SYNAPTOPHYSIN IN SPINAL ANTERIOR HORN IN AGING AND ALS - AN IMMUNOHISTOLOGICAL STUDY

Aged-related spinal cord changes such as neuronal loss have been relat ed to the degree of clinical severity of amyotrophic lateral sclerosis (ALS); morphological data on synapses are, however, wanting. Variatio ns in synaptophysin (Sph) expression in aging and ALS were thus studie d at the level of lower motor neurons in 40 controls with non-neurolog ical diseases and 11 cases of ALS. Control sections of formalin fixed paraffin embedded cervical (C7/8), thoracic (T10) and lumbar spinal co rd (L5) and C6, C7, C8 and L5 of ALS cases were stained with haematoxy lin and eosin, luxol fast blue (LFB), and immunostained with a mouse m onoclonal antibody against Sph. The neuropil of the anterior horn (AH) in all control cases demonstrated Sph positivity. A dot-like pattern of positivity of presynaptic terminals on soma of motor neurons and fi ne immunoreactivity along neuronal processes were observed. A signific ant reduction of Sph immunostaining was observed in the neuropil with increasing age and 3 different somatic patterns were seen: a-well pres erved Sph reactivity around the soma and the proximal dendrites of his tologically normal neurons; b- few chromatolytic neurons showing large numbers of dot-like presynaptic terminals around the cell body and in a ''fused'' pattern; c- intense, diffuse, and homogeneous reactivity of some neurons. Attenuation of Sph reactivity in the AH neuropil, to its complete loss? was observed in all ALS cases. In addition to patte rns a-c, two additional microscopic findings were noted in ALS: d- chr omatolytic neurons showing complete absence of Sph reactivity; e- abse nce of Sph reactivity around the soma and the proximal dendrites of hi stologically normal surviving neurons. Our findings demonstrate that t here is a decrease in Sph immunostaining with aging, thus suggesting a n alteration in dendritic networks of the AH with aging. Changes in th e pattern of Sph immunoreactivity in cell bodies may represent synapti c plasticity and/or degeneration. Reinnervation may also be a possible mechanism as a response to neuronal loss in oldest control cases. Sph reactivity results may thus lend support to the presence of superimpo sed aging components in ALS cases which may give an insight into expla ining the increasing severity of the disease which is encountered with advancing age.