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At least 757 records · Page 42Linked to original sources
PubMed1989

Effects of nicotinic agonists and antagonists on N-methyl-D-aspartate-induced 3H-norepinephrine release and 3H-(1-[1-(2-thienyl)cyclohexyl]-piperidine) binding in rat hippocampus.

The nicotinic agonists dimethylphenylpiperazinium iodide (DMPP) and carbachol (CARB) as well as (-)nicotine [-)NIC) were tested alone and in combination with N-methyl-D-aspartate (NMDA) for their abilities to enhance the efflux of 3H-norepinephrine (NE) from slices of rat hippocampus. CARB and (-)NIC produced small, transient increases in NE efflux, while DMPP produced larger, longlasting increases. Inasmuch as the nicotinic antagonists mecamylamine (MECA) and hexamethonium (C6) did not consistently inhibit the increases in NE efflux produced by these agonists, the role of a nicotinic receptor in mediating these responses is uncertain. CARB and DMPP enhanced the ability of NMDA to stimulate NE release, while (-)NIC did not. MECA, but not C6, was found to selectively antagonize NMDA-stimulated NE release that did not appear to involve a nicotinic receptor. Binding studies indicated that MECA and the related nicotinic antagonist pempidine produced an inhibition of NMDA-stimulated NE release by an action at the PCP receptor that is known to be linked to the NMDA receptor-ionophore complex. These data suggest that the actions of these ganglionic blocking agents on excitatory responses in the hippocampus involve inhibition of excitatory amino acid as well as nicotinic receptors.

Animals↗
PubMed1996

Nicotine injections into the ventral tegmental area increase locomotion and Fos-like immunoreactivity in the nucleus accumbens of the rat.

Systemic administration of nicotine has been shown to increase locomotor activity in rats, an effect which is enhanced by chronic pretreatment with the drug. Furthermore, administration of nicotine either systemically, or locally within the ventral tegmental area (VTA), increases extracellular levels of dopamine (DA) in the nucleus accumbens (NAc). In the present study, we examined the effect of local, bilateral injections into the VTA of nicotine (0.02, 0.2, 2.0 and 8.0 micrograms/0.5 microliter/side) on locomotor activity of rats in an open field. Nicotine (8.0 micrograms/side) significantly increased forward locomotion within 20 min after injection, whereas rearing was not affected. The stimulatory effect of locally applied nicotine was completely blocked by pretreatment with mecamylamine (1.0 mg/kg, s.c.). Repeated intra-tegmental injections of a subthreshold dose of nicotine (2.0 micrograms/side every 2 days), gradually increased locomotion, compared to the effect of acute intra-tegmental administration or control injections of saline, after the fifth and sixth injection. The effects of intra-tegmental injections of nicotine were further investigated on cells in several target areas for the VTA-DA neurons through determination of c-fos expression by means of Fos immunohistochemistry. Intra-tegmental injections of nicotine (8.0 micrograms/side) increased Fos-like immunoreactivity in the NAc, but did not affect the number of Fos-positive nuclei in the medial prefrontal cortex or in the dorsolateral striatum. The increase in accumbal Fos-like immunoreactivity was attenuated by pretreatment with mecamylamine (1.0 mg/kg, s.c.). Our data demonstrate that locomotor activating effects similar to those evoked by systemically administered nicotine, including behavioral sensitization, can be produced by intra-tegmental nicotine administration. Moreover, such local VTA administration of the drug was found to significantly affect neurons within DA target areas. Our findings support the notion that the effects of systemically administered nicotine in mesolimbic target areas are largely dependent on stimulation of nicotinic receptors in the VTA.

Animals↗
PubMed2001

Na(+)-dependent fluid absorption in intact perfused rat colonic crypts.

BACKGROUND & AIMS: The traditional paradigm of fluid movement in the mammalian colon is that fluid absorption and secretion are present in surface and crypt cells, respectively. We have recently demonstrated Na(+)-dependent fluid absorption in isolated crypts that are devoid of neurohumoral stimulation. We now explore the mechanism of Na(+)-dependent fluid absorption in isolated rat colonic crypts. METHODS: Net fluid absorption was determined using microperfusion techniques and methoxy[(3)H]inulin with ion substitutions and transport inhibitors. RESULTS: Net fluid absorption was reduced but not abolished by substitution of either N-methyl-D-glucamine- Cl(-) or tetramethylammonium for Na(+) and by lumen addition of 5-ethylisopropyl amiloride, an amiloride analogue that selectively inhibits Na(+)-H(+) exchange. Net fluid absorption was also dependent on lumen Cl(-) because removal of lumen Cl(-) significantly (P < 0.001) reduced net fluid absorption. DIDS at 100 micromol/L, a concentration at which DIDS is an anion exchange inhibitor, minimally reduced net fluid absorption (P < 0.05). In contrast, either 500 micromol/L DIDS, a concentration at which DIDS is known to act as a Cl(-) channel blocker, or 10 micromol/L NPPB, a Cl(-) channel blocker, both substantially inhibited net fluid absorption (P < 0.001). Finally, both the removal of bath Cl(-) and addition of bath bumetanide, an inhibitor of Na-K-2Cl cotransport and Cl(-) secretion, resulted in a significant increase in net fluid absorption. CONCLUSIONS: (1) Net Na(+)-dependent net fluid absorption in the isolated colonic crypt represents both a larger Na(+)-dependent absorptive process and a smaller secretory process; and (2) the absorptive process consists of a Na(+)-dependent, HCO(3)(-)-independent process and a Na(+)-independent, Cl(-)-dependent, HCO(3)(-)-dependent process. Fluid movement in situ represents these transport processes plus fluid secretion induced by neurohumoral stimulation.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

Kinetic properties of nicotinic receptors in cultured rat sympathetic neurons from superior cervical ganglia.

AIM: To analyze the kinetic properties of the effect of nicotine on nicotinic acetylcholine receptors (nAChR) in the cultured sympathetic neurons from neonatal rat superior cervical ganglia (SCG). METHODS: The whole-cell recording method of patch-clamp technique was used to record the currents induced by different concentrations of nicotine. The concentration-response of nicotine was fitted with Clark equation. RESULTS: Hill coefficient (1.097) was determined by fitting the nicotine responses of neuronal nAChR with Clark equation. The theoretical values of nicotine effect, calculated with Clark equation with H = 1, were basically identical with the practically recorded currents. CONCLUSIONS: Interaction of nicotine and nAChR in rat SCG fits a single binding site model.

Animals↗
PubMed1989

[The relationship between pilocarpine induced autonomic ganglia stimulating activity and salivary secretion of submandibular gland in pithed rat].

Superior cervical ganglion (SCG)-mediated effect of Pilocarpine (pilo.) on salivation of the rat submandibular gland was investigated. A total of 32 SD male rats, aged 12 weeks was divided into 4 experimental groups I to IV. They were anesthetized by pentobarbital (75 mg/kg, i.p.) and tracheotomized to allow artificial respiration. These rats were then ectomized only right SCG, leaving left SCG and injected with pilo. (8 mg./kg, i.v.). Rats of group I which were treated in the manner stated above were used as a control. Rats of group II and IV, of which adrenal glands were removed 18 hr before, were pithed 20 min before the injection of pilo. Rats of group III and IV were administered hexamethonium (C6) (1 mg/kg, i.v.). 5 min before the injection of pilo. Saliva from groups I to IV were collected separately from both salivary glands and flow rate of saliva were measured. Concentration of Na and K were also measured and total amounts of Na and K were calculated. 1) The flow rate induced by pilo. showed a tendency of increase in SCG-ectomized rats. 2) The flow rate showed also a tendency of increase in pithed rats. 3) The concentration and total amount of protein in saliva were decreased by SCG-ectomy. 4) The concentration of K was decreased in only SCG-ectomized rats whereas the total amount of K was closed in group I and II in spite of pithing and/or SCG ectomy. This reduction in K concentration seems to be caused by the increased flow rate as mentioned in paragraph 1). 5) SCG stimulating effect by pilo. was not antagonized, but rather activated by C6. 6) Submandibular ganglion-stimulating effect of pilo. was revealed in group III receiving C6, but this effect was extinguished in pithed rats of group IV. Considering of these results, it is proposed that SCG-stimulating ability of pilo., as shown previously by others, would be caused by activation of M1 receptor, which has sympathetic nerve stimulating effect on salivary glands, and may modify the salivation induced by stimulating effect of pilo. on M2 receptor. Moreover, results obtained with group III suggest that pilo. has submandibular ganglion-stimulating activity, although it's detailed mechanism is unknown.

Animals↗
PubMed1990

[Herpes simplex virus latency in the cornea].

We tried to identify herpes simplex virus type 1 (HSV-1) latency in the cornea obtained at the time of penetrating keratoplasty from patients with herpetic stromal keratitis in the non-active (subsided) stage. The subject consisted of 8 patients (3 males and 5 females; average age 42.3 years) who were diagnosed as having herpetic stromal keratitis and underwent penetrating keratoplasty during a period without active lesions (subsided stage) between August, 1984 and July, 1988. No infective virus was detected in the centrifugation supernatant following each corneal homogenization. Latent virus was detected from the culture supernatant of sections of the corneas in 4 of the 8 patients. Although the ganglion trigger theory of Hill et al. has been conventionally supported as the mechanism(s) of herpetic keratitis recurrence, our results suggest that HSV-1 proliferation from latency in the cornea (peripheral tissue) might stimulate the ganglion (ganglion and skin trigger theory). The present study is the first to demonstrate HSV-1 latency in the cornea.

Adult↗
PubMed2004

Calcium channel antagonists attenuate cross-sensitization to the rewarding and/or locomotor effects of nicotine, morphine and MK-801.

The present study focused on the evaluation of behavioural cross-sensitization, particularly in locomotor activities and conditioned rewarding effects, between nicotine and morphine, cocaine, amphetamine or MK-801. Nicotine (0.5 mg kg(-1))-experienced mice manifested an enhanced locomotor response to morphine (5 mg kg(-1)) or MK-801 (0.3 mg kg(-1)). No cross-sensitization was observed between nicotine and amphetamine (2 mg kg(-1)) or cocaine (15 mg kg(-1)). Additionally, the L-type voltage-dependent calcium-channel antagonists, nimodipine and verapamil, but not diltiazem, at a dose of 20 mg kg(-1) injected before morphine or MK-801 challenge, blocked the expression of this cross-sensitization. In the second test, an enhancement of morphine place conditioning in rats pre-exposed to nicotine (0.5 mg kg(-1), injected daily for 5 days) was demonstrated. After two conditioning sessions, morphine (5 mg kg(-1)) induced a clear place preference only in animals that had previously received nicotine injections. The administration of nimodipine (10 and 20 mg kg(-1)), verapamil (10 and 20 mg kg(-1)) and diltiazem (10 and 20 mg kg(-1)) prior to nicotine dose-dependently prevented this sensitization to the rewarding effect of morphine produced by prior injections of nicotine. These findings support the hypothesis that similar neural calcium-dependent mechanisms are involved in the appetitive effects of nicotine and morphine and in the sensitized locomotor stimulant effects of nicotine and morphine or MK-801.

Animals↗
PubMed2003

Sprouting of axon-like processes from axotomized retinal ganglion cells induced by normal and preinjured intravitreal optic nerve grafts.

The failure of axonal regeneration in the mammalian central nervous system (CNS) is currently attributed to the glial environment of the lesion site which elaborates a multitude of inhibitory factors. Less attention has been paid to the potential of trophic support associated with the CNS, especially in relation to the status of the damaged CNS after an injury has been evoked. Using a grafting paradigm to implant an optic nerve (ON) segment into the vitreous, we have addressed how a prior damage of the ON before grafting influences its ability to stimulate retinal ganglion cells (RGCs) to sprout axon-like processes. Our results showed that a normal noninjured ON implanted intravitreally stimulated sprouting of RGCs, as revealed by sliver staining of the sprouting cells, as well as increasing the number of RGCs which express GAP-43. A prior crush injury of the ON 7 days before its implantation into the vitreous resulted in a significant decrease in its ability to stimulate RGC sprouting when the crush lesion segment was used as the graft, whereas grafts taken from segments proximal and distal to the lesion segment had potencies similar to that of the noninjured graft. Both astrocytes and oligodendrocytes were drastically reduced in number in the lesion segment graft, suggesting their involvement in the secretion of soluble trophic factors that may play a role in the sprouting and regeneration of damaged neurons.

Animals↗
PubMed1963

THE RELEASE OF ACETYLCHOLINE BY SYMPATHETIC NERVE STIMULATION AT DIFFERENT FREQUENCIES.

Supramaximal stimulation of the periarterial nerves in the mesentery to the rabbit isolated ileum causes inhibition which is increased when hyoscine is added to the bath. This increase is, however, usually seen only when the stimulus frequency is low, and the addition of hyoscine usually makes no difference when the frequency is 10 shocks/sec or more. The observations suggest that, at low frequency, stimulation releases both acetylcholine and noradrenaline, but that at higher frequencies only noradrenaline is released. Similar observations have been made for the nictitating membrane of the cat. When the postganglionic fibres from the superior cervical ganglion were stimulated supramaximally, the contractions of the membrane increased in size as the frequency rose. In the presence of hyoscine the contractions were smaller, the greatest difference being for the lowest stimulus frequency, the difference diminishing as the frequency rose. These observations are consistent with the view that sympathetic cholinergic fibres in many situations release acetylcholine to act directly only at low frequencies, and that at higher frequencies the acetylcholine is almost entirely used to release noradrenaline.

Acetylcholine↗
PubMed1984

Nerve growth factor stimulates phospholipid methylation in target ganglionic neurons independently of the cyclic AMP and sodium pump responses.

Suspensions of neurons prepared from embryonic day 12 (E12) chick sympathetic ganglia were incubated with [methyl-3H]methionine in the absence of nerve growth factor (NGF). Presentation of the factor for different periods of time resulted in an approximate three-fold stimulation of radioactivity incorporated into total phospholipid, followed by a rapid decline thereafter. Both the magnitude and the time of the response were dependent on the NGF concentration used. Also examined were possible relationships of phospholipid methylation to two other short-latency responses to NGF, i.e., control of the Na+,K+-pump and elevation of cyclic AMP content. Incubation of E12 sympathetic neurons with known transmethylase inhibitors (shown to be active in the present system) failed to prevent reactivation of the Na+,K+-pump in response to NGF administration. E16 sympathetic neurons and E15 sensory neurons, which do not depend on exogenous NGF for control of their Na+,K+-pump, still show a stimulation of phospholipid methylation when challenged with the factor. Blockage of the pump with ouabain also fails to prevent a methylation response. Thus, the pump and methylation responses to NGF occur independently of each other. Intact E8 chick dorsal root ganglia, but not E12 sympathetic ganglia, display a rapid and transient rise in their cyclic AMP content when presented with NGF. At a concentration of 10 biological units/ml, NGF elicits a peak of phospholipid methylation at 4 min, and a peak of cyclic AMP at 10 min. Methylation inhibitors prevent the methylation response, but not that of cyclic AMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Modification of stimulated lacrimal gland flow by sympathetic nerve impulses in rabbit.

This study was undertaken to determine if sympathetic nerve impulses modify lacrimal gland fluid (LGF) flow, which was continuously recorded from a cannula in the excretory duct of the lacrimal gland in rabbits anesthetized with pentobarbital sodium. The preganglionic trunk of the superior cervical ganglion was stimulated with electrical stimuli during pilocarpine-induced and reflexly induced secretion. Stimuli equal to or 6-8 times stronger than the intensity that produced maximal pupil dilation caused inhibition followed by poststimulus enhancement of LGF flow when the prestimulus LGF flow was greater than 3.0 mul/min. When the prestimulus LGF flow was less than 0.8 mul/min, the stronger stimulation enhanced LGF flow but the weaker stimulation produced inhibition followed by poststimulus enhancement of LGF flow. Although no measurements of lacrimal gland blood flow were made, the alterations in these responses, which occurred during alpha- and beta-adrenergic blockade, were consistent with the changes in sympathetically induced blood flow that occur during alpha- and beta-blockade in other organs.

Animals↗
PubMed1981

Functional and structural studies concerning the control of activity in zygomatic glands of cats.

The zygomatic gland of the cat consists of at least two parts, separated by a septum, and each drains by a separate duct opening on a mucosal ridge postero-medial to the parotid orifice. It is composed on thin-walled ducts and tubulo-acini, containing mainly mucous cells, but scattered cap cells are also present. In cats under chloralose anaesthesia there is a spontaneous flow of extremely viscous saliva and often, in addition, there is a reflexly elicited component to the secretion. In fact, in contrast to the other major salivary glands, the zygomatic gland is easily made to secrete reflexly even in deep] anaesthesia, e.g. by pinching ipsilateral parts of the tongue, by stimulation of the oesophagus mimicking swallowing, or by afferent excitation of ipsilateral lingual, glossopharyngeal or vagal nerves. The efferent link of the reflex arc is contained in the buccal branch of the mandibular nerve. Section of this nerve abolishes these reflexes, and two weeks later a great loss of acetylcholinesterase positive nerves can be demonstrated in the gland. Efferent stimulation of the buccal nerve evokes a lively secretion that is not affected by hexamethonium but is abolished by atropine. Histochemically, adrenergic nerves are also found surrounding the acini and these nerves disappear after excision of the superior cervical ganglion. Electrical stimulation of the cervical sympathetic trunk causes some secretion, mainly by way of beta 1-adrenoreceptors. Myoepithelial cells are present around the tubulo-acini, and indications of the effect caused by their contraction on the flow from the glands have been observed. Such activity can be induced reflexly and it is then abolished by cutting the buccal nerve or by injecting atropine.

Acetylcholinesterase↗