Catecholaminergic projections to tuberoinfundibular neurones of the paraventricular nucleus: II. Effects of stimulation of the ventral noradrenergic ascending bundle: evidence for cotransmission.
In order to further elucidate the neural mechanisms underlying the control of adrenocortical secretion, responses of paraventricular nucleus (PVN) tuberoinfundibular neurones were examined following stimulation of the ventral noradrenergic ascending bundle (VNAB). Stimulation at low frequencies (0.5/5 Hz) excited the majority (52/64, 81%) of cells but only 15 showed a clear-cut, stimulus-locked, activation with onset latency of 44.5 +/- 10.0 msec and offset at 71.9 +/- 11.3 msec: the remaining 37 excited cells showed overall increases in firing after delivery of 5-10 stimuli. High frequency (50 Hz) trains of stimuli reversed the direction of response to inhibition for 14/52 of the excited cells. Inhibition of (nor)adrenaline synthesis by alpha-methylparatyrosine was without effect upon the firing of cells examined or the distribution and latencies of their responses following low frequency stimulation; high frequency trains reversed the response direction of only 4/35 cells, (p less than 0.05 vs. control rats; chi 2-test). Intracerebroventricular administration of 6-hydroxydopamine, a catecholaminergic neurotoxin, reduced the proportion of cells excited by the stimulation (10/47; p less than 0.005; chi 2-test). Unit responses to painful somatosensory stimuli were recorded from the majority of the cells tested (74%), except following 6-hydroxydopamine treatment, when only 38% were excited (p less than 0.005; chi 2-test). The results demonstrate that the VNAB provides an excitatory input to the PVN and that noradrenaline is probably responsible for this effect but a cotransmitter (neuropeptide Y?) may also be responsible for the observed excitatory responses. Inhibitory responses following high frequency stimulation were probably also mediated by (nor)adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
Saphier
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D
Department of Neurology, Hadassah University Hospital, Jerusalem, Israel.
Feldman
S
S
D000200:Action Potentials; D000818:Animals; D001933:Brain Stem / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004558:Electric Stimulation; D006892:Hydroxydopamines; D008297:Male; D008781:Methyltyrosines / Q000494:pharmacology; D009434:Neural Pathways / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism / Q000502:physiology*; D016627:Oxidopamine; D010146:Pain / Q000503:physiopathology; D010286:Paraventricular Hypothalamic Nucleus / Q000502:physiology* / Q000503:physiopathology; D051381:Rats; D019805:alpha-Methyltyrosine
D006892:Hydroxydopamines; D008781:Methyltyrosines; D019805:alpha-Methyltyrosine; D016627:Oxidopamine; D009638:Norepinephrine