The noradrenaline (NA)-containing innervation of the hippocampal formation arises exclusively in the brainstem nucleus locus coeruleus. The projection is 75--90% ipsilateral, originating predominantly in the large, multipolar cells of the compact component of the nucleus. The axons course into the hippocampal formation by three pathways. Ammon's horn receives its NA innervation principally through the ventral amygdaloid bundle-ansa peduncularis, with smaller contributions from the fornix and ipsilateral fasciculus cinguli. The innervation of the area dentata is to a larger extent bilateral, with the greatest contribution arising from the ipsilateral fasciculus cinguli and approximately equal proportions of fibers traveling via the contralateral cingulum, fornix, and the ventral path. In general, the endogenous content of NA is greater in the area dentata than in Ammon's horn, and in both structures is greater in the temporal than in the septal ends. The pattern of NA innervation is similar at all septotemporal levels, however. The dense plexuses of preterminal and terminal elements appear in the infragranular hilus of the area dentata, stratum lucidum of CA3, and in the molecular layer of the subiculum. Fluorescent varicosities often appear in perisomatic clusters, or, closely apposed to dendrites of granule and pyramidal cells.

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Frank-Ter Haar syndrome (FTHS), also known as Ter Haar syndrome, is an autosomal-recessive disorder characterized by skeletal, cardiovascular, and eye abnormalities, such as increased intraocular pressure, prominent eyes, and hypertelorism. We have conducted homozygosity mapping on patients representing 12 FTHS families. A locus on chromosome 5q35.1 was identified for which patients from nine families shared homozygosity. For one family, a homozygous deletion mapped exactly to the smallest region of overlapping homozygosity, which contains a single gene, SH3PXD2B. This gene encodes the TKS4 protein, a phox homology (PX) and Src homology 3 (SH3) domain-containing adaptor protein and Src substrate. This protein was recently shown to be involved in the formation of actin-rich membrane protrusions called podosomes or invadopodia, which coordinate pericellular proteolysis with cell migration. Mice lacking Tks4 also showed pronounced skeletal, eye, and cardiac abnormalities and phenocopied the majority of the defects associated with FTHS. These findings establish a role for TKS4 in FTHS and embryonic development. Mutation analysis revealed five different homozygous mutations in SH3PXD2B in seven FTHS families. No SH3PXD2B mutations were detected in six other FTHS families, demonstrating the genetic heterogeneity of this condition. Interestingly however, dermal fibroblasts from one of the individuals without an SH3PXD2B mutation nevertheless expressed lower levels of the TKS4 protein, suggesting a common mechanism underlying disease causation.

IOP elevation may directly damage mitochondria in the ONH axons by promoting reduction of COX, mitochondrial fission and cristae depletion, alterations of OPA1 and Dnm1 expression, and induction of OPA1 release. Thus, interventions to preserve mitochondria may be useful for protecting against ON degeneration in glaucoma.

Elevated hydrostatic pressure triggered mitochondrial fission, abnormal cristae depletion, Drp-1 translocation, and cellular ATP reduction in differentiated RGC-5 cells. Increased understanding of the molecular mechanisms that regulate the cellular response to elevated pressure including mitochondrial fission may provide new therapeutic targets for protecting RGCs from elevated hydrostatic pressure.

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Estimating the probability of RGC survival and measuring the rate of dendritic shrinkage could become a new paradigm for investigating neuronal degeneration and evaluating the response of neuroprotective treatment.