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Subiculum

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Subiculum

Details
Part ofTemporal lobe
ArteryPosterior cerebral Anterior choroidal
Identifiers
Acronym(s)S
NeuroNames188
NeuroLex IDbirnlex_1305
TA98A14.1.09.326
TA25519
FMA74414

Clinical, pathological, and physiological studies of focal epilepsy of temporal lobe origin have historically emphasized the role of the hippocampus. Certainly, damage to the hippocampus proper is central to temporal lobe epilepsy, with cell loss and gliosis of CA1 and CA3 subfields and dentate hilus representing pathologic hallmarks of the syndrome. However, emerging pathophysiological and imaging evidence strongly implicates a critical role for distal structures, including subiculum and parahippocampal region, in TLE as well. Although cell loss in the subiculum is not a significant feature of epilepsy, proximity of the subiculum to sites of hippocampal damage could endow it with a unique functional role in epileptogenesis. Subiculum, located between the hippocampus proper and parahippocampal region, represents anatomic transition zone between Ammon's horn and the entorhinal cortex. The Subiculum is the major output of the hippocampus and first brain region encountered by neural activity emanating from the hippocampus. With this privileged location, subiculum is exquisitely poised to modulate normal and abnormal neuronal firing as it propagates from the hippocampus to other cortical and subcortical regions. This review summarizes the anatomy and physiology of subiculum and correlates this information with its known and possible roles in epilepsy. The The of evidence suggests that the subiculum is not merely a back door out of the hippocampus, but a dynamic and interactive structure that processes and modifies epileptic discharges and in turn is modified by them. After summary of anatomy and physiology of the subiculum, exciting new findings about the subiculum's role in epilepsy and epileptogenesis are discuss. The hippocampal region consists of hippocampal formation and parahippocampal region. The hippocampal formation comprises dentate gyrus, Ammon's horn, and subiculum. In this review, term hippocampus refers to dentate gyrus and Ammon's horn, whereas subiculum refers to distinct hippocampal subregion distal to CA1 field. The word subiculum means support in Latin. The Subiculum forms the transition zone between the hippocampus and entorhinal cortex. Like the hippocampus, subiculum is a three-layer allocortex, consisting of a molecular layer, pyramidal cell layer, and a polymorphic / fiber layer. The molecular layer is contiguous with stratum lacunosum-moleculare and stratum radiatum of CA1. The cell layers contain large pyramidal neurons, less densely packed than in CA1, as well as variously shape, smaller interneurons that are presumably GABAergic inhibitory cells. The Parahippocampus or parahippocampal region is a transition zone between a three-layer allocortex and six-layer neocortex. The parahippocampal region consists of the presubiculum, parasubiculum, entorhinal cortex, perirhinal cortex, and, more posteriorly, postrhinal cortex or parahippocampal cortex. At the border of the three-layer subiculum and presubiculum, additional Cell layer appear, position more superficially and separated from the underlying continuation of three-layer subicular lamination by a Cell-free zone known as lamina dessicans. As the entorhinal cortex gives way to the postrhinal / parahippocampal cortex, lamina dessicans disappears, and more homogeneously layer cortex appears that resembles a six-layer neocortex, except that it lacks inner granular cell layer.

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Structure

Subiculum occupies a portion of parahippocampal gyrus in the mesial temporal lobe and is a component of the medial temporal memory system. It is made up of several cortical fields and, for this reason, is sometimes referred to as subicular complex. It is the position between the CA1 region of hippocampus proper and entorhinal cortex ventrally. Dorsally, it is bordered by retrosplenial cortex. Subicular complex is broken down into several distinct but related areas by their differing cytoarchitecture, however with slight variations between human, monkey, and rodent studies. These areas include prosubiculum, subiculum proper, presubiculum, postsubiculum, and parasubiculum. Sub: subiculum proper is border proximally by ProS, which separates it from the CA1 region of the hippocampus. Distally, it is bordered by PreS. ProS: area separating subiculum proper from CA1 region of hippocampus proper. PrS: this area borders subiculum proper ventrally and makes up part of the parahippocampal gyrus. PoS: PoS is bordered by presubiculum ventrally and laterally, with border between the two characterized by abrupt change in cyto-and histochemical staining. However, some sources treat this area as a dorsal part of the presubiculum. PaS: this area forms the ventral shoulder of parahippocampal gyrus and continues PrS ventrally. It is border laterally by the entorhinal cortex.

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Introduction

The Hippocampal formation of the mammalian brain is conventionally defined as consisting of the entorhinal cortex, dentate gyrus, Areas CA3 and CA1, and subiculum. 7. Early components of HF have been extensively investigated at anatomical, neurophysiological, biochemical and behavioural levels. By contrast, subiculum is comparatively under-investigate; consensus on its anatomical description and definition, for example, has only recently emerged brodmann, 1909; Lorente de No, 1934; Witter & Groenewegen, 1990; Amaral & Witter, 1995; o'mara et al. 2001. There is general agreement that the subiculum has three principal layers: molecular layer, continuous with strata lacunosum-moleculare and radiatum of adjacent hippocampal area CA1 field; enlarge pyramidal cell layer containing soma of principal neurons; and polymorphic layer. Cell packing in the pyramidal layer of subiculum is looser than that seen in hippocampal area CA1. The principal cell layer of the subiculum is populated with large pyramidal neurons: these are consistent in their shape and size and extend their apical dendrites into the molecular layer and their basal dendrites into deeper portions of the pyramidal cell layer. Among pyramidal cells are many smaller neurons; these are considered interneurons of subiculum Amaral & Witter, 1995. Hippocampal area CA1 sends its primary projection to all regions of the subiculum, which in turn projects to many cortical and subcortical targets figs 2 and and7. 7. Subiculum is therefore the major output structure of hippocampus Witter & Groenewegen, 1990; o'mara et al. 2001. Amaral et al. 1991 suggested that CA1 projection to subiculum is organized in a simple pattern, with all portions of CA1 projecting to subiculum, and all regions of subiculum receiving CA1 projections. Here, following Amaral et al. In 1991, I used the term proximal CA1 to refer to area bordering CA3 and distal CA1 for area bordering subiculum. Subiculum is similarly define, with proximal subiculum bordering CA1 and distal subiculum bordering presubiculum. To summarize these projections, Amaral et al. 1991; Fig. 3A: cells in proximal CA1 project to the distal subiculum, cells in mid-CA1 project to mid-subiculum and cells in distal CA1 project across the CA1-subiculum border into the proximal subiculum. Fibres arising in proximal CA1 travel to the subiculum mainly via alveus and the deepest portion of stratum oriens, whereas fibres originating in mid-CA1 do not enter the alveus but project to the subiculum through deep parts of stratum oriens. Axons of distal CA1 cells travel directly to the subiculum from all parts of stratum oriens Amaral et al. 1991. Neurophysiological depth profiles of CA1-subiculum projection, examining excitatory postsynaptic potentials evoke in subiculum following stimulation of different sites by bipolar stimulating electrode en route to hippocampal area CA1 of rat in vivo, confirm this neuroanatomical analysis o'mara et al. 2001. Stimulating electrodes were aimed at area CA1 and recording electrodes at dorsal subiculum; after passing primary visual cortex and corpus callosum, electrodes were allowed to settle in dorsal subiculum Fig.

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Summary

The hippocampal region consists of hippocampal formation and parahippocampal region. The hippocampal formation comprises dentate gyrus, Ammon's horn, and subiculum. In this review, term hippocampus refers to dentate gyrus and Ammon's horn, whereas subiculum refers to distinct hippocampal subregion distal to CA1 Field. The word subiculum means support in Latin. The Subiculum forms the transition zone between the hippocampus and entorhinal cortex. Like the hippocampus, subiculum is a three-layer allocortex, consisting of a molecular layer, pyramidal cell layer, and a polymorphic / fiber layer. The molecular layer is contiguous with stratum lacunosum-moleculare and stratum radiatum of CA1. The cell layers contain large pyramidal neurons, less densely packed than in CA1, as well as variously shape, smaller interneurons that are presumably GABAergic inhibitory cells. The Parahippocampus or parahippocampal region is a transition zone between a three-layer allocortex and six-layer neocortex. The parahippocampal region consists of the presubiculum, parasubiculum, entorhinal cortex, perirhinal cortex, and, more posteriorly, postrhinal cortex or parahippocampal cortex. At the border of the three-layer subiculum and presubiculum, additional cell layer appear, position more superficially and separate from the underlying continuation of three-layer subicular lamination by a cell-free zone known as lamina dessicans. As the entorhinal cortex gives way to the postrhinal / parahippocampal cortex, lamina dessicans disappears, and more homogeneously layer cortex appears that resembles a six-layer neocortex, except that it lacks inner granular cell layer. An important feature of connectivity of hippocampal region is that three-layer structures project unidirectionally, whereas parahippocampal structures with more than three layers have multidirectional, reciprocal interconnections to hippocampal formation and other parahippocampal regions. The Well-know trisynaptic circuit of hippocampus consists of three defined synaptic relay stations. First, input from the entorhinal cortex enters the hippocampus via a perforant path by synapsing onto dendrites of dentate granule cells in the outer two thirds of the dentate molecular layer. Dentate granule cells have been proposed to form a gate or filter of activity entering the hippocampus. Next, axons of dentate granule cells innervate hilar interneurons and CA3 pyramidal cells. Finally, via the Schaffer collateral pathway, CA3 neurons synapse onto CA1 pyramidal cells. Output of CA1 goes to the subiculum, and from the subiculum, activity exits the hippocampus to target entorhinal cortex and more distant subcortical and cortical areas. Use of glutamate in many of these pathways, and firing characteristics of target cells, predispose hippocampal circuit to reverberating neuronal firing, which has been considered to be conducive to paroxysmal, epileptiform firing. Subiculum receives dual afferent inputs from CA1 pyramidal neurons and from entorhinal cortex layer II / III neurons. The organization of CA1 afferents to subiculum is governed by several anatomic principles. First, CA1-to-subiculum inputs are organized topographically. Fibers from more proximal CA1 fibers innervate distal subiculum, whereas distal CA1 innervate proximal subiculum. Second, extensive longitudinal divergence exists from CA1 to subiculum, with the CA1 area making synaptic contacts over approximately one third of the longitudinal extent of subiculum.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

3.03.3.3 The Subiculum

Clinical, pathological, and physiological studies of focal epilepsy of temporal lobe origin have historically emphasized the role of the hippocampus. Certainly, damage to the hippocampus proper is central to temporal lobe epilepsy, with cell loss and gliosis of CA1 and CA3 subfields and dentate hilus representing pathologic hallmarks of the syndrome. However, emerging pathophysiological and imaging evidence strongly implicates a critical role for distal structures, including subiculum and parahippocampal region, in TLE as well. Although cell loss in the subiculum is not a significant feature of epilepsy, proximity of the subiculum to sites of hippocampal damage could endow it with a unique functional role in epileptogenesis. Subiculum, located between the hippocampus proper and parahippocampal region, represents anatomic transition zone between Ammon's horn and the entorhinal cortex. The Subiculum is the major output of the hippocampus and first brain region encountered by neural activity emanating from the hippocampus. With this privileged location, subiculum is exquisitely poised to modulate normal and abnormal neuronal firing as it propagates from the hippocampus to other cortical and subcortical regions. This review summarizes the anatomy and physiology of subiculum and correlates this information with its known and possible roles in epilepsy. The The of evidence suggests that the subiculum is not merely a back door out of the hippocampus, but a dynamic and interactive structure that processes and modifies epileptic discharges and in turn is modified by them. After summary of anatomy and physiology of subiculum, exciting new findings about subiculum's role in epilepsy and epileptogenesis are discuss., Schematic of transverse section of hippocampus and parahippocampal region. The Subiculum occupies the central position between the hippocampus proper and parahippocampal structures. Entorhinal cortex layers are identified with Roman numerals. DG, dentate gyrus; CA, cornu ammonis. B, select connections between hippocampal and parahippocampal regions. Note that hippocampal areas tend to project unidirectionally, whereas parahippocampal areas project to multiple targets. The dash line from subiculum to CA1 indicates one possible mechanism of epilepsy-induced plasticity, whereby excitatory connections between these two areas may be strengthen., Intracellular recordings from two subicular neurons, regular-spiking neuron and bursting neuron, in response to depolarizing current pulse. B, Field and patch-clamp recordings from subiculum slice bath in zero magnesium, showing appearance of synchronized epileptiform Field activity, and simultaneous whole-cell recordings in current-clamp and voltage-clamp modes. Illustrated traces indicate widespread activity. Vertical dashed line, beginning of bursting neuron activity, which fires before development of epileptiform Field activity about 25 msec later. These findings indicate that, during widespread epileptiform activity, burster cell is the leader cell. Later, neural firing begins in follower cells such as fast-spiking interneurons and regular spiking neurons. These results lead authors to propose a sequence of neuron recruitment in epileptic subiculum, with burster cells playing a prominent initiating role. Reproduce in modified form with permission from ref. 29, p. 5529. C, Intracellular recordings from bursting neurons in slices from the subiculum.

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Entorhinal Cortex (EC)

The Comparison of main trends in extrinsic and intrinsic connectivity patterns of MEC and LEC suggests that different phenotypes of both EC subdivisions likely depend on combinatorial effects of small differences in intrinsic organization and substantial differences in extrinsic inputs. Although this conclusion and following details are mainly based on studies in rodents, more sparse data in non-human and human primates seems to support a comparable organization. To understand the functional relevance of subtle intrinsic differences, more data is needed for which we likely will depend on the emergence of even more specific genetic tools to identify and manipulate activity of single classes of neurons. Eventually, detailed imaging studies in humans are expected to contribute to increased understanding of Functional diversification within EC. Extrinsic input differences as summarized above are still in overall support with notion that two functionally different input streams to the hippocampus are mediate by two entorhinal domains. MEC provides connectional routes with extensive posterior parts of the cortex, including posterior parahippocampal, retrosplenial, parietal and occipital networks, allowing representation of intrinsically generated signals about perceived and / or planned movements in stable contexts. In contrast, LEC mediates routes to and from the hippocampus with more anterior parahippocampal, sensory and pre-and orbitofrontal domains, providing access to evaluate information about the ever-changing external world. From a functional anatomical perspective, above provide suitable framework to keep adding details needed to mechanistically understand the role of EC. The Connectional scheme as presented here assumes that functionally different parts of EC share network structure to mediate cortical-hippocampal interactions in comparable matter. Neurons in layers II and III provide various combinations of information to the hippocampal circuit, and copy of that input is made available to neurons in layer V. Latter step might either be monosynaptic through inputs targeting extensive apical tufts of some of layer V pyramidal neurons or disynaptic through intrinsic projections from layer II to layer Vb. In view of the strict topology of reciprocal connectivity between EC and CA1 / subiculum, it is likely that at least some of these layer Vb neurons receive hippocampally process copy of that original input information. Layer Vb neurons are in position to integrate those inputs with additional sets of information, and to send resulting representations back to layers II and III. In the case of layer Va neurons, which apparently are the origin of the main output pathway of EC, hippocampally process copy might be disynaptical, mediate through Vb neurons, and it is currently not known whether other inputs integrate at the level of these Va neurons. In view of their apical dendrites reaching superficial layers of EC, it is likely that they, like layer Vb neurons, do receive superficially terminating inputs. If correct, connectional data strongly argue that differences in cortical inputs form the main feature underlying phenotypic differences between LEC and MEC.

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Afferent Connections

Base on assessments of fiber labeling following anterograde tracer injections, areas 35 and 36 provide only light projections to hippocampal structures. Two cases involving only deep layers do not result in any labeling in hippocampal or parahippocampal areas and so are not included in Table 3. This confirm, however, that projections arise in superficial layers. Both area 35 and area 36 provide light input to the ventral subiculum. Area 36 also provides light input to ventral CA1, dorsal presubiculum, and rostral and caudal parasubiculum. Few labeled fibers were observed in other regions, including CA2 and ventral CA3 arising from area 36 injections, but this level of labeling is considered negligible. Fiber labeling in hippocampal structures arising from tracer injections in POR was more substantial than that arising from PER areas 35 and 36, but still light. Area 36 projects lightly to dorsal CA1, as well as dorsal and ventral subiculum. POR projections of hippocampal structures were lighter than those arising from either of two Entorhinal subdivisions. The strongest projections from POR were to dorsal presubiculum and caudal parasubiculum. In contrast, labeling in ventral presubiculum and rostral parasubiculum was sparse. Base on densities of labeled cells arising from PER retrograde tracer injections, overall, hippocampal and parahippocampal structures project more heavily to area 35 than to area 36. One case that does not involve deep layers results in no labeled cells in any structure. Thus, input targets deep layers. Input was also stronger, overall, from ventral as compared to dorsal regions. There is essentially no projection of areas 35 and 36 arising in DG. Likewise, density of labeled cells in dorsal and ventral CA3 and CA2 was either very light or observed only in single case. Following area 35 injections, ventral CA1 and ventral subiculum were most densely label. Dorsal subiculum and rostral parasubiculum were also densely label. Following area 36 injections, again, ventral CA1 was most densely label, though not as densely as for area 35 injections. In general, dorsal subiculum provides the strongest hippocampal input to POR. Compared with area 35, POR receives greater input from dorsal CA1 and about the same from dorsal subiculum. Input from ventral CA1 and subiculum are weaker than that to either area 35 or area 36. Base on patterns of retrogradely-labeled cells, caudal parasubiculum targets POR very heavily, much more heavily than any of the other regions examine. Dorsal presubiculum also provides substantial input to POR, stronger than it provides to either area 35 or area 36. We also examine the percentage of input quantify as percent of the total number of labeled cells in afferent structures. For PER area 35, greatest input was from ventral CA1, which provides nearly 40 % of total input from different structures. Next strongest inputs were from dorsal CA1, and dorsal and ventral subiculum.

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Hippocampal Formation

The Hippocampal formation is composed of the Subiculum, Hippocampus, and Dentate gyrus, all of which constitute the allocortex of Brodmann. The Subiculum is laterally continuous with cortex of parahippocampal gyrus and area of periallocortex. Medially, edge of hippocampal formation is formed by Dentate gyrus and fimbria of the hippocampus. Developmentally, hippocampal formation originates dorsally and migrates into its ventral and medial positions in the temporal lobe. During this migration, small remnants of hippocampal formation remain behind to form medial and lateral longitudinal striae and their associated gray matter, indusium griseum. These structures are small in the human brain and extend rostrally along the dorsal aspect of corpus callosum into the subcallosal area.


Discussion

In summary, our results identify a new category of neuron, vector trace cell, defined by two properties. First, VTC responds when rat is at a specific distance and allocentric direction from small or extended cue, including environmental boundaries, by immediately generating a vector field. Second, vector field persists after cue that elicit it is subsequently remove, creating a vector trace field. Our findings build on the emerging picture of the prevalence of vector coding in hippocampal formation, but add a crucial dimension of vector memory. Thus, neurons in medial 12 and lateral 37 entorhinal cortex can encode allocentric vectors to discrete objects but do not show memory for previously-present cues. Likewise, recent reports of egocentric vector coding of environmental cues 38 39 also do not describe memory traces. Lateral entorhinal neurons 40, and a few CA1 place cells 13 can encode memory trace for previously-present objects, but these non-vectorial object fields, which develop only after cue removal, are confined to exact object locations so cannot retrieve locations in space between objects and boundaries, as is the case for VTCs. One study found 12 % of CA1 bat cells show egocentric vector tuning to goal, some with memory responses of 41. Interestingly, however, these goal-direct CA1 cells appear to encode vector to only a single goal at a time. The present study is the first to report cell classes that combine encoding location of multiple cues using allocentric vectors, with memory of those cue locations when cues are remove. VTCs suggest a vector-base model of computing spatial relationships between agent and multiple cues, free from constraints of direct perception of those cues, thus enabling spatial planning and imaginative cognition 4 7-9. Relative abundance and scarcity of VTCs in distal and proximal subiculum, respectively, provide strongest in vivo electrophysiological evidence for hypothesised spatial memory specialisation along CA1 / subiculum proximal-distal pathway 30, and provide cellular substrate for demonstration that selective inactivation of distal subiculum disrupts spatial memory 18. Finally, we note that, consistent with encoding-vs-retrieval scheduling and dual-input control models of theta 5 34 35, all cue-responsive neurons encode presence of inserted cue using earlier phase of theta. The shift to an earlier phase was specific to cue-field, therefore not driven by global state changes nor, give range of vectors, especially in VTCs, restricted to region in space. Rather, theta phase appears to define specific information channel for the presence of newly-insert cue within each neuron. Furthermore, degree of relative late-to-early shift, within each neuron, was linked to whether trace field would form. Thus, our findings extend theta-scheduling models 5 34 35 by demonstrating theta-phase shift as neural substrate for memory encoding. It will be important to determine VTC-specific factors, such as particular anatomical inputs and / or enhanced plasticity, underlying VTCs theta-link propensity to generate trace fields.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Discussion

5-HT 2C receptors are couple to G proteins consisting of G q and G complex. G induces phospholipase C to hydrolyze phosphatidylinositol 4 5-bisphosphate to inositol 1 45-triphosphate and diacyglycerol. IP 3 triggers release of CA 2 + from intracellular stores, which, together with dAG, activates protein kinase C. Activation of G q couple receptors has been reported to inhibit CA V 3 channels. In heterologous systems, G q couple neurokinin 1 receptor induces inhibition of recombinant CA V 3. 2 channels via pathway that involve G q, PLC, and PKC. In contrast, G q couple dopamine D1 receptor expressed in adrenocarcinomal cell line H295R inhibits CA V 3. 2 channels via G complex that bind to the intracellular loop of CA 2 + channel. More experiments will be required to determine if the inhibitory pathway we uncover in subiculum involves any of these two molecular mechanisms.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

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Sources

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