Mesencephalic trigeminal (MeV) neurons are primary sensory neurons of which
the cell soma is located within the brainstem, and is associated with syna
ptic contacts. In previous studies it has been reported that these cells ar
e resistant to kainic acid excitotoxicity, and have little or no responsive
ness to exogenously applied glutamate or selective agonists. In an in vitro
slice preparation with intracellular recording, we have found that these c
ells respond to pressure-applied glutamate, N-methyl-D-aspartic acid (NMDA)
, kainate (KA), and (R,S)-alpha-amino-3-hydroxy5-methyl-4-isoxazolepropioni
c acid (AMPA). The kainate and AMPA responses appear to be mediated by diff
erent receptors, at least in part, since they exhibit differing sensitivity
to an AMPA receptor selective antagonist. The agonists generally evoke lar
ger responses than glutamate and exhibit a long-duration desensitization re
quiring approximately 10 min for full recovery. Some cross-desensitization
between the glutamate agonists is also observed. Mesencephalic trigeminal n
eurons exhibit high-frequency oscillatory activity during depolarizations t
hat approach threshold potentials, and these could combine with transmitter
-induced depolarizations to enhance the excitability of these cells. Previo
us reports of nonsensitivity to glutamate and to kainate excitotoxicity are
attributable to relatively small responses, and to the desensitization exp
ressed by these neurons.