Removing the MTL results in anterograde amnesia (inability to form new memories) and some regregrade (temporally graded) amnesia (forgetting the past before injury).
Working memory can go through consolidation to become long term
The fornix is the most prominent hippocampal output pathway.
Hippocampus = dentate gyrus, hippocampus proper (CAs), and the subiculum(transitional zone that is continuous with HP at one edge and parahippocampal gyrus at the other).
The HP and dentate gyrus are three-layered(allocortex) with a molecular layer and a polymorphic layer and granular. The intermediate statum is a granule cell layer in the DG and a pyramidal cell layer in HP. The molecular layer of the DG faces the subarachnoid space and its output fibers project into the HP.
Granule cell axons enter CA as mossy fibers and synapse with the thorny dendritic shafts of pyramidal cells. Granule cells are glutamergic
In the subiculum there is a gradual change from 3 to 6 layers.
The hippocampal equivalent of subcortical white matter is a layer of fibers called the alveus that lies just beneath the ependymal lining of the ventricles. The alveus has afferents and efferents that collect into a bundle called the fimbria at the edge of the choroid fissure. The fimbria becomes the crus of the fornix and where the two crura converge begins the body of the fornix. At the interventricular foramen, the fornix turns inferiorly and posteriorly, diverging into the columns of the fornix, which passes through the middle of the hypothalamus toward the mammillary bodies.
The major source of input to the hippocampus is the enthorhinal cortex which receives some input from olfactory but mostly from association cortex, cingulate (via the cingulum), orbital cortex (via the uncinate fasciculus) and multimodal areas.
Also, modulatory cholinergic inptus from the septal nuceli reach the hippocampus through the fornix. Amygdala can reach the hippocampus directly as well. These two systems can modulate the probability that something will be encoded. Also, the hippocampus can get input from its contralateral half by way of the hippocampal commissure (right below the body of the fornix.
Hippocampal outputs are usually from the subiculum to go back to enthorhinal but the fornix carries info to septal and preoptic nuclei and nucleus accumbens(via precommisural fornix) and continue to orbital and anterior cingulate cortices. The postcommissural fornix go to anterior thalamus or hypothalamus and mammillary bodies and bed nucleus of the stria terminalis.
The mammilothalamic tract ends in the anterior nucleus, so hippocampus can influence this nucleus directly and indirectly.
The anterior thalamus projects to cingulate gyrus , completing a large circuit of inputs back to the hippocampus (cingulate projects to hipp via the cingulum).
The Papez Circuit: hippocampusfornixmammillary bodyanterior thalamic nucleicingulate--?parahippocampal/enthorhinal.
Damage to the mammillary bodies causes Korsakoff’s amnesia which leaves intact intelligence but the inability to form new episodic memories.
Bilateral damage of the cingulum does no damage, apparently.
Skills not centered around conscious recall does not require the hippocampus.
The emotional “tags” develop as patterns of strengthened synapses in the basolateral amygdala, in turn initiating autonomic and behavioral responses throught he central nuclei of the amygdala. Information about sights, sounds, and other stimuli reaches the basolateral amygdala rapidly through the thalamus and more slowly from cortical association areas.
An intrinsically pleasany or unpleasant stimulus (US) by itself causes an emotional response. Pairing this with neutral stimuli can cause activation of NMDA receptors and LTP in basolateral neurons. Protein synthesis consolidates this pairing and then alter exposure to the same formerly neutral stimulus (now a CS) can cause an emotional response. This is mediated quickly by the thalamus and slowly by the cortical pathway. Bilateral damage to the amygdala blocks the acquisition of such conditioned emotional responses without affecting declarative memory for the conditioning trials themselves. MTL damage does exactly the opposite.
Gradually acquired experience (nondeclarative memory) relies on interaction of the basal ganglia and the frontal lobes.
The dentate and the subventricular zone are the only regions where we can witness adult neurogenesis.
The anterior cingulate rounds out and is enveloped by a C shaped subcollasola area that is rich in serotonin and governs networks involving the hypothalamus and brainstem in mood and anxiety.
The septal area is a “way station” between the HF and the hypothalamus. It is recoiprically connected with the olfactory bulb, midbrain, cingulate, and thalamus. Serves as a feedback loop to the HF and modulates hypothalamic functions.
Dentate gyrus and CA3 interlock. Seperated by the fimbrio dentate sulcus.
Stratum oriens of CA has axons and basal dendrites of the pyramidal cells and inhibitory basket cells.
Stratum pyramidalis is the soma of the pyramidal cells (excitatory) and interneurons(inhibitory)
Stratum radiatum has the schaffer collateral fibers(CA3 to CA1) where the pyramidals have their apical dendrite.
Stratum lucidum in CA3 is where mossy fibers make contact with pyramidal cells.
Stratum lacunosum is continuous with the perforant path (EC to DG and CA).
Perforant path perforates through subiculum to get from EC to DG. DG mossy fibers synapse on CA3 which then pass to the alveus and use schafffer collaterals to pass to CA1 which then project to subiculum and EC
Septal and supramammillary regions help with theta regulation in the HF.
Lateral EC deals with cortical and medial EC deal with subcortical and leads to a convergence of exeteroceptive sensory information on the posterior HF; information from subcortical centers reflect the intrinsic state of the organism transmit more anteriorly.
Alzheimers can be partially attributed to loss of pyramidal neurons in CA1 field and subiculum.
Adrenal hormones can excite, with amino acids, plasticity, but too much might destroy. Stress can cause this and suppress ongoing neurogenesis in fear related learning and memory.