抄録
In previous study, we indicated that intraventricular administration of a dibenzoxazepine derived agent (DBZ-D) acts to enhance both the responses of regional cerebral blood flow and of the neurons in the nucleus basalis of Meynert (NbM) following electrical stimuli of the saphenous nerve. Glutamate (GLU) decarboxylase immunoreactivity is also identified in axonal terminals throughout the NbM neurons. In this study, therefore, it was examined if the direct application of DBZ-D may influence on the GLU-induced responses in the NbM neuron. Acetylcholine (Ach)-induced responses were also tested. All neurons examined (N=31) were antidromically identified from 18 Wistar male rat by cortical stimulation and also confirmed to be excited by electrical stimulation of the saphenous nerve under urethane anesthesia (1.1g/kg b.w.). Mean antidromic latency was 3.1+0.3 (1.2-10.1) msec.
GLU and Ach applied iontophoretically, had made an excitation of the firing discharge of all and 25 neurons tested, respectively. Simultaneous direct administration of DBZ-D enhanced the GLU-induced responses significantly (p<0.05), otherwise did not the Ach-induced responses at all.
These data suggest that 1) noxious stimuli cause an increased cortical blood flow via glutaminergic inputs and 2) that the intraventricular DBZ-D may act on the NbM neuron to modulate the glutaminergic synaptic inputs for increasing cortical blood flow following the neural stimulation in the rat. [Jpn J Physiol 54 Suppl:S197 (2004)]
