Pii: S0306-4522(99)00162-1

Voltage-dependent Ca21 channels constitute a major class of plasma membrane channels through which a significant amount of extracellular Ca21 enters neuronal cells. Their pore-forming a1 subunits are associated with cytoplasmic regulatory b subunits, which modify the distinct biophysical and pharmacological properties of the a1 subunits. Studies in animal models indicate altered expression of a1 and/or b subunits in epilepsy. We have focused on the regulatory b subunits and have analysed the immunoreactivity patterns of the b1 , b2 , b3 and b4 subunits in the hippocampus of patients with temporal lobe epilepsy (nˆ 18) compared to control specimens (nˆ 2). Temporal lobe epilepsy specimens were classified as Ammon’s horn sclerosis (nˆ 9) or focal lesions without alteration of hippocampal cytoarchitecture (nˆ 9). Immunoreactivity for the b subunits was observed in neuronal cell bodies, dendrites and neuropil. The b1, b2 and b3 subunits were found mainly in cell bodies while the b4 subunit was primarily localized to dendrites. Compared to the control specimens, epilepsy specimens of the Ammon’s horn sclerosis and of the lesion group showed a similar b subunit distribution, except for b1 and b2 staining in the Ammon’s horn sclerosis group: in the severely sclerotic hippocampal subfields of these specimens, b1 and b2 immunoreactivity was enhanced in some of the remaining neuronal cell bodies and, in addition, strongly marked dendrites. Thus, hippocampal neurons apparently express multiple classes of b subunits which segregate into particular subcellular domains. In addition, the enhancement of b1 and b2 immunoreactivity in neuronal cell bodies and the additional shift of the b1 and b2 subunits into the dendritic compartment in severely sclerotic hippocampal regions indicate specific changes in Ammon’s horn sclerosis. Altered expression of these b subunits may lead to increased currents carried by voltage-dependent calcium channels and to enhanced synaptic excitability. q 1999 IBRO. Published by Elsevier Science Ltd.