Noradrenergic hyperinnervation of the trigeminal sensory nuclei.

Administration of 6-hydroxydopamine to neonatal rats results in a permanent increase in the norepinephrine content in several brainstem areas. To assess the physiological effects of this hyperinnervation, we studied the noradrenergic inhibition of transmission of sensory information through the principal sensory and rostral spinal trigeminal nuclei. Unit activity produced by tactile stimulation of the face was recorded extracellularly from trigeminal sensory neurons in normal and hyperinnervated rats. The noradrenergic neurons projecting to the trigeminal sensory nuclei (locus coeruleus and the region of the lateral lemniscus) were stimulated 40 ms prior to delivery of a tactile stimulus to the face, producing complete inhibition. The interstimulus interval was then increased in 100 ms increments until the sensory response returned to control values. Compared with controls, the duration of inhibition was 30% longer in hyperinnervated rats and 25% shorter in rats depleted of catecholamines with reserpine and alpha-methyl-p-tyrosine. While the beta-adrenergic blocker, propranolol, had no effect on the duration of inhibition in normal animals, the mean latency of response to tactile stimulation was decreased from 15.3 to 10.4 ms. Propranolol given to hyperinnervated rats decreased the latency of the response to tactile stimulation from 15.1 to 9.1 ms and decreased the duration of inhibition by 40% compared with untreated hyperinnervated rats, suggesting an alteration in numbers or sensitivity of beta-receptors. Since the drug treatment never eliminated the inhibition due to locus coeruleus stimulation, there is also a non-noradrenergic component. We conclude from these observations that noradrenergic hyperinnervation is not completely counteracted by receptor down regulation.