Sympathetic mediation of salivation induced by intracerebroventricular pilocarpine in rats

Cecanho, Rodrigo; Anaya, Marcelo; Renzi, Antonio; Menani, José Vanderlei; Luca, Laurival A. De

doi:10.1016/s0165-1838(99)00002-8

Cited by 14 publications

(10 citation statements)

References 24 publications

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“…This suggestion is in accordance with results from viral tracing studies that showed mainly parasympathetic efferent fibers from the lamina terminalis to salivary glands (Hübschle et al, 2001). However, the salivation induced by icv administration of pilocarpine can be reduced by cervical ganglionectomy or antagonism of systemic ␣ 1 -adrenoceptors (Cecanho et al, 1999), which suggests that pilocarpine can also act on the brain to increase sympathetic output to the salivary glands. Since the reduction in salivation after cervical ganglionectomy is not total (Cecanho et al, 1999), it is possible that the activation of parasympathetic efferent fibers contributes to the effect of pilocarpine, which would be in agreement with the present results.…”

Section: Discussionsupporting

confidence: 89%

“…However, the salivation induced by icv administration of pilocarpine can be reduced by cervical ganglionectomy or antagonism of systemic ␣ 1 -adrenoceptors (Cecanho et al, 1999), which suggests that pilocarpine can also act on the brain to increase sympathetic output to the salivary glands. Since the reduction in salivation after cervical ganglionectomy is not total (Cecanho et al, 1999), it is possible that the activation of parasympathetic efferent fibers contributes to the effect of pilocarpine, which would be in agreement with the present results. Therefore, it is possible that the regulation of salivation by central cholinergic receptors depends on an interaction of sympathetic and parasympathetic mechanisms, perhaps an interaction in a synergistic manner (Emmelin, 1987;Garrett, 1987).…”

Section: Discussionmentioning

confidence: 99%

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Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

et al. 2003

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Although cholinergic agonists such as pilocarpine injected peripherally can act directly on salivary glands to induce salivation, it is possible that their action in the brain may contribute to salivation. To investigate if the action in the brain is important to salivation, we injected pilocarpine intraperitoneally after blockade of central cholinergic receptors with atropine methyl bromide (atropine-mb). In male Holtzman rats with stainless steel cannulas implanted into the lateral ventricle and anesthetized with ketamine, atropine-mb (8 and 16 nmol) intracerebroventricularly reduced the salivation induced by pilocarpine (4 micro mol/kg) intraperitoneally (133 + 42 and 108 + 22 mg/7 min, respectively, vs. saline, 463 + 26 mg/7 min), but did not modify peripheral cardiovascular responses to intravenous acetylcholine. Similar doses of atropine-mb intraperitoneally also reduced pilocarpine-induced salivation. Therefore, systemically injected pilocarpine also enters the brain and acts on central muscarinic receptors, activating autonomic efferent fibers to induce salivation.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 99%

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

et al. 2003

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“…Moreover, removal of the SCG as well as systemic injection of α-adrenoceptor antagonists reduced the icv pilocarpine-stimulated salivation by 40% compared to sham-operated rats (33). This evidence suggests that sympathetic nerves involved in salivary secretion could be stimulated by direct activation of brain cholinergic receptors.…”

Section: Discussionmentioning

confidence: 80%

Anandamide injected into the lateral ventricle of the brain inhibits submandibular salivary secretion by attenuating parasympathetic neurotransmission

Fernández‐Solari

Prestifilippo

Vissio

et al. 2009

Braz J Med Biol Res

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Our objective was to determine the effect of arachidonylethanolamide (anandamide, AEA) injected intracerebroventricularly (icv) into the lateral ventricle of the rat brain on submandibular gland (SMG) salivary secretion. Parasympathetic decentralization (PSD) produced by cutting the chorda tympani nerve strongly inhibited methacholine (MC)-induced salivary secretion while sympathetic denervation (SD) produced by removing the superior cervical ganglia reduced it slightly. Also, AEA (50 ng/5 μL, icv) significantly decreased MC-induced salivary secretion in intact rats (MC 1 μg/kg: control (C), 5.3 ± 0.6 vs AEA, 2.7 ± 0.6 mg; MC 3 μg/kg: C, 17.6 ± 1.0 vs AEA, 8.7 ± 0.9 mg; MC 10 μg/kg: C, 37.4 ± 1.2 vs AEA, 22.9 ± 2.6 mg). However, AEA did not alter the significantly reduced salivary secretion in rats with PSD, but decreased the slightly reduced salivary secretion in rats with SD (MC 1 μg/kg: C, 3.8 ± 0.8 vs AEA, 1.4 ± 0.6 mg; MC 3 μg/kg: C, 14.7 ± 2.4 vs AEA, 6.9 ± 1.2 mg; P < 0.05; MC 10 μg/kg: C, 39.5 ± 1.0 vs AEA, 22.3 ± 0.5 mg; P < 0.001). We showed that the inhibitory effect of AEA is mediated by cannabinoid type 1 CB1 receptors and involves GABAergic neurotransmission, since it was blocked by previous injection of the CB1 receptor antagonist AM251 (500 ng/5 μL, icv) or of the GABA A receptor antagonist, bicuculline (25 ng/5 μL, icv). Our results suggest that parasympathetic neurotransmission from the central nervous system to the SMG can be inhibited by endocannabinoid and GABAergic systems.

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“…Ma et al 1999; Singh et al 2001) and is used clinically to treat dry mouth (Wiseman & Faulds, 1995). Systemic administration of pilocarpine can induce salivation through at least two mechanisms: (i) direct – through activation of glandular cholinergic receptors, and (ii) neural – through the stimulation of the central nervous system (Renzi et al 1993; Cecanho et al 1999; Renzi et al 2002; Takakura et al 2003). Therefore, one possible explanation for this difference between the submandibular and parotid glands in vivo is that they display different sensitivities to cholinergic agonists.…”

Section: Discussionmentioning

confidence: 99%

Regulation of membrane potential and fluid secretion by Ca²⁺‐activated K⁺ channels in mouse submandibular glands

Romanenko

Nakamoto

Srivastava

et al. 2007

The Journal of Physiology

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We have recently shown that the IK1 and maxi-K channels in parotid salivary gland acinar cells are encoded by the K Ca 3.1 and K Ca 1.1 genes, respectively, and in vivo stimulated parotid secretion is severely reduced in double-null mice. The current study tested whether submandibular acinar cell function also relies on these channels. We found that the K + currents in submandibular acinar cells have the biophysical and pharmacological footprints of IK1 and maxi-K channels and their molecular identities were confirmed by the loss of these currents in K Ca 3.1-and K Ca 1.1-null mice. Unexpectedly, the pilocarpine-stimulated in vivo fluid secretion from submandibular glands was essentially normal in double-null mice. This result and the possibility of side-effects of pilocarpine on the nervous system, led us to develop an ex vivo fluid secretion assay. Mammals express three major paired salivary glands, the parotid, submandibular and sublingual. The morphology, histology and saliva composition are unique for each gland type (Young & Van Lennep, 1977). These differences are most evident in the secretory endpieces, also known as acini, the cells which secrete the water and most of the protein found in saliva. In rodents, the parotid acinar cells are serous, while submandibular acinar cells are seromucous. In contrast, the secretory endpieces of sublingual glands are mixed in nature, containing both mucous and serous demilune cells. The composition of the saliva collected from individual glands varies according V. G. Romanenko and T. Nakamoto contributed equally to this work. This paper has online supplemental material.to the acinar cell type. Parotid glands produce a watery fluid and sublingual glands secrete a thick, ropey saliva due to the exocytosis of heavily glycosylated mucins, whereas submandibular saliva has an intermediate consistency.The mechanism of fluid secretion is generally studied at two levels: (i) the cellular level gives detailed information under well controlled conditions but is an over-simplified model and (ii) the in vivo level provides access to whole organ function, but the interpretation of results is complicated by systemic effects. In the latter case, saliva secretion is often induced by cholinergic agonists such as pilocarpine. It is well established that pilocarpine can stimulate saliva secretion through glandular muscarinic receptors. However, systemic administration of a cholinergic agonist also activates receptors in the brain and peripheral nervous

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Sympathetic mediation of salivation induced by intracerebroventricular pilocarpine in rats

Cited by 14 publications

References 24 publications

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Anandamide injected into the lateral ventricle of the brain inhibits submandibular salivary secretion by attenuating parasympathetic neurotransmission

Regulation of membrane potential and fluid secretion by Ca²⁺‐activated K⁺ channels in mouse submandibular glands

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Sympathetic mediation of salivation induced by intracerebroventricular pilocarpine in rats

Cited by 14 publications

References 24 publications

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Central Muscarinic Receptors Signal Pilocarpine-induced Salivation

Anandamide injected into the lateral ventricle of the brain inhibits submandibular salivary secretion by attenuating parasympathetic neurotransmission

Regulation of membrane potential and fluid secretion by Ca2+‐activated K+ channels in mouse submandibular glands

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Regulation of membrane potential and fluid secretion by Ca²⁺‐activated K⁺ channels in mouse submandibular glands