Abstract

In rat thalamus, histamine H 1 receptor and isoforms of H 3 receptor were expressed predominantly in the midline and intralaminar areas. Correspondingly, higher H 1 and H 3 receptor binding was also detected in these areas. All isoforms of H 3 receptor were expressed in several thalamic nuclei, but there were minor differences between their expression patterns. H 1 mRNA expression was high in the ventral thalamus, but the H 1 binding level was low in these areas. Since increased brain histamine appears to have an antiepileptic effect through the H 1 receptor activity, kainic acid (KA)-induced status epilepticus in rat was used to study modulation of H 1 and H 3 receptors in the thalamus following seizures. After systemic KA administration, transient decreases in mRNA expression of H 1 receptor and H 3 receptor isoforms with full-length third intracellular loops were seen in the midline areas and the H 1 receptor mRNA expression also decreased in the ventral thalamus. After 1 week, a robust increase in mRNA expression of H 3 receptor isoforms with a full-length third intracellular loop was found in the ventral posterior, posterior, and geniculate nuclei. The changes indicate a modulatory role of H 3 receptor in the sensory and motor relays, and might be involved in possible neuroprotective and compensatory mechanisms after KA administration. However, short-term increases in the H 3 receptor binding appeared earlier (72 h) than the increases of H 3 mRNA expression (1–4 w). The elevations in H 3 binding were evident in the intralaminar area, laterodorsal, lateral posterior, posterior and geniculate nuclei, and were likely to be related to the cortical and subcortical inputs to thalamus.

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