Norepinephrine (NE) is an important
neurotransmitter in the brain, and regulates antinociception. However, the mechanism of action of NE on
pain-related neurons in the hippocampal CA3 region is not clear. This study examines the effects of NE,
phentolamine on the electrical activities of
pain-excited neurons (PENs) and
pain-inhibited neurons (PINs) in the hippocampal CA3 region of rats. Trains of electric impulses applied to the right sciatic nerve were used as noxious stimulation. The electrical activities of PENs or PINs in the hippocampal CA3 region were recorded by using a glass
microelectrode. Our results revealed that, in the hippocampal CA3 region, the intra-CA3 region microinjection of NE decreased the
pain-evoked discharged frequency and prolonged the discharged latency of PEN, and increased the
pain-evoked discharged frequency and shortened discharged inhibitory duration (ID) of PIN, exhibiting the specific
analgesic effect of NE. While intra-CA3 region microinjection of
phentolamine produced the opposite response. It implies that
phentolamine can block the effect of endogenous NE to cause the enhanced response of PEN and PIN to noxious stimulation. On the basis of above findings we can deduce that NE,
phentolamine and alpha-
adrenoceptor are involved in the modulation of nociceptive information transmission in the hippocampal CA3 region.