Brain, Vol. 119, No. 4, 1327-1347, 1996
© 1996 Guarantors of Brain
research-article |
Inhibitory neurons in the human epileptogenic temporal neocortex
An immunocytochemical study
1Instituto Cajal Madrid 2Departments of Neurosurgery, Hospital de la Princesa Madrid 3Departments of Neurophysiology, Hospital de la Princesa Madrid 4Department of Pathology, Clinica Puerta de Hierro Madrid
Correspondence to:
Correspondence to: Dr J. DeFelipe, Instituto Cajal (CSIC), Avenida Dr Arce, 37, Madrid 28002, Spain
Immunocytochemical methods were used to study alterations in inhibitory neuronal circuits in human neocortex resected during surgical treatment of intractable temporal epilepsy associated or not with brain tumours. The epileptogenic cortex was characterized and divided into spiking or non-spiking zones by intraoperative electrocorticography (ECOG). The resected cortex was cut into blocks, sectioned and stained immunocytochemically for visualization of glutamic acid decarboxylase (GAD), the calcium-binding protein, parvalbumin (PV) and glial fibrillary acidic protein (GFAP). A variety of alterations in cortical neuronal circuits as revealed by immunocytochemical and histological methods were found. Similar alterations in inhibitory neuronal circuits appear to occur independently of the primary epileptogenic site and pathology associated with epilepsy, which suggests that there is possibly a common basic underlying mechanism that leads to seizure activity. These changes were apparently unrelated to ECOG findings at surgery, which bring into question the value of the use of interictal epileptic discharges recorded by ECOG to guide cortical resections. The most conspicuous and common change was the loss of chandelier cells. The finding that these cells are among the most vulnerable types of GABAergic interneurons in the epileptogenic temporal cortex indicates that they might be of great functional importance, since the axon terminals of chandelier cells are likely to exert powerful regulation of impulse generation in cortical pyramidal cells. Therefore, these cells might represent a key component in the aetiology of human epilepsy.
focal epilepsy; brain tumours; glutamic acid decarboxylase; parvalbumin; gliosis
Received November 22, 1995. Revised February 19, 1996. Accepted February 26, 1996.
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