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PubMed2000

Assessment of trigeminal somatosensory evoked potentials in burning mouth syndrome.

OBJECTIVE: The measurement of pain threshold (PT) and the assessment of trigeminal somatosensory evoked potentials (TSEPs) were performed. These experiments indicated the pathological conditions of nerve afferent and efferent pathways in patients with burning mouth syndrome (BMS). This study also explored the probable pathophysiological mechanisms in BMS. MATERIALS AND METHODS: The dorsum linguae of 38 samples in 19 subjects (22 BMS with pain, 10 BMS with numbness, and 6 controls) were stimulated by electroneuromyography. PT was measured as the lowest stimulation intensity the subjects could detect. N3, P4 latency, and spike potential latency of TSEP were recorded by stimulating the lingual nerve. RESULTS: Pain thresholds were significantly lower, N3, P4 latencies were significantly shorter, and the spike potential appeared earlier in the BMS with pain group (P < 0.01). The opposite tendency of these values presented in the BMS with numbness group (P > 0.05). CONCLUSIONS: The results indicated that the nerve sensitivity was elevated in the BMS with pain group, and that these patients were easily affected by etiological factors. In the BMS with numbness group, partial or complete nerve blockage may have been indicated. This study suggested that selfreports of BMS pain appeared to be of value, and that there were pathological conditions in nerve transmission. It supported the theory that peripheral or central nervous system involvement might play an important role in BMS. It was possible to show the pathogenesis of BMS. All of these objectively explain the clinical understanding of BMS, and may be of assistance in the treatment of BMS.

Afferent Pathways↗
PubMed1977

[Branchial vascularization in the eel: action of acetylcholine and adrenaline on the distribution of polymerizable resin in the different vascular compartments].

The current findings from gill vascular cast preparations in the eel emphasize the division in each primary lamella of the afferent vasculature into two efferent pathways: an arterial pathway (via the secondary lamellae and the efferent branchial artery to the dorsal aorta), a venous pathway (via the central lamellar compartment and the branchial vein to the sinus venosus). By the same technique two antagonist mechanisms have been shown presumably controlling the blood flow in both pathways. 1. Acetylcholine increases the filling of the central lamellar compartment by constricting the efferent arterial sphincters and therefore increases the venous return. 2. Epinephrine impairs the filling of the central lamellar compartment (by acting on alpha receptors) and dilates the arterial pathway (by acting on beta receptors). Therefore the stimulation of these two synergic receptors by epinephrine increases the systemic blood flow.

Acetylcholine↗
PubMed2000

Centrifugal pathways protect hearing sensitivity at the cochlea in noisy environments that exacerbate the damage induced by loud sound.

Loud sounds damage the cochlea, the auditory receptor organ, reducing hearing sensitivity. Previous studies demonstrate that the centrifugal olivocochlear pathways can moderately reduce these temporary threshold shifts (TTSs), protecting the cochlea. This effect involves only the olivocochlear pathway component known as the crossed medial olivocochlear system pathway, originating from the contralateral brainstem and terminating on outer hair cells in the cochlea. Here I demonstrate that even moderate noise backgrounds can significantly exacerbate the cochlear TTSs induced by loud tones, but this is prevented because in such conditions there is additional activation of uncrossed olivocochlear pathways, enhancing protection of cochlear hearing sensitivity. Activation of the uncrossed pathways differs from that of the crossed pathway in that it is achieved only in noise backgrounds but can then be obtained under monaural conditions of loud tone and background noise. In contrast, activation of the crossed pathway is achieved only by binaural loud tones and is not further enhanced by background noise. Thus, conjoint activation of both crossed and uncrossed efferent pathways can occur in noise backgrounds to powerfully protect the cochlea under conditions similar to those encountered naturally by humans.

Acoustic Stimulation↗
PubMed1981

Extratelencephalic pathways and feeding behavior in the pigeon (Columba livia).

Electrolytic lesions were placed in the tractus septomesencephalicus (TSM) and tractus occipitomesencephalicus (TOM), efferent pathways originating in visual and somatosensorimotor areas of the avian telencephalon and distributing widely to brain stem and spinal nuclear regions. Lesion effects upon several aspects of ingestive behavior were examined using high speed cinematography, operant conditioning procedures and monitoring of intake and feeding responses. While there was no evidence for direct effects upon drinking, both TSM adn TOM lesions were followed by periods of reduced food intake. Disruptions of feeding in TSM birds were mild and relatively transient but birds were hypophagic for prolonged periods. While there were no deficits in the efficiency or accuracy of their feeding responses or their performance in an operant situation, TSM birds displayed an inappropriate seed "sorting" behavior suggestive of lesion effects upon visually controlled food preferences. TOM lesions produced a significant reduction in responsiveness to food (aphagia, hypophagia), impairments in the control of grasping and peck accuracy and a disruption in operant key pecking reinforced by food. These "sensorimotor" and "motivational" deficits were similar to those seen after damage to central trigeminal structures in the pigeon and suggest that TOM is also a component of a putative "feeding system" in the pigeon.

Animals↗
PubMed1996

A functional neuroanatomy of anxiety and fear: implications for the pathophysiology and treatment of anxiety disorders.

This paper reviews the evidence that provides the basis for a functional neuroanatomy of anxiety and fear. The afferent arm of the anxiety circuit includes the exteroceptive sensory systems of the brain, which convey the sensory information contained in a fear- or anxiety-inducing stimulus to the dorsal thalamus. Visceral afferent pathways alter the function of the locus coeruleus and the amygdala. The thalamus relays sensory information to the primary sensory receptive areas of the cortex, which project to adjacent unimodal and polymodal cortical association areas. The cortical association areas send projections to the amygdala, entorhinal cortex, orbitofrontal cortex, and cingulate gyrus. A pivotal role for the amygdala in the transmission and interpretation of fear and anxiety is suggested by extensive afferents to the amygdala from thalamic and cortical exteroceptive systems, as well as by subcortical visceral afferent pathways. The neuronal interactions between the amygdala enable the individual to initiate adaptive behaviors to threat based upon the nature of the threat and prior experience. The efferent pathways involving the amygdala, locus coeruleus, hypothalamus, periaqueductal gray, and striatum mediate autonomic, neuroendocrine, and skeletal-motor responses associated with fear and anxiety. The proposed brain structures, neural mechanisms, and neural circuits related to anxiety provide a basis for increased understanding of the pathophysiology of anxiety disorders.

Afferent Pathways↗
PubMed1995

Morphology and connections of neurons in area 17 projecting to the extrastriate areas MT and 19DM and to the superior colliculus in the monkey Callithrix jacchus.

Neurons of area 17, the primary visual cortex, project to various anatomically and physiologically different extrastriate areas and subcortical regions. In the present investigation, we addressed the question of whether the efferent neurons in area 17 can contribute to functional diversity between these regions. We approached this question by analyzing the dendritic morphology of neurons in area 17 projecting to area MT, area 19DM, and the superior colliculus in the new world simian primate Callithrix jacchus, because dendritic morphology is an important factor in determining physiological properties of nerve cells. Retrograde transport of fluorochromes injected into the target regions, and intracellular injections of Lucifer yellow in the prelabelled neurons, revealed the following. 1) Morphologically identical large pyramidal cells in layer VI of area 17 project to all three targets. Some of them possess axon collaterals to two or all three targets, suggesting that they provide common information to all three areas. 2) Pyramidal cells in layer IIIc projecting to area MT form a morphologically homogeneous population. 3) Three small to medium-sized pyramidal cell types in layers IIIa-c, spiny stellate cells in layer IIIc, and another large pyramidal cell type in layer VI project to area 19DM. 4) Pyramidal cells in the lower two-thirds of layer V in area 17 project to the superior colliculus. In conclusion, we have shown that in Callithrix one efferent pathway may originate from several cell types. However, with the exception of the large cells in layer VI, efferent cells projecting to area MT, area 19DM, and the superior colliculus were morphologically distinct. This suggests that functional differences between brain regions could arise in part from morphological heterogeneity between and within the efferent cell populations.

Animals↗
PubMed2005

Lateralization of the effects of the benzodiazepine drug oxazepam on medial olivocochlear system activity in humans.

Benzodiazepines (Bzd) are known to interact with GABAergic inhibitory neurotransmission. Previous research on their effect on human auditory efferent pathways--through evoked otoacoustic emissions suppression by contralateral acoustic stimulation (CAS)--indicated a decrease in medial olivocochlear (MOC) efferent system inhibitory activity, after oral intake of oxazepam--representative of the Bzd drug class. To date, this pharmacological effect was only assessed in the right ear. Since a leftward asymmetry of Bzd receptors localization in human auditory cortex has been described recently, we explored in this study the hypothesis of an asymmetrical action of Bzd on MOC efferent functioning. The results revealed a significant difference of Bzd effect probing the right ear versus the left ear, with CAS-induced suppression being less effective in the right than left ear after oxazepam intake. This finding raises the question of possible neurochemical left-right asymmetry in the descending auditory pathways. The potential localization of this asymmetry is discussed.

Adult↗
PubMed1978

Topographical organization of the striatonigral pathway revealed by anterograde and retrograde neuroanatomical tracing techniques.

L-[4,5-3H]leucine was injected stereotaxically into various regions of the rat neostriatum. Light microscopic autoradiographic techniques were used to plot the entire efferent pathways of the neostriatum, and in particular, the projections to the substantia nigra (SN). The terminal distribution of the pathways projecting to the ipsilateral SN was predominantly restricted to the zona reticulata region. The dorsal part of the head of the striatum was found to innervate the anterior and medial portions of the zona reticulata, while the ventral area of the head projected to more posterior regions of the SN. A pathway from the tail of the striatum to the lateral and dorsal parts of SN was also demonstrated. Horseradish peroxidase injections, restricted to different areas of the SN, led to retrograde labelling of neurons in the striatum whose distribution confirmed the topographic organization of the striatonigral pathway demonstrated in the autoradiographic studies.

Animals↗
PubMed1988

Excitant amino acids and audiogenic seizures in the genetically epilepsy-prone rat. II. Efferent seizure propagating pathway.

Previous studies indicate that the inferior colliculus is the brain stem auditory nucleus most sensitive to the chemical blockade of audiogenic seizures in the genetically epilepsy-prone rat. Other auditory structures do not appear to be as important. This study attempted to define the efferent pathways involved in propagation of the seizure from the colliculus to the spinal cord where the motor components of the convulsion are generated. This study also determined whether certain nuclei which have been implicated in the propagation of seizures in other epilepsy models are involved in audiogenic seizures. The excitant amino acid antagonist, 2-amino-7-phosphonoheptanoate, was infused bilaterally into several of those sites. The drug was effective in significantly reducing seizure severity with infusion of 5 nmol bilaterally into the midbrain and the pontine reticular formation or the substantia nigra. However, similar drug doses were not effective when infused into the entopeduncular nucleus even though prominent behavioral effects were observed with this infusion. Infusion of 2-amino-7-phosphonoheptanoate into the prepiriform cortex resulted in a small but significant reduction in seizure severity. These results suggest that inhibition of excitatory transmission within the substantia nigra and the reticular formation effectively blocks the output pathway for the audiogenic seizures, whereas the role of the prepiriform cortex in this process is relatively minor.

2-Amino-5-phosphonovalerate↗
PubMed1995

Catecholamine and NPY efferents from the ventrolateral medulla to the amygdala in the rat.

Anatomical tracing studies have demonstrated an efferent pathway to central nucleus of the amygdala (CeA) from the ventrolateral medulla. The combined retrograde tracing/immunohistochemical method was used to test for the presence of catecholamines and neuropeptide Y (NPY) in ventrolateral medulla neurons that innervate the CeA. Numerous retrogradely labeled neurons were observed in the ventrolateral medulla caudal to the area postrema. Fewer retrogradely labeled neurons were also observed in the rostral ventrolateral medulla. Retrogradely labeled neurons immunoreactive for both tyrosine hydroxylase and NPY were found in the caudal ventrolateral medulla. Double-labeled phenylethanolamine-N-methyltransferase neurons were present at levels rostral to the area postrema. A substantial portion of the ventrolateral medulla projection to the CeA arises from adrenergic cells of the C1 group, because nearly 40% of the retrogradely labeled cells were also immunoreactive for phenylethanolamine-N-methyl-transferase. The high percentage of double-labeled NPY-immunoreactive neurons suggests NPY is colocalized in CeA-projecting catecholamine neurons, indicating that input from the ventrolateral medulla to the CeA primarily arises from C1 adrenergic neurons that also express NPY. This contrasts with previous data suggesting the catecholaminergic projection from the nucleus of the solitary tract to the CeA originates from the A2 noradrenergic cell group. Thus, the input to the CeA from catecholaminegic groups in the caudal medulla is chemically coded in terms of a dorsal noradrenergic and a ventrolateral adrenergic pathway.

Amygdala↗
PubMed1991

Cochlear efferent neurones and protection against acoustic trauma: protection of outer hair cell receptor current and interanimal variability.

We have measured the changes in neural and microphonic sensitivity in the basal turn of the guinea-pig cochlea produced by intense acoustic overstimulation (10 kHz, 115 dB SPL for 60 s and 150 s). As reported previously, the drop in neural and microphonic sensitivities observed after overstimulation were highly correlated [Patuzzi et al. (1989) Hear. Res. 39, 189-202]. Presentation of a non-traumatizing pure-tone to the contralateral ear (10 kHz, 80 dB SPL) during acoustic overstimulation reduced the amount of acoustic trauma measured using the neural response or the microphonic response. Transection of the medial olivo-cochlear system of efferent fibres at the floor of the fourth ventricle abolished this protective effect of contralateral sound and dramatically reduced the variability in the data. Since the low-frequency microphonic is a simple measure of the receptor current through the outer hair cells, and this current probably plays a part in enhancing the mechanical sensitivity of the cochlea, the protection of the microphonic we have observed suggests that the efferent system protects neural sensitivity by protecting the mechano-electrical transduction of outer hair cells. The drop in variability after sectioning the efferents also suggests that inter-animal variations in susceptibility to noise trauma may be a consequence of differing tonic activity of the efferents, and/or a variation in the sensitivity of the efferent pathway.

Action Potentials↗
PubMed2000

Striatal nitric oxide signaling regulates the neuronal activity of midbrain dopamine neurons in vivo.

A major component of the cortical regulation of the nigrostriatal dopamine (DA) system is known to occur via activation of striatal efferent systems projecting to the substantia nigra. The potential intermediary role of striatal nitric oxide synthase (NOS)-containing interneurons in modulating the efferent regulation of DA neuron activity was examined using single-unit recordings of DA neurons performed concurrently with striatal microdialysis in anesthetized rats. The response of DA neurons recorded in the substantia nigra to intrastriatal artificial cerebrospinal fluid (ACSF) or drug infusion was examined in terms of mean firing rate, percent of spikes fired in bursts, cells/track, and response to electrical stimulation of the orbital prefrontal cortex (oPFC) and striatum. Intrastriatal infusion of NOS substrate concurrently with intermittent periods of striatal and cortical stimulation increased the mean DA cell population firing rate as compared with ACSF controls. This effect was reproduced via intrastriatal infusion of a NO generator. Infusion of either a NOS inhibitor or NO chelator via reverse microdialysis did not affect basal firing rate but increased the percentage of DA neurons responding to striatal stimulation with an initial inhibition followed by a rebound excitation (IE response) from 40 to 74%. NO scavenger infusion also markedly decreased the stimulation intensity required to elicit an IE response to electrical stimulation of the striatum. In single neurons in which the effects of electrical stimulation were observed before and after drug delivery, NO antagonist infusion was observed to decrease the onset latency and extend the duration of the initial inhibitory phase induced by either oPFC or striatal stimulation. This is the first report showing that striatal NO tone regulates the basal activity and responsiveness of DA neurons to cortical and striatal inputs. These studies also indicate that striatal NO signaling may play an important role in the integration of information transmitted to basal ganglia output centers via corticostriatal and striatal efferent pathways.

Animals↗
PubMed1980

Carotid sinus nerve efferents: properties and physiological significance.

The significance of a sympathetic efferent nerve supply, vasoconstrictor to the carotid body and hence facilitatory to carotid chemoreceptors, is well understood. The significance of a second efferent pathway, whose impulses, passing down the sinus nerve, are inhibitory to the chemoreceptors, is less certain. Activity in these sinus nerve efferents is increased by injection of pressor agents, by hypoxia, by hypercapnia, by application of alkaline solutions to the ventral medulla, and by severe hypocapnia. All these stimuli appear to act centrally. Sinus nerve efferents can also be activated reflexly by stimulating ipsilateral carotid chemoreceptors. The mechanism of efferent inhibition is disputed. A purely cholinergic vasodilator role is unlikely because inhibitory effects are abolished by alpha-adrenergic antagonists. Sinus efferents probably cause release of an inhibitory transmitter, dopamine, but convincing evidence for a releasing mechanism has yet to be obtained. Stimulation of nociceptive endings in the heart has reciprocal effects on sinus nerve efferents and sympathetic efferents to the carotid body, inhibiting the former and stimulating the latter. Recent results are cited which indicate that the responses of sinus nerve efferents to changes in blood pressure are more variable than is generally believed, and that the conventional explanation of the relationship between sinus efferent activity and arterial pressure needs to be revised.

Animals↗
PubMed1983

Changes in coronary blood flow produced by the coronary artery occlusion.

The influence of the occlusion of one coronary artery on coronary blood flow in an intact myocardium was investigated in narcotised dogs with open chest by using the crossed circulation method. Interruption of blood inflow to one of the branches of the left coronary artery under autoperfusion of the coronary bed led to a drop in the blood flow rate in the intact branch of the same artery, which was caused by decreased perfusion pressure. Stabilization of coronary perfusion pressure made it possible to detect the dilatatory reaction of the intact coronary bed to the occlusion of one of the coronary arteries. On the basis of an analysis of the dilatatory reaction, conclusions are drawn about the reflex nature of the observed phenomenon. The results of experiments with selective pharmacological blockade of both parts of the autonomous nervous system suggest that the afferent and efferent pathways run in the sympathetic nervous system.

Afferent Pathways↗
PubMed1981

The neural pathway involved in "efferent inhibition" of chemoreceptors in the cat carotid body.

This study was done to determine whether a pathway of efferent axons in the carotid sinus nerve is necessary for the phenomenon of "efferent inhibition" (inhibition induced in carotid body chemoreceptors by electrical stimulation of the carotid sinus nerve). Our approach was to eliminate efferent axons in the carotid sinus nerve of cats without destroying the sensory axons. This was achieved by cutting the ipsilateral glossopharyngeal and vagus nerves central to their sensory ganglia and/or by removing the nodose and superior cervical ganglia. In neurophysiological studies we found that the response of chemoreceptors in cats 10 days after surgery was the same as that in controls. chemoreceptor activity was decreased by electrical stimulation of the carotid sinus nerve and was increased by hypoxia and cyanide. In operated cats as in control animals, "efferent inhibition" was abolished by haloperidol and dihydroergotamine, drugs that block the inhibitory action of dopamine. Electron microscopic studies disclosed that the number of nerve endings in glomus cell/sheath cell complexes was not measurably different in control and experimental carotid bodies. By contrast, 10 days after the carotid sinus nerve was cut the number of nerve endings next to such ells was reduced by more than 99%. cutting the nerve roots and excising the ganglia eliminated most nerve endings on blood vessels: The number of noradrenergic-type nerve endings was reduced 99% and other types of nerve endings (presumptive cholinergic and peptidergic types) were reduced by more than 90%. Our experiments indicate that "efferent inhibition" is not abolished by operations that destroy inputs to blood vessels and to carotid boy glomus cells from (1) the nodose ganglion, (2) superior cervical ganglion, or from (3) neurons in the brain stem whose axons run in the glossopharyngeal or vagus nerves. We conclude that " efferent inhibition" may be caused by antidromic stimulation of sensory axons.

Animals↗
PubMed1999

Effects of cholinergic blockers on auditory brain-stem evoked potentials in rats.

The pharmacology of auditory brain-stem evoked potentials (ABEP) pathways is poorly understood. There are anecdotal reports on the involvement of various neurotransmitters but they were not investigated systematically. The aim of this study was to investigate the effects on ABEP of muscarinic and nicotinic blockers, administered into the cerebral ventricles. Atropine sulfate, d-Tubocurarine and saline were injected stereotactically into the lateral cerebral ventricle of anesthetized male rats. Auditory clicks were given at a rate of 20 s(-1). ABEP recording was performed before and 30 min after injection. Pre- and post-injection peak latencies and peak-to-peak amplitudes of positive waves were compared for each animal. Atropine reduced the amplitudes of waves P1, P3 and P4 and increased mildly the brain stem transmission time. d-Tubocurarine reduced the amplitudes of P1 and P4 with no significant effect on the peak latencies. Saline injection had no effect on any of the parameters. These results show that both cholinergic systems are involved in ABEP generation or transmission. Mechanism of action could be either direct inhibition of afferent pathways or indirect effect, via modulating efferent pathways.

Animals↗
PubMed1997

Myogenic vestibular-evoked potentials in normal subjects: a comparison between responses obtained from sternomastoid and trapezius muscles.

Brief intense clicks cause short latency microcontraction of cervical muscles. Several studies have supported the hypothesis that these microcontractions are of vestibular origin. Averaging these muscular responses enables us to obtain myogenic vestibular evoked potential (MVEP). The receptor of these responses is thought to be the saccule, afferent pathways being the vestibular nerve and efferent pathways the vestibulospinal tract. However, discrepancies are reported with regard to results obtained in healthy subjects: some authors obtained symmetrical response to monaural clicks whereas others obtained responses of greater amplitude on the muscle ispilateral to stimulation. These discrepancies may be due to the presence of different recording sites (inion, sternomastoid or trapezius muscles). The aim of this study was to clarify MVEP results in healthy subjects, using a simple non-traumatic method, and to compare the results obtained on sternomastoid (SM) and trapezius muscles (TRP). Sixteen normal hearing healthy subjects were involved. Latencies and amplitude of both SM and TRP muscle were reproducible in the same subject. Patterns of response were similar to those obtained in previous studies. Following binaural and monaural stimulations, latencies of MVEP were symmetrical on both muscles and amplitudes tended to be greater on muscles contralateral to stimulation, which conflicts with previous results in the literature. Whatever the type of stimulation, latencies of responses obtained on SM were significantly shorter (mean = -3.8 ms), and amplitudes lower (mean = -7.1 microV), than those obtained on TRP. Binaural stimulation resulted in responses of greater amplitude compared to monaural (mean = 0.45 microV). Given the intrasubject reproducibility of the responses, these methods allow MEVP to be recorded in a standardized and reproducible way.

Adult↗
PubMedDate not supplied

Contrastive effects of prostaglandin F2 alpha on normal cardiac rhythm and ouabain-induced cardiac arrhythmias in cats: possible neural basis.

The effects of prostaglandin F2 alpha (PGF2 alpha) on normal cardiac rhythm and ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. PGF2 alpha (1-16 micrograms/kg i.v. bolus) produced ventricular arrhythmias and few incidences of AV conduction disturbances in normal cats. Changes in heart rate and blood pressure caused by PGF2 alpha in normal cats were complex, namely a decrease, an increase, or an initial decrease followed by an increase. Bilateral vagotomy antagonized the ventricular arrhythmias, AV conduction disturbances and hemodynamic changes produced by 16 micrograms/kg i.v. PGF2 alpha. On the other hand, atropine (2 mg/kg i.v.) pretreatment blocked the AV conduction disturbances and the reduction in heart rate and blood pressure, but not the ventricular arrhythmias or the increase in heart rate and blood pressure caused by 16 micrograms/kg i.v. PGF2 alpha. The ventricular arrhythmogenic effect of PGF2 alpha was prevented by propranolol (1 mg/kg i.v.). Intervention with cardiotoxic doses of ouabain augmented the PGF2 alpha-induced AV conduction disturbances, sinus bradycardia and hypotension, and attenuated the ventricular arrhythmias. Subsequent bilateral vagotomy prevented the ouabain-potentiated PGF2 alpha-induced AV block and sinus bradycardia, attenuated the hypotension and further reduced the ventricular arrhythmias. PGF2 alpha (2-16 micrograms/kg i.v.), contrary to its arrhythmogenic effect in normal cats, mainly suppressed ouabain-induced ventricular and supraventricular arrhythmias in ouabain-intoxicated cats, but aggravated the same in few cats. PGF2 alpha (16 micrograms/kg), prior to ouabain administration, produced ventricular arrhythmias in a group of 8 cats and later, in the same group of animals, when tested on ouabain-induced arrhythmias, it mainly antagonized them. These results suggest that PGF2 alpha evokes an arrhythmogenic effect on cardiac rhythm of normal hearts and mainly an antiarrhythmic effect on ouabain-induced arrhythmias largely through the mediation of two functionally opposing excitatory and inhibitory autonomic neural reflex pathways, respectively. The afferents of these pathways are of vagal origin. The efferent pathways of the inhibitory and excitatory reflexes involve in part increased vagal activity and increased sympathetic activity to the heart, respectively. Alteration by ouabain of the arrhythmogenic nature of PGF2 alpha on normal heart to its antiarrhythmic effect on the arrhythmic heart may be due to its selective potentiating effect on the inhibitory reflex pathway.

Anesthesia↗