The pathophysiological mechanisms underlying the loss of intestinal fluid in diarrhea have been the subject of much debate for decades . Diarrhea may be caused by an increase in osmotic load within the intestine, excessive secretion of electrolytes and water into the intestinal lumen, exudation of protein and fluid from the mucosa, infection and inflammation; and altered intestinal motility, resulting in rapid transit . In most instances, multiple processes are simultaneously affected involving several factors, a particular factor becoming a dominant player in a given environment, however, motility and/or secretory disturbances usually remain a common denominator in most cases . The mucosal lining of the gastrointestinal tract is provided with an extensive nerve supply from the enteric nervous system . Neurotransmitters such as acetylcholine and noradrenaline and neurotransmitter candidates such as ATP, CGRP, CCK-8, ENK, GAL, GABA, serotonin, NO, somatostatin, SP, VIP etc have been implicated to different extents in normal and pathophysiological situations. Based on the knowledge gained about the divergent factors controlling the processes of secretion of electrolytes and motility, many interventional strategies have been adopted by researchers and numerous antidiarrheal compounds have been developed but not many compounds are without side effects and therefore there has always been a need for finding new ones.
Acetylcholine is the endogenous neurotransmitter at cholinergic synapses in the central and peripheral nervous system. The stimulation of vagal input to the gastrointestinal tract increases tone, amplitude of contraction and secretory activity of the stomach and intestine. Since such responses are inconsistently seen with administered acetylcholine, possibly because of poor perfusion and rapid hydrolysis by plasma butryl cholinesterase, use of neostigmine was made in the present investigation. Neostigmine is an inhibitor of acetylcholinesterase and increases the amount of acetylcholine at the synapse  and thus exerts a pro-kinetic effect. The results show that the Lantana camara leaf powder and LCME significantly reduced the % intestinal transit in a dose dependent manner. Lantadene A also produced a statistically significant reduction in % intestinal transit.
The induction of diarrhea with castor oil results from the action of ricinoleic acid formed from hydrolysis of its triglyceride in the oil [20, 21]. The released ricinoleic acid produces changes in the transport of water and electrolytes resulting in a hypersecretory response and speeds intestinal transit . The involvement of nitric oxide from neurons in the diarrhea induced by the castor oil has also been proposed . Castor oil increases the induction of prostaglandins , causes changes in the permeability and mucosal injuries and stimulates PAF  biosynthesis which may result in inflammation of intestinal mucosa. The preventive administration of LCME was associated with significant protection against diarrhea induced by castor oil in mice. Lantana camara might possess some compounds with antisecretory properties which may account for its efficacy against diarrhea induced by castor oil in mice.
Lantana camara has been reported to be toxic to grazing animals such as cow, buffaloes, sheep and goats [7, 25] and laboratory animals such as guinea pigs  and female rats . In spite of its widespread toxicity in the Lantana affected animals, various parts of this plant have been used in the traditional medicines for treating cuts, ulcers, swelling, eczema, inflammation, fever etc . Gastrointestinal stasis, ruminal stasis, constipation, discolorization of conjunctiva, photosensitization, decreased bile flow and urinary retention in the Lantana poisoned animals has been noticed [27–29]. These symptoms resembled those due to atropine toxicity i.e., anticholinergic excess [30, 31].
Anti-dysenteric and anti-diarrheal properties of medicinal plants have been suggested to be due to tannins, alkaloids, saponins, flavonoids, sterols and triterpenes and reducing sugars . The sesquiterpene lactones have been reported to have the ability to relax smooth muscles and thereby relieve gastrointestinal disorders . The phytochemical analysis of the Lantana camara leaf extract has earlier been shown to contain flavonoids , terpenes  and their derivatives and pentacyclic triterpenoids . These constituents may mediate the anti-diarrheal action of the Lantana camara extract. A verbascoside  isolated from Lantana camara has been shown to be an inhibitor of protein kinase C. The role of this enzyme has been demonstrated in signal transduction, inflammation and smooth muscle contraction  and an inhibition of its activity by a constituent of Lantana camara shall result in decrease in motility. Although the anti-diarrheal properties of the reported active terpenoids are well established, aspects of their mechanism of action remain poorly understood. Terpenes, flavonoids and terpenoid derivatives may act by inhibiting release of autocoids and prostaglandins [39, 4] thereby inhibit the motility and secretion induced by neostigmine. Intestinal motility alterations in Lantana camara foliage poisoned sheep has been described by Pass et al.  but no mechanism has been suggested.