Summary: Introduction. The entire hippocampus is derived from the telencephalon. Embryologically, it is made up of the most archaic cortices. Through special phylogenetic and ontogenetic telencephalization processes, it will arrive at its particular mesial basal position. This structure has three components: a) Retrocommisural hippocampus, or hippocampus proper (RH). b) Supracommisural hippocampus (SH). c) Precommisural hippocampus (PH). The RH is situated in the most medial part of the 5th temporal gyrus (5 TG). The outer/upper face of the RH is to be found in the temporal recess of the lateral ventricle. It is called pes hippocampi or albeus. Inwards, it is limited by the choroid fissure, outwards and downwards by the parenchyma of the 5th TG, forwards, by the amygdala of the striatal body and, backwards, by the isthmus. The fornix is a continuation of efferent pathways from CA3, CA1 and the subiculum. By means of a circular course, it ascends over the thalamus and, descending in front of Monro's foramina and traversing the hypothalamus, reaches the mammillary bodies. It consists of fimbria, posterior pillars and a body and anterior pillars. The latter pass behind the anterior white commisure (AWC), and make up the anterior portion of Monro's foramina. The SH originates in the RH. At the level of the splenium of the corpus callosum (CC), the fornix produces two striae, medial and lateral, and the dentate gyrus turns from fasciola cineria into induceum griseum. These structures are to be found in both hemispheres and, traveling over the CC, will reach the preoptic and hypothalamic septal areas, as well as the PH. The PH is a small fiber contingent which stems from the fornix at the level and in front of the AWC. Memory. General aspects. There is general agreement that the main role of the hippocampus is that of creating new memories relative to experienced events (episodic or autobiographic memory). Some researchers, however, prefer to think of the hippocampus as part of a major medial temporal lobe memory system responsible for declarative memory. This memory would include, besides episodic memory, memory of events. Another very important hippocampal function would relate to storage of semantic (conceptual) memories. Engrams. Memory and synaptic plasticity. Engrams are hypothetical means whereby memory traces are stored as physical or chemical changes in the brain in response to external stimuli. The existence of engrams has been proposed by diverse scientific theories which try to explain the persistence of memory and how some memories are stored in the brain. The term engram was coined by Sermon and explored by Pavlov Lashley tried to locate the engram and failed in finding a sole biological locus for the same which made him think that memories were not localized in any particular part of the brain, but distributed throughout the cerebral cortex. Afterwards, in 1949, Hebb, a student of Lashley's, published his empiricist theories in The Organization of Behavior. Hebb referred to Lorente de Nó's reverberating circuits to propose a mechanism for maintaining activity in the cerebral cortex after the external stimulus had ceased: the so called central autonomous process. This led him to consider the cellular assembly, a complex reverberating circuit which could be assembled by experience. Changes in synaptic resistance with experience were eventually named Hebb's, or the Hebbian, synapse. Hebbian theory describes a basic mechanism for synaptic plasticity by means of which an increment in synaptic efficacy stems from repetitive and persistent stimulation of the post-synaptic cell. This theory receives the name of Hebb's rule. The fact that memory is persistent stresses the relevance of understanding those factors which maintain synaptic strength and prevent undesired synaptic changes. There is evidence that recurrent inhibitory connections in region CA1 of Ammon's horn of the hippocampus might contribute in this sense by modulating the ability to induce long-term potentiation (LTP) or long-term depression (LTD) of synaptic activity, given by a sequence of high-or low-frequency stimulations, respectively. The hippocampus seems to be able to select the most relevant from the least relevant aspects of a definite experience in order to transform them into long-term memory. According to the concept of Emotional Tagging, for example, through the activation of the amygdala by emotionally suggestive events, the experience will be tagged as important and synaptic plasticity promoted in other cerebral regions, such as the hippocampus. Recently, it has been shown that activation of the amygdala transforms transient plasticity into long-term plasticity. This finding directly relates to the afore mentioned hypothesis of emotional tagging, since activation of this organ could trigger neuromodulatory systems, further reduce the activation threshold of the synaptic marker and facilitate transformation of early into late memory at the level of the hippocampus via direct amygdalar action on the latter organ. γ-aminobutyric acid. γ-aminobutyric acid (GABA), together with its different receptor subunits, functions as an inhibitor neurotrans-mitter in hippocampus and memory activities. GABA and memory. LTP has been a widely studied mechanism of synaptic plasticity and, as we have mentioned, it is intimately related to diverse memory and learning processes in mammals. It has been observed in pyramidal cells of area CA1 of the hippocampus of young C57BL/6 mice that the pairing of pre-synaptic stimulation with just one post-synaptic action potential will be sufficient to induce LTP, whereas in the adult animal this stimulation must be paired with several post-synaptic action potentials to achieve such induction. This change might result from a modification during maturation of GABAergic inhibitory processes. A bath of muscimol, a GABAA agonist, given to sections of hippocampal area CA1 will increase the range of frequencies inducing LTD, while in the presence of picrotoxin, a GABAA antagonist, LTD will be induced only at very low stimulation frequencies. The resulting recurrent inhibition appears to stem from GABAergic input to pyramidal neurons of CA1. In this way, post-synaptic spike activity could increase GABAergic feedback inhibition, and thus favor LTD. However, in experiments in which the pairing of stimulating action potentials is set apart in time, LTD, LTP or no plasticity may be observed. An explanation for these results could be that, in the presence of picrotoxin, and therefore GABA inhibition, the first action potential may have a greater tendency to "back propagate", so that only one spike would be enough to cause LTP instead of LTD, and affect memory processes differently.
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