On the non-adrenergic, non-cholinergic contribution to the parasympathetic nerve-evoked secretion of parotid saliva in the rat.
A secretion of parotid saliva in the anaesthetized rat in response to stimulation of the parasympathetic nerve occurs in the presence of atropine and adrenoceptor antagonists, albeit reduced and transient in the face of continuous high-frequency stimulation (40 Hz). In non-atropinized rats prolonged stimulation of the parasympathetic nerve at a high frequency (40 Hz, 40 min), aiming at depletion of the neuronal stores of transmitters thought to be responsible for the non-adrenergic, non-cholinergic (NANC) secretion of parotid saliva, was performed. The magnitude of the secretory response to various stimulation frequencies (0.2-60 Hz) applied to the parasympathetic nerve was assessed before and after the period of high-frequency stimulation. The second time, the frequency-response curve was shifted to the right and, moreover, the initial maximal secretory response was not reached. Control experiments suggested that this reduction in secretory responses could be attributed neither to impaired cholinergic neurotransmission nor to decreased responsiveness of the secretory cells. The secretory responses to parasympathetic nerve stimulation after high-frequency stimulation are thought to be evoked by acetylcholine predominantly. When these responses were compared with (1) those obtained before high-frequency stimulation and thought to be evoked by acetylcholine and non-adrenergic, non-cholinergic transmitters in conjunction and (2) those depending on non-adrenergic, non-cholinergic transmitters only it appears that the non-adrenergic, non-cholinergic transmission contributes to the parasympathetic secretory response at a frequency (0.2 Hz) far below threshold frequency (5 Hz) for the non adrenergic, non-cholinergic evoked secretory response. At frequencies below 20 Hz it appears that acetylcholine and non-adrenergic, non-cholinergic transmitters interact positively thereby enhancing the secretory responses.
Månsson
B
B
Department of Physiology and Biophysics, Lund University, Sweden.
Ekström
J
J
D000818:Animals; D001285:Atropine / Q000008:administration & dosage / Q000494:pharmacology; D004338:Drug Combinations; D005260:Female; D007275:Injections, Intravenous; D016210:Methacholine Chloride / Q000008:administration & dosage / Q000494:pharmacology; D018377:Neurotransmitter Agents / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000502:physiology*; D010306:Parotid Gland / Q000378:metabolism / Q000502:physiology*; D010830:Physostigmine / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012463:Saliva / Q000378:metabolism*; D013373:Substance P / Q000008:administration & dosage / Q000494:pharmacology; D014660:Vasoactive Intestinal Peptide / Q000008:administration & dosage / Q000494:pharmacology
D004338:Drug Combinations; D018377:Neurotransmitter Agents; D016210:Methacholine Chloride; D013373:Substance P; D014660:Vasoactive Intestinal Peptide; D001285:Atropine; D010830:Physostigmine