Microinjections of small amounts of the cholinergic receptor agonists carbachol and nicotine into the pontine reticular formation (PRF) of rats were shown to induce catalepsy. Catalepsy was used in this work as an experimental model for studying the interactions between cholinergic mechanisms and excitatory amino acid mechanisms in the PRF. The excitatory amino acid (EAA) receptor agonists glutamate, NMDA, kainate and AMPA were microinjected in subcataleptic doses before carbachol in the same location into the PRF. All the EAA receptor agonists injected induced a significant potentiation of the cataleptogenic effect of carbachol. The NMDA receptor antagonist MK-801 and the non-NMDA receptor antagonist DNQX microinjected in picomol doses before the EAA receptor agonists attenuated their potentiating effect. These results support the suggestion that EAA neuronal mechanisms contribute synergistically with the cholinergic mechanisms to the PRF neuronal interactions involved in the generation of catalepsy. Similar synergistic interactions might be active in the generation of other pontine behavioral manifestations like REM sleep.
- Excitatory amino acids
- Interaction between carbachol and excitatory amino acids
- Pontine reticular formation