Control of ICP and the cerebrovascular bed by the cholinergic basal forebrain.

Abstract

The involvement of the cholinergic basal forebrain in the control of ICP and the cerebrovascular bed was investigated by simultaneous measurement of CBF, BP, ICP and ETCO2 in rats and cats. Single unit spikes were also continuously recorded during ICP changes in the dorsomedial hypothalamic nucleus (DMH) of cats. Glutamate or acetylcholine (Ach) microinjection into the magnocellular basal nucleus (nucleus basalis Meynert: NBM, substantia innominata: SI) of rats or the DMH of cats caused persistent increases in ICP associated with slightly decreased BP. Microinjection of Ach into the NBM or the DMH also induced consistent increases in CBF in the cerebral cortex. Spike activities in DMH neurons increased before and during spontaneous ICP elevation. The firing rate of the DMH neurons increased in phase with the plateau wave-like ICP variations elicited by microinjection of Ach into the cholinoceptive pontine area or the contralateral DMH. Glutamate- or Ach-induced increases in ICP resulted from an increased CBV in response to a reduced cerebral vasoconstrictor tone. Activity within the cholinergic basal forebrain, as well as the central noradrenergic system, contribute to ICP changes and may be the intrinsic neuronal origin of the plateau waves occurring in some pathological conditions.