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PubMed2001

Neural hormonal regulation of exocrine pancreatic secretion.

Exocrine pancreatic secretion is regulated by hormone-hormonal and neural-hormonal interactions involving several regulatory peptides and neurotransmitter from the gut, the pancreas and the vagus nerve. The roles of the gastrointestinal peptides including secretin, CCK, neurotensin, motilin, PYY and pancreatic islet hormones including insulin, pancreatic polypeptide and somatostatin have been established. Interactions among secretin, CCK and neurotensin produce synergistic stimulatory effect. Motilin modulates the cyclic pattern of pancreatic secretion while local insulin provides a permissive role for the action of secretin and CCK at physiological concentration. Somatostatin, PYY and pancreatic polypeptide are inhibitory regulators, acting either on the release of secretin and CCK or on the action of the two stimulatory hormones. The vagal afferent-efferent pathway mediates the actions of many of these regulatory peptides, particularly of secretin and CCK. Acetylcholine and nitric oxide are the neurotransmitters known to mediate the actions of secretin and CCK. Serotonin (5-HT) released from enterochromaffin cells in the intestinal mucosa and nerve terminals of the enteric nervous system and intrapancreatic nerves may be involved in both stimulatory and inhibitory mechanism through its various receptor subtypes. 5-HT also mediates the action of secretin and CCK. The regulatory roles of neuropeptides, PACP and GRP, are now established, whereas those of others are being uncovered. Pancreatic juice provides both positive and negative feedback regulation of pancreatic secretion through mediation of both secretin- and CCK-releasing peptides. Three CCK-releasing peptides have been purified: monitor peptide from pancreatic juice, diazepam-binding inhibitor from porcine intestine, and luminal CCK-releasing factor from rat intestinal secretion. All have been shown to stimulate CCK release and pancreatic enzyme secretion. Pancreatic phospholipase A2 from pancreatic juice and intestinal secretion appears to function as a secretin-releasing peptide. However, the detailed map of neurohormonal regulatory pathways of exocrine pancreatic secretion is yet to be constructed.

Animals↗
PubMed1995

The forebrain of gnathostomes: in search of a morphotype.

A morphotype of the forebrain of gnathostomes, i.e. those characters that must have been present in the forebrain of ancestral gnathostomes, was generated by using out-group analysis to identify the shared primitive characters present in the forebrains of extant gnathostomes. The nature of morphotypes and the steps in generating a morphotype are described. Because hypotheses of phylogenetic relationships profoundly affect the resulting morphotype, current hypotheses of gnathostome interrelationships are reviewed, and particular attention is paid to the problematic relationships of lobe-finned fishes. Ontogenetic studies provide the most common basis for how neural characters are grouped, and a review of the developmental literature indicates that gnathostome forebrains are segmented, with the diencephalon arising from a rostral parencephalic neuromere, which subsequently forms anterior and posterior divisions, and a more caudal synencephalic neuromere. Unfortunately, there is no agreement concerning the number of segments that form the secondary prosencephalon (telencephalon and hypothalamus). For this reason, the characters of the secondary prosencephalon must be analyzed in a topological manner. An out-group analysis of the characters of the diencephalon of extant gnathostomes reveals that the diencephalon of ancestral gnathostomes must have arisen from three segments: an anterior parencephalic segment, which gave rise to intermediate, ventrolateral and ventromedial thalamic nuclei; a posterior parencephalic segment, which gave rise to dorsal and ventral habenular nuclei, anterior, dorsal posterior, dorsal central, and, possibly, lateral posterior thalamic nuclei, and posterior tubercular nuclei; a synencephalic segment, which gave rise to pretectal nuclei, accessory optic nuclei and the nucleus of the medial longitudinal fascicle. The pretectal and posterior tubercular regions of ray-finned fishes appear to be highly derived, due to extensive cellular proliferations that give rise to numerous nuclei. The secondary prosencephalon of ancestral gnathostomes was probably divided rostrally into inverted and evaginated cerebral hemispheres, with paired olfactory bulbs arising directly from the hemispheres, and caudally into preoptic and hypothalamic areas. The cerebral hemispheres likely comprised a dorsally situated pallium divided into medial, dorsal and lateral pallial formations, as well as an intercalated pallial nucleus situated ventrolateral to the lateral pallium, and a ventrally situated subpallium divided medially into septal nuclei and a medial amygdalar nucleus and laterally into a corpus striatum. Both pallial and subpallial centers of ancestral gnathostomes probably received ascending thalamic and posterior tubercular inputs, with telencephalic efferent pathways terminating primarily in the hypothalamus, posterior tubercle and midbrain tegmentum. An out-group analysis further indicates that some taxa in each gnathostome radiation exhibit highly derived telencephalic characters due to the independent expansion of one or more pallial formations.

Animals↗
PubMed1994

Axial myoclonus mediated by the propriospinal tract: a case report.

We describe a patient with axial myoclonus. Myoclonus first occurred in the upper abdominal muscle and spread up to the neck muscle and down to the lower abdominal muscle. Physiological studies of the jerks revealed that the myoclonus arose in the thoracic spinal cord and spread slowly up and down the spinal cord at about 3 m/s. We conclude that the myoclonus is mediated by the propriospinal tract.

Adult↗
PubMed1988

Opposite changes of pituitary and ovarian receptors for LHRH in ageing rats: further evidence for a direct neural control of ovarian LHRH receptor activity.

Hypophyseal and ovarian receptors for the neurohormone LHRH (LHRH-R) have been measured in young (3-4 months), middle-aged (8-11 months), constant estrous (CE, 10-14 months) and pseudopregnant (PR, 16-18 months) rats in order to study whether changes in hypothalamic and/or peripheral LHRH-like peptide production might precede and/or accompany the onset of reproductive failure observed in aging rats. Furthermore, we have investigated whether the neural efferent system from the brain to the ovary is affected with aging. The pattern of pituitary LHRH-R modifications during the estrous cycle of middle-aged rats shows lower LHRH-R levels on the second day of diestrus, resulting in a shift of the maximal LHRH binding capacity in the morning of proestrus. On the other hand, when comparing pituitary LHRH-R of animals exhibiting constant vaginal cornification (CVC) or repetitive PP with young estrus rats, no significant difference could be observed. Young rats responded to electrical stimulation (ES) of the medial preoptic area with an acute elevation of LHRH-R while ES performed in CVC, or PP animals resulted in a significant increase of hypophyseal LHRH binding capacity similar to the one observed in young estrous controls, indicating an impairment in the neural signals impinging in the pulse generating system, in old rats, and not an intrinsic defect of the LHRH-R per se. Ovarian LHRH-R concentration is higher in middle-aged cycling animals on the day of vaginal proestrus, compared to levels measured in young animals at any phase of the estrous cycle. Similarly, CE rats displaying CVC as well as PP animals show significantly higher numbers of LHRH-R with no change in affinity, than young estrus rats. CVC and PP rats receiving unilaterally an intraovarian injection of the potent LHRH antagonist, Ac-D-Cl-Phe1,2, D-Trp3, D-Phe6, D-Ala10, LHRH, showed an acute drop of LHRH-R measured within the treated ovary with no significant changes taking place in the vehicle-treated contralateral gland, suggesting that changes of endogenous ovarian LHRH-like peptide might participate in the mechanism(s) responsible for LHRH receptor increase observed in aging rats. In order to investigate the participation of a direct neural efferent pathway in ovarian LHRH-R regulation, young and old rats were subjected to spinal cord transection (above T10-T11). Bilateral transection of the spinal cord in young animals in the morning of proestrous markedly increased ovarian LHRH-R concentration in the afternoon (17.00 h) of the same day.(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1985

Quantitative studies of the cat carotid body. III. The type I cells.

The work reported here examines the quantitative ultrastructure of cat carotid body type I cells, and the effects of hypoxia on the cells. On the basis of size and density of electron-dense cored vesicle (EDCV) we were unable to identify more than one major population of type I cells. Prior ventilation of the animals with 10% O2 resulted in an increase in the volume percentage (Vv%) of mitochondria and a decrease in the Vv% of EDCV as compared to the values after ventilation with 100% O2. The lack of effect of prior denervation of the carotid body on the hypoxic changes suggests that the effects are not mediated via an efferent pathway.

Animals↗
PubMed1982

The oto-respiratory reflex.

The oto-respiratory (O-R) reflex consists of the cough reflex produced by direct mechanical stimulation of the deep portion of the posterior wall of the external auditory meatus. Because the efferent pathways are different for coughing and bronchoconstriction, some subjects can have an O-R reflex (coughing) without the oto-bronchial (O-B) reflex (bronchoconstriction). This study also states that on stimulation of the mechanoreceptors in the external ear, 20 out of 125 normal subjects (16%) presented with the O-R reflex; in 7 of the 20 subjects, bronchoconstriction ('responders') was also documented (O-B reflex). The O-B reflex was particularly evident in 3 of the 7 responders. These normal subjects referred a family history of atopy. Only through animal experimentation can the exact nervous pathway of the O-R reflex be defined. From the physiological point of view, it is difficult to imagine how this 'irritative' reflex could have a protective function against auditory aggression.

Acoustic Stimulation↗
PubMed2001

AT(1) antisense distinguishes receptors mediating angiotensin II actions in solitary tract nucleus.

Angiotensin (Ang) II receptors in the solitary tract nucleus (nTS) are located on vagal sensory-afferent fiber terminals as well as on neuronal cell bodies. Results from in vitro slice preparations indicate that approximately 50% of the neuronal excitatory actions of Ang II result from actions at presynaptic receptors. The differential contribution of actions on fiber terminals versus neuronal cell soma to the cardiovascular effects of Ang II in the nTS is not known. We used antisense oligonucleotides to the angiotensin type 1 (AT(1)) receptor, which should reduce receptors on neurons within the injection site but not those on fiber terminals projecting to the nTS. Ang II injections (250 fmol/30 nL) into the nTS reduced blood pressure by 14+/-1 mm Hg and heart rate by 13+/-1 bpm (n=8) in male Sprague-Dawley rats anesthetized with chloralose/urethane. Although there was still a significant fall in pressure that was induced by Ang II at 90 and 150 minutes after AT(1) antisense (164 pmol/120 nL) was injected into the nTS, the response was blunted 50% (P<0.01). Heart rate responses were completely blocked at the 150-minute time point. Scrambled sequence oligonucleotides did not alter Ang II responses at any time. There was a 40% reduction in (125)I[Sar(1)Thr8]-Ang II binding when antisense-injected and noninjected sides of the nTS were compared with receptor autoradiography. This finding is consistent with the continued presence of AT(1) receptors on afferent fibers. This unique strategy illustrates that both presynaptic fiber terminals and nTS neurons are involved in the blood pressure lowering actions of Ang II, whereas heart rate responses are largely due to actions directly on nTS neurons and activation of vagal efferent pathways.

Angiotensin I↗
PubMed1976

Reflex suppression of renin secretion during distention of cardiopulmonary receptors in dogs.

We studied the effect of brief periods of left atrial-pulmonary vein distention on the rate of renin secretion in sodium-restricted dogs anesthetized with chloralose and breathing spontaneously. Series 1 consisted of 32 trials in seven dogs with intact renal nerves and intact vagi. Renin secretion, calculated as the product of renal venous minus arterial renin activity (radioimmunoassay) times renal plasma flow (electromagnetic flowmeter), was depressed to 56% of control during atrial distention despite no change in arterial pressure, central venous pressure, or renal blood flow. Series 2 consisted of 58 trials in 12 dogs which had undergone unilateral renal denervation several days prior to the studies. Simultaneous, bilateral determinations indicated that renin secretion from the innervated kidney was depressed to 58% of control during atrial distention; secretion from the denervated kidney was unchanged. Series 3 consisted of 30 trials in six dogs with bilateral cervical vagotomy. Atrial distention evoked no changes in renin secretion. We conclude that left atrial distention reflexly reduces the rates of renin secretion via vagal afferent and renal sympathetic efferent pathways.

Animals↗
PubMed1994

Motor recovery after early brain damage. A case of brain plasticity.

BACKGROUND: Motor recovery is remarkable when the brain is damaged early in life. We describe a case of early damage to the right hemisphere with remarkable reorganization and plastic functional changes, studied by computed neuroimaging. CASE DESCRIPTION: A 31-year-old man had a left-sided hemiplegia at the age of 12, followed by good motor recovery despite a large right cortical-subcortical lesion. Single-photon emission computed tomography with motor activation study showed cerebral blood flow increase in the left premotor and sensorimotor cortices irrespective of the hand he was moving, without flow changes in the right hemisphere. CONCLUSIONS: A remarkable reorganization and plastic brain functional changes occurred in a patient after early diffuse damage of the right hemisphere. The study points to a potential role of ipsilateral cortical efferent pathways in subserving hand movements after early cerebral damage.

Adult↗
PubMed2001

Chronic AT(1) receptor blockade alters autonomic balance and sympathetic responses in hypertension.

In the coarctation hypertension model, we have shown that chronic treatment with losartan causes both normalization of impaired reflex control of heart rate and partial correction of the depressed aortic nerve activity/pressure relationship, even with the persistence of hypertension. In the present study, we analyzed the effects of angiotensin II blockade on the efferent pathways of coarcted and sham-operated groups treated chronically with vehicle or losartan (10 mg/kg per day PO). Hypertension was induced by subdiaphragmatic aortic coarctation, and the treatments lasted 9 days (4 control and 5 experimental days). On day 5, autoregressive power spectral analysis was performed on heart rate recordings made in conscious rats. Other groups were used for sympathetic splanchnic nerve activity recordings made simultaneously with pressure (anesthetized rats) at basal condition and during loading/unloading of baroreceptors. Losartan treatment induced a significant reduction in basal pressure but did not interfere with the development of hypertension (similar pressure increases of 24% and 28% over control values in losartan and vehicle groups, respectively). In vehicle-treated rats, establishment of hypertension was accompanied by a marked change in power spectral density from high- (1.19+/-0.06 Hz, 33+/-6%) to low-frequency components (0,42+/-0.03 Hz, 54+/-6%), with increased low-frequency-to-high-frequency ratio. When compared with sham-operated vehicle-treated rats, there was also increase in the gain of sympathetic activity/pressure relationship, with displacement of lower plateau toward high levels of sympathetic activity. No changes in the power spectral density and sympathetic activity/pressure relationship were observed when hypertension developed in the presence of chronic angiotensin type 1 (AT(1)) receptor blockade. The data suggest that angiotensin II, activated during the establishment of coarctation hypertension, acts via AT(1) receptors to alter sympathovagal balance, facilitating the sympathetic outflow to heart and peripheral circulation during baroreceptors unloading. Data also indicate that the observed effects are not conditioned by preexisting pressure levels.

Angiotensin Receptor Antagonists↗
PubMed1999

A cerebellar model of timing and prediction in the control of reaching.

A simplified model of the cerebellum was developed to explore its potential for adaptive, predictive control based on delayed feedback information. An abstract representation of a single Purkinje cell with multistable properties was interfaced, using a formalized premotor network, with a simulated single degree-of-freedom limb. The limb actuator was a nonlinear spring-mass system based on the nonlinear velocity dependence of the stretch reflex. By including realistic mossy fiber signals, as well as realistic conduction delays in afferent and efferent pathways, the model allowed the investigation of timing and predictive processes relevant to cerebellar involvement in the control of movement. The model regulates movement by learning to react in an anticipatory fashion to sensory feedback. Learning depends on training information generated from corrective movements and uses a temporally asymmetric form of plasticity for the parallel fiber synapses on Purkinje cells.

Adaptation, Physiological↗
PubMed1992

Local application of atropine attenuates the upper airway reaction to cold, dry air.

In some individuals, inhalation of cold, dry air (CDA) provokes symptoms of rhinitis, accompanied by an increase in the levels of inflammatory mediators and markers of plasma leakage of recovered nasal lavages. Because rhinorrhea is a major component of this reaction and because nasal glands are heavily innervated by the parasympathetic system, we assessed the effect of atropine on the nasal reaction to CDA. Using a double-blind, randomized, crossover design, we administered a total dose of 0.5 mg of atropine or placebo intranasally to 18 volunteers before provocation with CDA. The reaction was monitored with symptom scores and by measuring the concentrations of histamine, N-alpha-p-tosyl-L-arginine methyl ester (TAME)-esterase activity and albumin, as well as the osmolality of lavage fluids before and after the provocation. Atropine significantly reduced rhinorrhea, the levels of histamine, and TAME-esterase activity as well as the osmolality of recovered lavage fluids, but had no effect on nasal congestion or albumin. Even with atropine, however, rhinorrhea and TAME-esterase activity were still significantly increased over the prechallenge baseline. Our results demonstrate that atropine-sensitive parasympathetic efferent pathways contribute to the CDA-induced rhinitis. We speculate that (1) the glandular and the vascular events of the upper airway reaction to dry air have different pathophysiologic mechanisms; (2) a significant component of TAME-esterase activity in lavage fluids may be of glandular origin; and (3) in addition to parasympathetic nerve activation, other mechanisms are involved in the upper airway reaction to dry air. The mechanism(s) leading to the reduction of histamine is unknown.

Administration, Intranasal↗
PubMed1973

Reflex vascular responses to left ventricular outflow obstruction and activation of ventricular baroreceptors in dogs.

Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured. Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5+/-3 (SE) and -42+/-11 mm Hg in muscle and -1+/-1 and -3+/-2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels. Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction. Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine. The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.

Animals↗
PubMed2000

T cell-mediated Fas-induced keratinocyte apoptosis plays a key pathogenetic role in eczematous dermatitis.

Clinical and histologic similarities between various eczematous disorders point to a common efferent pathway. We demonstrate here that activated T cells infiltrating the skin in atopic dermatitis (AD) and allergic contact dermatitis (ACD) induce keratinocyte (KC) apoptosis. KCs normally express low levels of Fas receptor (FasR) that can be substantially enhanced by the presence of IFN-gamma. KCs are rendered susceptible to apoptosis by IFN-gamma when FasR numbers reach a threshold of approximately 40,000 per KC. Subsequently, KCs undergo apoptosis induced by anti-FasR mAb's, soluble Fas ligand, supernatants from activated T cells, or direct contact between T cells and KCs. Apoptotic KCs show typical DNA fragmentation and membrane phosphatidylserine expression. KC apoptosis was demonstrated in situ in lesional skin affected by AD, ACD, and patch tests. Using numerous cytokines and anti-cytokine neutralizing mAb's, we found no evidence that cytokines other than IFN-gamma participate in this process. In addition, apoptosis-inducing pathways other than FasR triggering were ruled out by blocking T cell-induced KC apoptosis by caspase inhibitors and soluble Fas-Fc protein. Responses of normal human skin and cultured skin equivalents to activated T cells demonstrated that KC apoptosis caused by skin-infiltrating T cells is a key event in the pathogenesis of eczematous dermatitis.

Apoptosis↗
PubMed1990

Differential elimination of circadian and ultradian rhythmicity by hypothalamic lesions in the common vole, Microtus arvalis.

Effects of hypothalamic lesions on the ultradian and circadian organization of wheel running and feeding were studied in the common vole, Microtus arvalis. Circadian organization broke down within 30 days in continuous darkness in 24% of intact voles (n = 135). Ultradian rhythmicity of feeding (period 2-3 hr) persisted in constant conditions in all intact voles. Following lesions of the suprachiasmatic nuclei (SCN), circadian rhythmicity disappeared when lesions were complete (n = 8) or more extensive than 25% of the total SCN volume (n = 5). Absence of circadian rhythmicity was also found in animals with substantial lesions in the diencephalic paraventricular area (PVA) and in the retrochiasmatic area (RCA) and/or adjacent arcuate nucleus (Arc). Complete loss of ultradian and circadian organization occurred in eight voles with damage to the RCA and/or Arc. In three of these, the SCN was intact. The SCN is a likely candidate for a circadian pacemaker in voles (as in other rodents), while the loss of circadian rhythmicity following PVA and RCA/Arc lesions may be due to destruction of efferent pathways from the SCN. The RCA/Arc area is apparently necessary for the expression of ultradian rhythms. The intact SCN is neither necessary nor sufficient for the generation of ultradian rhythmicity.

Activity Cycles↗
PubMed2006

Sleep to remember.

Recently, compelling evidence has accumulated that links sleep to learning and memory. Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory. Consolidation is an active process that is presumed to rely on the covert reactivation and reorganization of newly encoded representations. Hippocampus-dependent memories benefit primarily from slow-wave sleep (SWS), whereas memories not depending on the hippocampus show greater gains over periods containing high amounts of rapid eye movement sleep. One way sleep does this is by establishing different patterns of neurotransmitters and neurohormone secretion between sleep stages. Another central role for consolidating memories is played by the slow oscillation, that is, the oscillating field potential change dominating SWS. The emergence of slow oscillations in neocortical networks depends on the prior use of these networks for encoding of information. Via efferent pathways, they synchronize the occurrence of sharp wave ripples accompanying memory reactivations in the hippocampus with thalamocortical spindle activity. Thus, hippocampal memories are fed back into neocortical networks at a time when these networks are depolarized and, because of concurrent spindle activity, can most sensitively react to these inputs with plastic changes underlying the formation of long-term memory representations.

Animals↗
PubMed2006

Differential activation of nerve fibers with magnetic stimulation in humans.

BACKGROUND: Earlier observations in our lab had indicated that large, time-varying magnetic fields could elicit action potentials that travel in only one direction in at least some of the myelinated axons in peripheral nerves. The objective of this study was to collect quantitative evidence for magnetically induced unidirectional action potentials in peripheral nerves of human subjects. A magnetic coil was maneuvered to a location on the upper arm where physical effects consistent with the creation of unidirectional action potentials were observed. Electromyographic (EMG) and somatosensory evoked potential (SEP) recordings were then made from a total of 20 subjects during stimulation with the magnetic coil. RESULTS: The relative amplitudes of the EMG and SEP signals changed oppositely when the current direction in the magnetic coil was reversed. This effect was consistent with current direction in the coil relative to the arm for all subjects. CONCLUSION: A differential evocation of motor and sensory fibers was demonstrated and indicates that it may be possible to induce unidirectional action potentials in myelinated peripheral nerve fibers with magnetic stimulation.

Action Potentials↗
PubMed2005

Initiation and suppression of saccades by the frontal eye field in the monkey.

After a saccadic eye movement occurs to an interesting object appearing in the visual field, visual fixation holds its image on the fovea and suppresses saccades to other objects appearing in the visual field. To understand the neural mechanism of visual fixation, the effects of electrical stimulation of the frontal eye field (FEF) on the generation of electrically evoked saccades (Esacs) and the suppression of saccades in trained monkeys were investigated. When the properties of the electrically evoked suppression of visually guided (Vsacs) and memory-guided saccades (Msacs) were examined, two types of suppression were found. Stimulation of a wide area of the FEF suppressed only ipsiversive Vsacs and Msacs at stimulus intensities lower than those for eliciting Esacs, whereas stimulation of a localized area of the FEF suppressed the initiation of both Vsacs and Msacs in any direction during and approximately 50 ms after stimulation. However, neither stimulation affected the vector of these saccades. The thresholds for suppression were usually less than 50 microA. The most effective stimulation timing for the suppression of ipsiversive and contraversive Vsacs was approximately 40 to 50 ms before saccade onset. Therefore, suppression occurred in the efferent pathway for Vsacs at the premotor rather than the motoneuronal level, most likely in the superior colliculus and/or the paramedian pontine reticular formation. The results suggest that the suppression in the FEF may play a role in maintaining visual fixation by suppressing the generation of saccades.

Animals↗