title: Locus coeruleus and dorsal pontine reticular influences on the gain of vestibulospinal reflexes.
abstract: Experimental anatomical and physiological studies have shown that noradrenergic locus coeruleus (LC) neurons, which are NE-sensitive due to inhibitory adrenoceptors, send inhibitory afferents to neurons of the peri-LC alpha and the adjacent dorsal pontine reticular formation (pRF); on the other hand these tegmental neurons, which are, in part at least, cholinergic as well as cholinoceptive, send excitatory afferents to the medullary inhibitory reticulospinal (RS) system. Experiments performed in precollicular decerebrate cats indicate that these pontine structures exert a regulatory influence on posture as well as on the gain of vestibulospinal (VS) reflexes. In particular, the increased discharge of dorsal pontine reticular neurons, and the related inhibitory RS neurons induced by microinjection of cholinergic agonists into the peri-LC alpha and the adjacent pRF of one side, decreased the postural activity, but greatly increased the response gain of the ipsilateral triceps brachii in response to stimulation of labyrinth receptors resulting from roll tilt of the animal (at 0.15 Hz, +/- 10 degrees). Similar results were also obtained when the discharge of these pontine and medullary reticular neurons was raised, either by local injection into the peri-LC alpha and the dorsal pRF of the beta-adrenergic antagonist propranolol, which blocked the inhibitory influence of the noradrenergic LC neurons on these structures, or by local injection into the LC complex of an alpha 2- or beta-adrenergic agonist (clonidine or isoproterenol) which led to functional inactivation of the noradrenergic neurons; in the latter case the effects were bilateral. Just the opposite results were obtained after microinjection into the LC of a cholinergic agonist, leading to activation of the corresponding neurons. Evidence was also presented indicating that the cholinergic excitatory afferents to the LC originated from the ipsilateral dorsal pRF. The effects described above were dose-dependent and site-specific, as shown by histological controls. Under given conditions, the decrease in postural activity induced either by direct activation of presumptive cholinergic and cholinoceptive pRF neurons or by inactivation of noradrenergic and NE-sensitive LC neurons was followed by transient episodes of postural atonia which lasted several minutes and affected the ipsilateral and sometimes also the contralateral limbs. In these instances, the EMG modulation of the corresponding triceps brachii to animal tilt was suppressed. These findings suggest two different ranges of operation for the noradrenergic and cholinergic structures located in the dorsolateral pontine tegmentum, leading either to a decrease or to an increase in gain of the VS reflexes. The cellular basis of these gain changes is discussed.(ABSTRACT TRUNCATED AT 400 WORDS)
authors.affiliation: Department of Physiology and Biochemistry, University of Pisa, Italy.
authors.forename: O
authors.initials: O
authors.lastname: Pompeiano
authors.forename: E
authors.initials: E
authors.lastname: Horn
authors.forename: P
authors.initials: P
authors.lastname: d'Ascanio
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D002415:Cats; D002799:Cholinergic Fibers / Q000502:physiology; D003000:Clonidine / Q000494:pharmacology; D003655:Decerebrate State / Q000503:physiopathology; D004347:Drug Interactions; D007545:Isoproterenol / Q000494:pharmacology; D008125:Locus Coeruleus / Q000502:physiology; D011149:Pons / Q000187:drug effects / Q000502:physiology*; D011187:Posture / Q000502:physiology; D011433:Propranolol / Q000494:pharmacology; D012018:Reflex / Q000502:physiology*; D012154:Reticular Formation / Q000187:drug effects / Q000502:physiology; D012399:Rotation; D012895:Sleep, REM / Q000502:physiology; D014722:Vestibule, Labyrinth / Q000502:physiology*
chemical_list: D002217:Carbachol; D011433:Propranolol; D007545:Isoproterenol; D003000:Clonidine