Accommodative response of the eye to electrical stimulation of the ciliary ganglion in cats.
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In the frog optic tectum, at the depth of 200-270 micron extracellular monosynaptic PSPS of one axon were recorded under threshold electrical stimulation of the retina by a short train of stimuli. The latency of presynaptic spike was 8-12 ms. At a 5-25 ms interval between successive stimuli a negative spike was observed on the top of the testing EEG quanta enlarged 1.5-2.5 times. This spike is considered to be a population discharge evoked by the firing of a single fibre of the optic tract. This fibre terminates in layer F or G, while the population spike is generated by the tectum units of layers 6-8. A possibility that the firing of the 3d-5th class detectors excites tectal ganglionic cells whose axons form the main part of the tectobulbospinal tract is discussed.
Developmental changes in heartbeat pacemaker mechanisms were examined electrophysiologically in the isopod crustacean Ligia exotica. The heartbeat of embryos and early juveniles was myogenic. The heart muscle cells were coupled electrically, and no localized pacemaker activity was found in the heart. In newly hatched juveniles, the cardiac ganglion exhibited no spontaneous activity, although stimulation of the cardiac ganglion produced excitatory junctional potentials (EJPs) in the heart muscle. The myogenic activity of the heart was reset and entrained by the EJPs evoked by ganglionic stimulation. During juvenile development, spontaneous EJPs appeared irregularly in the heart muscle. Later in development, the cardiac ganglion started rhythmic bursting, and each muscle response followed a ganglionic burst discharge and overlapped the EJPs evoked by ganglionic activity. At this point, the activity of the cardiac ganglion was suppressed by application of tetrodotoxin (TTX); however, even in old adults, both muscle activity and the heartbeat continued following TTX application. Heartbeat frequency was lower in TTX-containing saline than in normal saline. These results show that, during juvenile development, the heart pacemaker is transferred from the heart muscle to the cardiac ganglion, which becomes the primary pacemaker and entrains the heart muscle activity to a higher frequency via EJPs.
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The reaction of rat parietal cortical vessels to stimulation of the sympathetic ganglion was studied by intravital microscopy. stimulation induced constriction of cerebral arterioles. Clamping of one or both carotid arteries led to myogenic vasodilatation in the majority of cases. Constrictive response of brain arterioles to ganglion stimulation under conditions carotid occlusion did not differ from that under conditions of baseline cerebral blood supply.
Effects of selective applications of drugs to the guinea pig hypogastric ganglion were studied on the contractile response of the vas deferens to the hypogastric nerve stimulation or to ganglionic stimulating drugs. Both acetylcholine (ACh) and dimethylphenylpiperazinium (DMPP) contracted the vas deferens. Neostigmine potentiated the ACh-induced contractions but not those which were DMPP-induced. Hemicholinium-3 (HC-3) reduced the response to nerve stimulation (R-NS) but affected neither the ACh-induced contractions nor the DMPP-induced contractions. Morphine blocked R-NS but not the ACh-induced and the DMPP-induced contractions. Hexamethonium reduced R-NS and the contractions to ACh or to DMPP. Methacholine and bethanechol applied before and after preganglionic tetanic stimulation of the hypogastric nerve produced no change of tone of the vas deferens. Atropine did not antagonize the responses which were produced by nerve stimulation, ACh or DMPP. These results support the classic hypothesis that ganglionic transmission is mediated by nicotinic receptors but do not provide evidence that muscarinic receptors exist at the synapses of this preparation.
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The effects of increased synaptic stimulation of sympathetic neurons on the tyrosine hydroxylase activity of these cells were studied. Seventy-two hours after unilateral stimulation of the preganglionic cervical sympathetic trunk at 10 Hz for 30 min tyrosine hydroxylase activity was 32% higher in stimulated than in control superior cervical ganglia. Stimulation at 10 Hz for only 10 min increased enzyme activity by 25% when measured 72 h later, while stimulation for 60 min increased activity by 73%. No further change in enzyme activity was found after 90 min of stimulation although electrophysiological recordings from the ganglion demonstrated that synaptic transmission was maintained throughout the period of stimulation. Ganglionic neurons also follow high frequency trains of stimuli when they are interrupted by silent periods. Stimulation with 40 Hz trains (250 msec on/500 msec off) for 30 min and 90 min produced a 50% and a 92% increase in tyrosine hydroxylase activity, respectively. Stimulation of ganglia with the same number of pulses administered either continuously or in trains produced the same size increase in enzyme activity. The relationship between preganglionic nerve activity and tyrosine hydroxylase activity may represent an adaption of sympathetic neurons to situations requiring increased transmitter release.
1. Direct electrical stimulation (0.05 ms, 5.0 V and 30 Hz) caused negative chronotropic and inotropic effects on the blood-perfused, isolated dog atrium. 2. These negative effects of electrical stimulation were significantly blocked not only by treatment with atropine or tetrodotoxin, but also by hexamethonium, although hexamethonium did not modify the effects of injected acetylcholine. 3. These results suggest that direct electrical stimulation on the isolated, blood-perfused dog atrium readily causes a release of acetylcholine by excitation of parasympathetic pre-ganglionic fibers.
The central terminals of the primary sensory trigeminal ganglion (TG) neurons projecting into the caudal trigeminal nucleus (CTN) of the rat exhibit neurokinin A (NKA)-, substance P (SP)-, and calcitonin gene-related peptide (CGRP)-immunoreactivities (IRs). We stimulated the TG in the rat to induce some of the alterations which might occur during migraine (neurogenic inflammation). Under a stereotaxic apparatus and by means of a bipolar electrode, one-side TG of the animals were electrically stimulated (7.5 Hz, 5 ms, 0.8-1. 4 mA) with square pulses for 5 min. Then, using immunohistochemical methods, the lower medulla of each rat was studied for NKA-, SP- and CGRP-IRs. Light microscopic examination of brain-stem sequencial sections revealed a simultaneous decrease in the immunoreactivities of all neuropeptides (NKA, SP and CGRP) in the CTN ipsilateral to TG stimulation in comparison with the other (not stimulated) side CTN. It is suggested that this decrease in immunoreactivity would be due to the co-release of neuropeptides following noxious stimuli and that NKA, SP and CGRP might therefore act as co-transmitters or co-modulators at the first central synapses of the trigeminal sensory pathway.
BACKGROUND: Nicotine has been shown to release nitric oxide from nerves in human sigmoid colon. This effect has been used to investigate the innervation and functional relationship of the longitudinal and circular muscle layers. METHODS: Strips of longitudinal and circular muscle were obtained from 19 patients with colorectal cancer. The strips from ten patients were subjected to electrical field stimulation (EFS) in vitro using stimulus parameters for selective stimulation of nerves. The effect of nicotine 1-10 micromol/l on EFS responses was then measured in the presence and absence of a nitric oxide synthase inhibitor, nitro-L-arginine methyl ester (L-NAME) 200 micromol/l. The effect of nicotine on spontaneous activity was investigated in the muscle strips from the other nine patients. RESULTS: Both longitudinal and circular strips responded to EFS with contraction. The time to achieve a peak contractile response (time to peak; TTP) was significantly longer (P<0.001) in circular strips. L-NAME reduced the mean(s.e.m.) TTP in circular muscle from 23.3(2.0) to 17.2(1.5) s (P=0.007) and altered its pattern of response to resemble that of longitudinal muscle. Nicotine 10 micromol/l reduced the contraction to EFS in circular (P<0.001) but not in longitudinal (P=0.347) muscle. The nicotine-induced reduction in circular muscle contraction was blocked by L-NAME 200 micromol/l (P=0.005). CONCLUSION: These findings suggest that nitric oxide release on neural stimulation is greater in circular than in longitudinal muscle.
1. Anaesthetized rabbits were infused for 20 min with 85 mug-kg-1-min-1(+/-)-alpha-methyladrenaline. The hearts dissected 15 min after the infusion contained 1.49 mug/g alpha-methyladrenaline; the endogenous noradrenaline content was correspondingly decreased. 2. Hearts from alpha-methyladrenaline-infused animals were isolated with the right sympathetic nerves intact and perfused. Ventricular rate, right atrial and right ventricular tensions were recorded using the transverse method. 3. Electrical stimulation (10 Hz, 1 ms, 1 min) of sympathetic nerves, perfusion with the nicotinic drug, p-aminophenethyltrimethylammonium (PAPETA) or perfusion with 54 mM KCl (high K+) solution evoked an output of both alpha-methyladrenaline and noradrenaline. The ratio of the amines in the perfusates was similar to that found in the hearts after termination of the experiments or in non-perfused hearts. 4. Methacholine perfused before and during sympathetic nerve stimulation, PAPETA or high K+ inhibited the release of both false transmitter and noradrenaline. These effects were reversed by atropine. Similarly, lowering the calcium chloride concentration of the medium from 1.8 to 0.1 mM decreased amine outputs. This was reversed by washing. 5. Tyramine evoked a preferential release of the false transmitter that was not altered by methacholine or calcium deprivation. 6. These experiments whow that the muscarinic inhibition of neuronal noradrenaline release and the requirement of calcium ions for its liberation by depolarizing stimuli can be extended to a false transmitter amine. It is suggested that the proportion of alpha-methyladrenaline to noradrenaline occurring in the perfusate during administration of tyramine reflects the relative concentrations of the amines in the axoplasm.
RATIONALE: The effects of drugs on performance of tasks used to assess attention might be confounded with changes in motivation. Few studies have investigated the role of motivational factors in such situations. OBJECTIVES: To determine how changes in motivation for food influence performance of the 5-choice serial reaction time task and whether the effects of nicotine and amphetamine can be explained by motivational changes. METHODS: Male hooded Lister rats were trained to respond to a 1-s light stimulus presented randomly in one of five apertures in order to obtain food reinforcers. For three groups of rats (n=9-10), access to food was restricted to maintain body weights at 80, 90 or 95% of control weights. Saline and nicotine (0.025-0.2 mg/kg) were tested in each group, with and without pre-feeding (5 g). In a second experiment, saline and amphetamine (0.03-0.9 mg/kg s.c.) were tested without pre-feeding. RESULTS: High levels of motivation for food were associated with increases in anticipatory responses, fewer omission errors, shorter response latencies and completion of more trials, without change in accuracy. Nicotine, but not amphetamine, increased accuracy and the number of trials completed; whereas amphetamine, but not nicotine, increased omission errors. Both drugs decreased anticipatory responding at the largest doses tested. There were few interactions of motivational level with drug effects. CONCLUSIONS: The improvements in performance produced by nicotine did not resemble the effect of increased motivation, but some effects of amphetamine resembled those of reducing the level of motivation for food. Motivational levels did not confound assessments of the attentional effects of the drugs in terms of response accuracy.
Intracellular recordings were made from neurons in rabbit vesical pelvic ganglia (VPG), in vitro. Increasing the frequency of preganglionic-nerve stimulations from 0.1-1 Hz to 10-20 Hz facilitated fast excitatory postsynaptic potentials (EPSPs), resulting in a generation of action potentials. Acetylcholine-induced response was not altered during the facilitation of the fast EPSP. Serotonin blocked action potentials elicited by preganglionic-nerve stimulations at 0.1 Hz, while it caused no blockade at 10 Hz. Serotonin may potentiate the feature of high-pass filter in transmission of VPG. Immunohistochemical study demonstrated serotonin-like varicose terminals in rabbit VPG.
Inhibitory actions of the medial trigon of the caudal medulla (ITM) with special reference to the paramedian reticular nucleus (PRN) were explored in cats under chloralose (40 mg/kg) and urethane (400 mg/kg) anesthesia. Stimulation with square wave pulses (80 Hz, 1 msec, 100-200 microA) produced a reduction of mean systemic arterial blood pressure (MSAP) of 15-90 mmHg, and change in heart rate (HR) that varied from mild increase of 15 to reduction of 85 beats/min. These responses were not affected by mid-collicular decerebration nor by bilateral vagotomy. Destruction of PRN did not change the resting MSAP, HR or baroreceptor reflex responses. Stimulation of PRN suppressed the sympathetic pressor and cardioacceleratory and the vagal bradycardia responses resulting from activating cardiovascular (CV) regulatory mechanisms in the hypothalamus, midbrain and medulla, or from activating the somatic or the baroreceptive afferents. Activation of the PRN suppressed the MSAP-increase produced by direct stimulation of the stellate or celiac ganglion. PRN stimulation could eliminate the pronounced CV reactions consequent either to asphyxial anoxia during occlusion of the trachea or to cerebral ischemia following occlusion of vertebral and carotid arteries. Furthermore, PRN activation could stop the general convulsion of the animal induced by picrotoxin, 4 mg/kg, IV. Our findings suggest that in the trigon area especially in the PRN, there resides an independent mechanism which exerts very powerful and broad inhibitory actions on the autonomic as well as somatic nervous system.
Little research has addressed McNally's hypothesis [(1996). Anxiety sensitivity is distinguishable from trait anxiety. In: R. M. Rapee (Ed.), Current controversies in the anxiety disorders (pp. 214-227). New York: The Guilford Press.] that anxiety sensitivity (AS) should be negatively associated with the use of arousal-increasing substances. In the present study, we examined the relationship between AS and the self-reported use of two widely available stimulants--nicotine and caffeine--and exercise frequency in a sample of 256 university students. A measure of trait anxiety was also incorporated within the design. The associations between use of both substances and levels of AS and trait anxiety were weak and nonsignificant. Although inconsistent with McNally's hypothesis, some significant findings were found when the lower-order components of AS (i.e., fears of physical, psychological, and publicly observable symptoms of anxiety) were examined. The associations between exercise frequency and the anxiety measures, indicating a negative relationship, were generally consistent with McNally's hypothesis. Implications of these findings are discussed with reference to future investigation.