oscillation. The optimal oscillation frequency can be calculated analytically, is directly related to the plasticity rule, and for experimentally determined values of the plasticity window in rodent slices gives values in the theta range. A major prediction of this model is that the pairwise correlation of place cells which encode for neighboring locations should increase during initial exploration, leading up to the critical transition. We find such an increase in a population of simultaneously recorded CA1 pyramidal cells from a rat exploring a novel track. Furthermore, in a rat in which hippocampal theta is reduced through inactivation of the medial septum we find no such increase. Our model is the first to show how theta-modulation can speed up learning by facilitating the emergence of environment-specific network-wide patterns of synaptic connectivity in hippocampal circuits.

Calcium Accumulation and Neuronal Damage in the Rat Hippocampus following Cerebral Ischemia

1987 ◽  
Vol 7 (1) ◽  
pp. 89-95 ◽  
Author(s):  
J. K. Deshpande ◽  
B. K. Siesjö ◽  
T. Wieloch
Keyword(s):  
Calcium Concentration ◽  
Neuronal Damage ◽  
Dorsal Hippocampus ◽  
Pyramidal Cells ◽  
Calcium Content ◽  
Early Recovery ◽  
Neuronal Necrosis ◽  
Calcium Accumulation ◽  
Ca1 Pyramidal Cells ◽  
Ischemic Period

The present study was undertaken to correlate calcium accumulation with the development of neuronal necrosis following transient ischemia. After 10 min of forebrain ischemia in the rat—a period that leads to reproducible damage of CA1 pyramidal cells—determination of calcium concentration and evaluation of morphological signs of cell body necrosis in the dorsal hippocampus were performed at various recirculation times. Tissue calcium concentration was not different from control at the end of ischemic period and did not change after 3, 6, 12, or 24 h of recirculation. However, after 48 h, calcium content increased significantly, with a further increase being seen after 72 h. At early recovery periods, only scattered necrotic neurons were observed. after 48 h, only 2 of 12 hemispheres showed more than 25 necrotic cells per section. More conspicuous neuronal death was observed after 72 h. The results thus demonstrate that net accumulation of calcium in regio superior of the hippocampus precedes marked necrosis of CA1 pyramidal cells. The results suggest that one primary event in the delayed death of these cells is membrane dysfunction with increased calcium cycling.

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