The ability to find one's way depends on neural algorithms that integrate information about place, distance and direction, but the implementation of these operations in cortical microcircuits is poorly understood. Here we show that the dorsocaudal medial entorhinal cortex (dMEC) contains a directionally oriented, topographically organized neural map of the spatial environment. Its key unit is the 'grid cell', which is activated whenever the animal's position coincides with any vertex of a regular grid of equilateral triangles spanning the surface of the environment. Grids of neighbouring cells share a common orientation and spacing, but their vertex locations (their phases) differ. The spacing and size of individual fields increase from dorsal to ventral dMEC. The map is anchored to external landmarks, but persists in their absence, suggesting that grid cells may be part of a generalized, path-integration-based map of the spatial environment.
perience correlate with subsequent choices offers strong evidence for the existence of intrinsic preferences. Although it is not clear how malleable these preferences are, their existence may have health implications for the way in which individuals deal with events that are known to be unpleasant-for example, going to the doctor for painful procedures. The neurobiological mechanisms governing dreading behavior may hold clues for both better pain management and improvements in public health.
Gamma oscillations are thought to transiently link distributed cell assemblies that are processing related information, a function that is probably important for network processes such as perception, attentional selection and memory. This 'binding' mechanism requires that spatially distributed cells fire together with millisecond range precision; however, it is not clear how such coordinated timing is achieved given that the frequency of gamma oscillations varies substantially across space and time, from approximately 25 to almost 150 Hz. Here we show that gamma oscillations in the CA1 area of the hippocampus split into distinct fast and slow frequency components that differentially couple CA1 to inputs from the medial entorhinal cortex, an area that provides information about the animal's current position, and CA3, a hippocampal subfield essential for storage of such information. Fast gamma oscillations in CA1 were synchronized with fast gamma in medial entorhinal cortex, and slow gamma oscillations in CA1 were coherent with slow gamma in CA3. Significant proportions of cells in medial entorhinal cortex and CA3 were phase-locked to fast and slow CA1 gamma waves, respectively. The two types of gamma occurred at different phases of the CA1 theta rhythm and mostly on different theta cycles. These results point to routeing of information as a possible function of gamma frequency variations in the brain and provide a mechanism for temporal segregation of potentially interfering information from different sources.
Conclusions. Our study is part of recent attempts in "neuroeconomics" and the "cognitive neuroscience of social behavior" to understand the social brain and the associated moral emotions (37-44). However, this study sought to identify the neural basis of the altruistic punishment of defectors. The ability to develop social norms that apply to large groups of genetically unrelated individuals and to enforce these norms through altruistic sanctions is one of the distinguishing characteristics of the human species. Altruistic punishment is probably a key element in explaining the unprecedented level of cooperation in human societies (1-3). We hypothesize that altruistic punishment provides relief or satisfaction to the punisher and activates, therefore, reward-related brain regions. Our design generates five contrasts in which this hypothesis can be tested, and the anterior dorsal striatum is activated in all five contrasts, which suggests that the caudate plays a decisive role in altruistic punishment. Caudate activation is particularly interesting because this brain region has been implicated in making decisions or taking actions that are motivated by anticipated rewards (17)(18)(19)(20). The prominent role of the caudate in altruistic punishment is further supported by the fact that those subjects who exhibit stronger caudate activation spend more money on punishing defectors. Moreover, our results also shed light on the reasons behind this correlation. Subjects who exhibit higher caudate activation at the maximal level of punishment if punishment is costless for them also spend more resources on punishment if punishment becomes costly. Thus, high caudate activation seems to be responsible for a high willingness to punish, which suggests that caudate activation reflects the anticipated satisfaction from punishing defectors. Our results therefore support recently developed social preference models (6-8), which assume that people have a preference for punishing norm violations, and illuminate the proximate mechanism behind evolutionary models of altruistic punishment. As the interface between hippocampus and neocortex, the entorhinal cortex is likely to play a pivotal role in memory. To determine how information is represented in this area, we measured spatial modulation of neural activity in layers of medial entorhinal cortex projecting to the hippocampus. Close to the postrhinal-entorhinal border, entorhinal neurons had stable and discrete multipeaked place fields, predicting the rat's location as accurately as place cells in the hippocampus. Precise positional modulation was not observed more ventromedially in the entorhinal cortex or upstream in the postrhinal cortex, suggesting that sensory input is transformed into durable allocentric spatial representations internally in the dorsocaudal medial entorhinal cortex.An extensive body of evidence suggests that the hippocampus is essential for fast encoding and storage of new episodic memories but has a more limited role in remote memory, which is thought to be st...
A fundamental property of many associative memory networks is the ability to decorrelate overlapping input patterns before information is stored. In the hippocampus, this neuronal pattern separation is expressed as the tendency of ensembles of place cells to undergo extensive 'remapping' in response to changes in the sensory or motivational inputs to the hippocampus. Remapping is expressed under some conditions as a change of firing rates in the presence of a stable place code ('rate remapping'), and under other conditions as a complete reorganization of the hippocampal place code in which both place and rate of firing take statistically independent values ('global remapping'). Here we show that the nature of hippocampal remapping can be predicted by ensemble dynamics in place-selective grid cells in the medial entorhinal cortex, one synapse upstream of the hippocampus. Whereas rate remapping is associated with stable grid fields, global remapping is always accompanied by a coordinate shift in the firing vertices of the grid cells. Grid fields of co-localized medial entorhinal cortex cells move and rotate in concert during this realignment. In contrast to the multiple environment-specific representations coded by place cells in the hippocampus, local ensembles of grid cells thus maintain a constant spatial phase structure, allowing position to be represented and updated by the same translation mechanism in all environments encountered by the animal.
Theta-phase precession in hippocampal place cells is one of the best-studied experimental models of temporal coding in the brain. Theta-phase precession is a change in spike timing in which the place cell fires at progressively earlier phases of the extracellular theta rhythm as the animal crosses the spatially restricted firing field of the neuron. Within individual theta cycles, this phase advance results in a compressed replication of the firing sequence of consecutively activated place cells along the animal's trajectory, at a timescale short enough to enable spike-time-dependent plasticity between neurons in different parts of the sequence. The neuronal circuitry required for phase precession has not yet been established. The fact that phase precession can be seen in hippocampal output stuctures such as the prefrontal cortex suggests either that efferent structures inherit the precession from the hippocampus or that it is generated locally in those structures. Here we show that phase precession is expressed independently of the hippocampus in spatially modulated grid cells in layer II of medial entorhinal cortex, one synapse upstream of the hippocampus. Phase precession is apparent in nearly all principal cells in layer II but only sparsely in layer III. The precession in layer II is not blocked by inactivation of the hippocampus, suggesting that the phase advance is generated in the grid cell network. The results point to possible mechanisms for grid formation and raise the possibility that hippocampal phase precession is inherited from entorhinal cortex.
To determine whether entorhinal spatial representations are continuous or fragmented, we recorded neural activity in grid cells while rats ran through a stack of interconnected, zig-zagged compartments of equal shape and orientation (a hairpin maze). The distribution of spatial firing fields was markedly similar across all compartments in which running occurred in the same direction, implying that the grid representation was fragmented into repeating submaps. Activity at neighboring positions was least correlated at the transitions between different arms, indicating that the map split regularly at the turning points. We saw similar discontinuities among place cells in the hippocampus. No fragmentation was observed when the rats followed similar trajectories in the absence of internal walls, implying that stereotypic behavior alone cannot explain the compartmentalization. These results indicate that spatial environments are represented in entorhinal cortex and hippocampus as a mosaic of discrete submaps that correspond to the geometric structure of the space.
To determine how hippocampal backprojections influence spatially periodic firing in grid cells, we recorded neural activity in the medial entorhinal cortex (MEC) of rats after temporary inactivation of the hippocampus. We report two major changes in entorhinal grid cells. First, hippocampal inactivation gradually and selectively extinguished the grid pattern. Second, the same grid cells that lost their grid fields acquired substantial tuning to the direction of the rat's head. This transition in firing properties was contingent on a drop in the average firing rate of the grid cells and could be replicated by the removal of an external excitatory drive in an attractor network model in which grid structure emerges by velocity-dependent translation of activity across a network with inhibitory connections. These results point to excitatory drive from the hippocampus, and possibly other regions, as one prerequisite for the formation and translocation of grid patterns in the MEC.
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