Violeta Bucinskaite

Effects of Repeated Sensory Stimulation (Electro- acupuncture) and Physical Exercise (Running) on Open- field Behaviour and Concentrations of Neuropeptides in the Hippocampus in WKY and SHR rats

The effects of repeated sensory stimulation (electro‐acupuncture) and physical exercise (running) on open‐field behaviour and on hippocampal concentrations of neuropeptide Y, neurokinin A, substance P, galanin and vasoactive intestinal peptide (VIP)‐like immunoreactivities were studied in WKY (Wistar‐Kyoto) and SHR (spontaneously hypertensive) rats. Significantly higher concentrations of substance P‐like immunoreactivity, neurokinin A‐like immunoreactivity and neuropeptide Y‐like immunoreactivity were found in the hippocampus immediately after 3 weeks of treatment (electro‐acupuncture and running), but not 1 week after the last (tenth) intervention. No changes in galanin‐like immunoreactivity and VIP‐like immunoreactivity were found. The changes in neuropeptide concentrations were similar in the two rat strains. Open‐field behaviour was significantly reduced during the treatment period in both strains. There were significant negative correlations between behaviour and neuropeptide concentrations in SHR rats, suggesting interdependency with sympathetic activity. It is proposed that the effects of electro‐acupuncture and physical exercise in rats are related to increases in neuropeptide Y, neurokinin A and substance P in the hippocampus.

Interleukin-1β sensitizes the response of the gastric vagal afferent to cholecystokinin in rat

Interleukin-1beta (IL-1beta) and cholecystokinin (CCK) are important mediators in the development of anorexic response during disease. The role of IL-1beta and CCK in the peripheral mechanisms of anorexia was studied by recording the mass afferent activity of the gastric vagal nerve in anesthetized rats. The i.v. administration of CCK (1 nmol) increased the activity of the vagal nerve, and this response was raised by 55-72% 2 h after i.v. injection of IL-1beta. It is proposed that IL-1beta-induced anorexia is mediated via the sensitization of type A CCK receptors in the periphery.

Effects of electro-acupuncture and physical exercise on regional concentrations of neuropeptides in rat brain

The effects of single or repeated treatments with manual acupuncture (ACU), electro-acupuncture (ELACU) or physical exercise on neuropeptide Y (NPY), neurokinin A (NKA), substance P (SP), galanin (GAL) and vasoactive intestinal peptide (VIP)-like immunoreactivity (-LI) in different regions of the rat brain were studied. Initially the effect of microwave irradiation (MWI) was compared to decapitation on the recovery of neuropeptides, and significantly higher concentrations of SP-LI, NKA-LI and NPY-LI were found in the hippocampus, occipital cortex, pituitary and striatum following MWI. Repeated ELACU treatments significantly increased SP-LI, NKA-LI and NPY-LI in the hippocampus and NPY-LI in the occipital cortex. No changes were found in animals receiving ACU or performing physical exercise.

Response of the gastric vagal afferent activity to cholecystokinin in rats lacking type A cholecystokinin receptors

A systemic administration of cholecystokinin (CCK) increases gastric vagal afferent activity via type A CCK receptors (CCKAR). In the present study, the response of gastric vagal afferent activity to an intravenous administration of CCK was investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which lack CCKAR, and compared with its control strain, Long-Evans Tokushima Otsuka (LETO) rats. The intravenous administration of 300 pmol kg(-1) and 3 nmol kg(-1) of CCK elicited dose-dependent increases in the gastric vagal afferent activity in LETO rats. The responses were not influenced by the pretreatment with L-365,260, a type B CCK receptor (CCKBR) antagonist, while they were significantly diminished by pretreatment with MK-329, a CCKAR antagonist. After pretreatment with MK-329, 3 nmol kg(-1) (but not 300 pmol kg(-1)) of CCK still elicited a small but significant increase in the activity. In the OLETF rats, both 300 pmol kg(-1) and 3 nmol kg(-1) of CCK produced small increases in the vagal afferent activity, and the responses were not influenced by pretreatment with either L-365,260 or MK-329. In addition, the systemic administration of CCK did not change gastric motility in the OLETF rats, indicating that the response of the vagal afferent activity in OLETF rats was independent of the gastric motility change. These results demonstrate that neither CCKAR nor CCKBR contributes to the response of the afferent activity of the gastric vagal nerve to a systemic administration of CCK in OLETF rats, suggesting an involvement of novel (non-A, non-B) CCK receptors.

Cholecystokinin-8 (CCK-8) has no effect on heart rate in rats lacking CCK-A receptors

Heart rate responses to i.v. administration of cholecystokinin-8 (CCK-8) were investigated in Otsuka Long-Evans Tokushima Fatty (OLETF) rats lacking CCK-A receptors and control Long-Evans Tokushima Otsuka (LETO) rats. The heart rate decreased after i.v. administration of 3 nmol.kg(-)(1) of CCK-8 in LETO rats, but not in OLETF rats. Bradycardia in the LETO rats disappeared after treatment with MK-329, but not after treatment with L-365,260. The expression of CCK-A receptor precursor mRNA was found exclusively in the atrium in LETO rats. These results suggest that CCK-8 decreases heart rate via CCK-A receptors located in the atrium of the rats.

Exogenous cholecystokinin‐8 reduces vagal efferent nerve activity in rats through CCKA receptors

It has been proposed that the vagus nerve plays a role in mediating cholecystokinin‐8 (CCK‐8) effect on such gastric functions as motility, emptying and gastric acid secretion. To examine the contribution of the efferent pathways in realizing these effects, efferent mass activity in the ventral gastric vagal nerve in Sprague‐Dawley rats was recorded. Intravenous infusion of CCK‐8 (0.1–1 nmol) suppressed the efferent activity. The effect of CCK‐8 was significantly reduced in animals with total subdiaphragmatic vagotomy in comparison to those with partial vagotomy. Intravenous infusion of CCKA receptor antagonist L‐364,718 (1–100×10−6 g) blocked the response of vagal efferent activity to 0.1 nmol CCK‐8, but the CCKB receptor antagonist L‐365,260 (1–100×10−6 g) did not in the conditions of either partial or total vagotomy. Intracisternal infusion of L‐364,718 (1×10−6 g) blocked the response of vagal efferent activity to 0.1 nmol CCK‐8 i.v. Infusion of exogenous CCK‐8 did not affect the activity of supradiaphragmatic vagal afferents. The results suggest that the effect of systemically administered CCK‐8 on vagal efferent activity is mediated by both peripherally (subdiaphragmatically) and centrally localized CCKA receptors.

Effect of interleukin-1β on subdiaphragmatic vagal efferents in the rat

Interleukin-1beta (IL-1beta) is an important mediator of fever and illness. Recent studies have demonstrated that IL-1beta (2 microg kg(-1)) increases gastric vagal afferent activity. The peripheral mechanisms of the action of lower doses were studied by recording the mass efferent and afferent activity of the gastric branch of the ventral vagal nerve in anesthetized rats. Twenty min after i.v. administration of IL-1beta (1 microg kg(-1)) the efferent activity of the vagal nerve was decreased to 62+/-6% in totally but not in partly vagotomized rats. Preadministration of indomethacin (5 mg kg(-1)) 30 min before IL-1beta blocked this reduction. Administration of 1 microg kg(-1) of IL-1beta had no effect on the afferent activity of the gastric branch of the vagal nerve. The present results suggest that the subdiaphragmatic vagal afferents modulate the parasympathetic efferent outflow in response to IL-1beta partly through prostaglandin dependent mechanisms and that supradiaphragmatic afferents or central sites are more sensitive to the low doses of IL-1beta which becomes evident after elimination of the subdiaphragmatic vagal input.

Changes of neuropeptide concentrations in the brain following experimentally induced mononeuropathy in Wistar Kyoto and spontaneously hypertensive rats

The effect of unilateral, experimentally induced, mononeuropathy on concentrations of neuropeptide Y (NPY), neurokinin A (NKA), substance P (SP), calcitonin gene-related peptide CGRP) and galanin- (GAL-) like immunoreactivities (-LI) was studied in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rat brains. Two weeks following ligation of the sciatic nerve, significantly higher concentrations of NPY-LI were found in the hippocampus, striatum and occipital cortex of both rat strains. CGRP-LI and GAL-LI were increased in the hippocampus of WKY rats. NKA-LI and SP-LI were decreased to different degrees in the pituitary of the WKY and SHR rats, indicating that the changes of the tachykinins, CGRP and GAL were selectively associated with the basal level of sympathetic tone. The increased concentrations of NPY-LI in the brain, not influenced by sympathetic tone, may be part of a general defense reaction in response to trauma.

Increased concentrations of calcitonin gene.related peptide-like immunoreactivity in rat brain and peripheral tissue after ischaemia: correlation to flap survival

The effects of experimentally induced ischaemia after free-flap surgery on concentrations of neuropeptide Y (NPY), neurokinin A (NKA), substance P (SP) and calcitonin gene-related peptide (CGRP)-like immunoreactivity (-LI) were studied in flap tissue and in different regions of the rat brain (striatum, hippocampus, pituitary, hypothalamus, frontal and occipital cortex). Ten days after the operation, CGRP-LI and NKA-LI were decreased in the ischaemic tissue but increased in the surrounding tissue. In the brain, CGRP-LI was increased in five of six regions analysed, with the exception of the striatum. SP-LI and NKA-LI were increased in the pituitary and hippocampus, but decreased in other brain regions. Changes of CGRP-LI in the brain correlated positively with the CGRP-LI concentrations in the surrounding flap tissue and the CGRP-LI concentrations in the ischaemic flap tissue with the extent of flap survival. The results of the present study suggest that higher concentrations of CGRP-LI are related to tissue survival and that endogenous CGRP has a regulatory effect in ischaemia.

Effects of systemic injection of interleukin-1β on gastric vagal afferent activity in rats lacking type A cholecystokinin receptors

We have shown that systemic administration of interleukin-1beta (IL-1beta) excites gastric vagal afferent activity in part via stimulation of type A cholecystokinin (CCK-A) receptors in rats. The present study was undertaken to determine whether the response of the gastric vagal afferent nerve to systemic IL-1beta is altered in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, which lack CCK-A receptors. The response was compared with that of the control strain, Long-Evans Tokushima Otsuka (LETO) rats. All animals were anesthetized with pentobarbital and artificially ventilated. Intravenous administration of 4 microg/kg of IL-1beta increased gastric vagal afferent activity in both LETO and OLETF rats, whereas a smaller dose of 2 microg/kg of IL-1beta increased activity only in the OLETF rats. The present results demonstrate that the response of the gastric vagal afferent activity in CCK-A receptor deficient OLETF rats was more sensitive to intravenous administration of IL-1beta than was in control LETO rats.