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PubMed1981

Cardiovascular changes in elicited by vagal gastric afferents in the rat.

Cardiovascular changes elicited by gastric distension in the urethane anaesthetized rat are described. Heart rate changes were mediated via a vago-vagal pathway with 'in-series' tension receptors in the stomach wall providing the afferent input and cholinergic cardio-inhibitory fibres forming the efferent pathway. Blood pressure changes occurred independently of the heart rate changes; the main afferent pathway was again vagal but the efferent outflow was non-cholinergic and probably sympathetic.

Animals↗
PubMed1989

Sagittal organisation of the olivocerebellonuclear pathway in the rat. III. Connections with the nucleus dentatus.

The organization of olivary afferents and nuclear efferents of the D-zone of the rat cerebellum was studied by means of tracing with wheat-germ agglutinin-coupled peroxidase using tetramethylbenzidine as a chromagen. The tracer was injected iontophoretically within the cerebellar cortex. This allowed us to study both afferent and efferent pathways of the cerebellar lobules concerned with retrograde and anterograde tracing, respectively. Retrograde cellular labelling in the inferior olive was restricted to the principal olive (PO). Anterograde terminal labelling was found only within the various subdivisions of the nucleus lateralis or dentatus (ND). For any one of our small cortical injections there was a corresponding sagittal band of retrogradely labelled cells in the contralateral PO, and a sagittal band of terminal labelling through the ND. Based on both their olivary and nuclear connections, 3 sagittal subzones can be distinguished within the D-zone of the rat. From medial to lateral, we call them D0, D1 and D2. The 3 subzones run through part of the anterior and posterior lobes. D1 and D2 run continuously from their rostral to their caudal extents whereas D0 is discontinuous. It is interrupted through lobule VIc (crus I). The olivary projections to D0 arise within the medial half of the ventral lamella of the PO, including the dorsomedial cell column. Those to D1 arise within the dorsal lamella of the PO. Those to D2 arise within the lateral half of the ventral lamella of the PO. Rostrocaudally, widely distant cells of the same subdivision of the PO project to the same cerebellar lobule. This indicates extensive convergence of the olivary afferents within each of the 3 hemispheric compartments, D0, D1 and D2. Each of the 3 hemispheric subzones specifically projects to one of the 3 subdivisions distinguished within the ND of the rat, without apparent mediolateral overlapping. The medialmost D0 projects onto the dorsolateral hump; D1 projects more laterally onto the main, magnocellular part of the ND, and D2 projects ventrally onto the parvicellular subdivision of the ND. Thus the sagittal partition of the hemispheric cortex is reflected at the nuclear level. In contrast, Purkinje cell axons from individual lobules appear to branch extensively in the rostrocaudal direction. Therefore, within each of the 3 compartments D0, D1 as well as D2, the nuclear projection of the anterior lobe and the posterior lobe are largely coextensive.

Animals↗
PubMed1977

The prenatal development of some of the visual pathways in the cat.

Lesions were made in the visual system in a series of cat fetuses of known gestational age, and fiber and terminal degeneration were stained by the Eager method. The times of development of the retinal projection, of the thalamcortical and corticothalamic projections of area 17 of the visual cortex, and of the intrinsic fibers in the visual cortex were examined. Enucleation of one eye resulted in degeneration being detected bilaterally in the lateral geniculate nuclei (LGN), superior colliculi (SC) and optic tracts. The optic nerves reached the optic chiasm by the thirtieth embryonic day (E30) and the optic tract connections with the LGN and SC were made by E37. The projection always appeared stronger in the contralateral LGN and SC, and the amount of degeneration increased in both sides with increasing age. A parasagittal knife cut was made in the dorsomedial crest of the visual cortex. Where the lesion passed through the cellular layers of the cortex, intrinsic fibers were cut when these were present. The deeper part of the incision through the white matter undercut the medial wall of the visual cortex, interrupting thalamocortical and corticothalamic fibers when these were present. The longer horizontal fibers that were intrinsic to the visual cortex began to develop during the last two weeks of gestation but were not fully developed at birth. In the undercut visual cortex distant from the place of entry of the lesion, and before the intrinsic fibers of the cortex had developed, degeneration was found in layers 1 and 4, demonstrating the presence of a thalamocortical pathway. The youngest fetus to show this degeneration was operated at E48. This degeneration was not present three days earlier at E45. Fiber plexuses that have been described earlier in development (Marin-Padilla, '71; Cragg, '75) do not appear to degenerate after undercutting the cortex. The corticothalamic pathway to the lateral posterior nucleus medial to the LGN was developed at E45. The descending pathways to the ipsilateral LGN and SC were developed by E48, but it is not known whether they are present before this. Thus degeneration has been used to detect the development of axonal pathways in the fetus for the first time; the major afferent and efferent pathways are developed at an earlier stage than has previously been described.

Animals↗
PubMed2004

Role of sirtuin proteins in life extension by caloric restriction.

The deacetylase activity of sirtuin proteins may play a key role in the life extending action of caloric restriction in organisms ranging from yeast to mammals. Recent research has been focused on the possible afferent pathway by which caloric restriction increases the deacetylase activity and on the efferent pathway by which the increased deacetylase activity extends life. Further research is needed to firmly establish the role of sirtuin proteins in life extension by caloric restriction in mammals.

Animals↗
PubMed2005

Elevated serum cytokines correlated with altered behavior, serum cortisol rhythm, and dampened 24-hour rest-activity patterns in patients with metastatic colorectal cancer.

PURPOSE: Incapacitating symptom burden in cancer patients contributes to poor quality of life (QOL) and can influence treatment outcomes because of poor tolerance to therapy. In this study, the role of circulating cytokines in the production symptoms in cancer patients is evaluated. EXPERIMENTAL DESIGN: Eighty patients with metastatic colorectal cancer with either normal (group I, n = 40) or dampened (group II, n = 40) 24-hour rest/activity patterns measured by actigraphy were identified. Actigraphy patterns were correlated with QOL indices, serum cortisol obtained at 8:00 a.m. and 4:00 p.m. and with serum levels of transforming growth factor-alpha, tumor necrosis factor-alpha, and interleukin 6 (IL-6) obtained at 8:00 a.m. and analyzed in duplicate by ELISA. Cytokine levels and survival were also correlated. RESULTS: Group II patients had significantly higher pre treatment levels of all three cytokines, displayed significantly poorer emotional and social functioning, had higher fatigue, more appetite loss, and poorer performance status compared with group I patients. Transforming growth factor-alpha (TGF-alpha) and IL-6 were significantly increased in the patients with WHO performance status >1 and in those with appetite loss. Fatigue was significantly associated with elevated TGF-alpha only. IL-6 was increased in those patients with extensive liver involvement and multiple organ replacement, and it was significantly correlated with dampened cortisol rhythm. In a multivariate analysis, IL-6 was correlated with poor treatment outcome. CONCLUSIONS: Significant correlations were found between serum levels of TGF-alpha and IL-6, circadian patterns in wrist activity and serum cortisol and tumor-related symptoms in patients with metastatic colorectal cancer. These data support the hypothesis that some cancer patient's symptoms of fatigue, poor QOL, and treatment outcome are related to tumor or host generated cytokines and could reflect cytokine effects on the circadian timing system. This interplay between cytokine signaling pathways, the hypothalamic-pituitary-adrenal axis, the autonomic nervous system, and efferent pathways of the suprachiasmatic nucleus that control circadian physiology, opens the way to new rational interventions for symptom management in cancer patients.

Activities of Daily Living↗
PubMed1975

Reflex heart rate control via specific aortic nerve afferents in the rabbit.

Reflex bradycardia was elicited in rabbits via repetitive electrical stimulation of the central end of the sectioned left aortic nerve. Supramaximal stimulation produced a 16.9 plus or minus 1.3% (SE) increase in the R-R interval when vagal and sympathetic efferent pathways were intact. Reducing the stimulation voltage allowed selective stimulation of the myelinated (A) fibers, and polarizing electrodes placed central to the stimulus site permitted A fiber blockade and selective stimulation of the unmyelinated (C) fibers. When afferent A fibers were selectively stimulated, 64% of the maximum response was obtained; selective C fiber activation elicited 63% of the maximum observed response. Selective stimulation of A or C fibers after either vagotomy or stellectomy indicated that A fiber afferents elicit heart rate responses via both vagal and sympathetic efferents, whereas C fiber afferent information is mediated predominantly via vagal efferents. This afferent-efferent specificity of the aortic baroreceptor pathways suggests baroreceptor mechanisms normally used to modulate heart rate. Small increments in blood pressure would activate low-threshold A fibers and result in reciprocal changes in vagal and sympathetic efferent activity. More substantial increases in blood pressure would activate afferent C fibers and produce additional heart rate effects via vagal efferents.

Animals↗
PubMed2002

Diagnosis and treatment of neurally mediated syncope.

BACKGROUND: Syncope is caused by a severe but reversible reduction in blood flow to the brain stem neurons responsible for supporting consciousness (reticular activating system). Neurally mediated syncope, also referred to as vasovagal or reflex syncope, is the most frequent cause of loss of consciousness in apparently normal subjects. REVIEW SUMMARY: Neurally mediated syncope is believed to be a reflex response with afferent, central, and efferent pathways. Characteristic autonomic changes in neurally mediated syncope are an increase in parasympathetic efferent activity causing bradycardia and a reduction in sympathetic vasoconstrictor outflow causing vasodilatation. Premonitory symptoms, such as nausea, diaphoresis, abdominal discomfort, and blurred vision, are caused by autonomic activation and are distinguishing features of neurally mediated syncope. Neurally mediated syncope frequently has a characteristic trigger, although this may not be apparent. Testing orthostatic tolerance during passive head-up tilt is the best available diagnostic procedure to evaluate patients with syncope in whom a cardiac cause has been excluded. In many cases, once the diagnosis of neurally mediated syncope is confirmed, it may suffice to reassure the patient and teach him to avoid known triggers and to recognize and act upon early warning symptoms. Because subjects with neurally mediated syncope may potentially be sodium depleted, increasing salt intake can be beneficial in improving their orthostatic intolerance. CONCLUSIONS: Neurally mediated syncope is the most common form of syncope in healthy adults. The best diagnostic tools are the clinical history and passive head-up tilt. The best treatment strategies are the avoidance of triggering factors as well as intravascular volume expansion.

Journal Article↗
PubMed1980

Motor reflexes of stomach elicited by phenyldiguanide in the rat.

Intragastric pressure (IGP) as an index of gastric motor activity was used to investigate gastric motor responses elicited by phenyldiguanide (PDG) in rats under pentobarbitone anaesthesia. Phenyldiguanide injected into the atrium produced an inhibitory gastric motor response whereas an aortic injection resulted in an increase in IGP. Intracarotid injections were without effect. Atropine reduced the response to atrial PDG but not to aortic PDG. Cervical vagotomy abolished the response to both atrial and aortic PDG. Guanethidine and spinal transection abolished the response to atrial PDG only. It is concluded that PDG acts by stimulation of nonmedullated vagal afferents. The efferent pathway for PDG-evoked gastric relaxation is through sympathetic nerves and the efferent system for gastric contraction involves a noncholinergic, nonadrenergic excitatory mechanism.

Animals↗
PubMed1985

The effect of cyclooxygenase inhibitors on the low filling rate cystometrogram in urethane anesthetized rats.

The effect of two widely used cyclooxygenase inhibitors (indomethacin and ketoprofen) on the low filling rate cystometrogram was investigated in urethane anesthetized rats. Both indomethacin and ketoprofen significantly increased volume threshold to elicit neurogenic bladder contractions without affecting their amplitude. Also the pressure threshold was unaffected by both drugs while the volume/pressure relationship was significantly flattened compared to controls. These findings indicate that acute suppression of arachidonic acid metabolism along the cyclooxygenase pathway increases the micturition threshold without affecting bladder muscle contractility and/or neurotransmission along the efferent pathway of the micturition reflex.

Anesthesia↗
PubMed1980

Responses of the heart to stimulation of aortic body chemoreceptors in dogs.

We stimulated the aortic chemoreceptors in dogs that were anesthetized with chloralose and artificially ventilated by perfusing the isolated aortic arch with venous blood. Inotropic responses were determined by measuring the maximum rate of change of left ventricular pressure (dP/dt max) with aortic pressure and heart rate held constant. Stimulation of the aortic chemoreceptors resulted in an average increase in heart rate of 14 +/- 2.0 beats/min (mean +/- SE) from 166 +/- 7.7 beats/min and an increase in dP/dt max of 501 +/- 85 mm Hg/sec from 3508 +/- 154 mm Hg/sec. These changes were statistically significant (P less than 0.001). The afferent pathway of the reflex was shown to be in the vagus nerves and the efferent pathway in the cardiac sympathetic nerves. In some of the dogs, the carotid chemoreceptors were also stimulated. This resulted in decreases in heart rate and dP/dt max of 48 +/- 24 beats/min and 795 +/- 142 mm Hg/sec. Thus we have shown that stimulation of aortic chemoreceptors evokes chronotropic and inotropic responses opposite to those evoked from stimulation of carotid chemoreceptors.

Animals↗
PubMed1976

Tolerance and contact sensitivity to DNFB in mice. VI. Inhibition of afferent sensitivity by suppressor T cells in adoptive tolerance.

Tolerance in contact sensitivity to DNFB can be adoptively transferred to normal mice with lymph node cells from tolerant donors. This tolerance is antigen specific and is mediated by T cells, i.e., "suppressor" T cells. Experiments were carried out to investigate the mechanism(s) by which the suppressor T cells induce tolerance to DNFB contact sensitivity. The suppressor cells were effective only if they were present during the early stages of the afferent limb of sensitization. As measured by DNA synthesis, cell proliferation in the draining lymph nodes of recipients of suppressor cells was found to be significantly less than in control animals indicating that the suppressor cells acted, at least in part, by limiting or inhibiting DNFB-induced cell proliferation. This inhibition was shown to be antigen specific since the DNFB suppressor cells did not inhibit cell proliferation induced by oxazolone, an unrelated contact sensitizer. The ability to DNFB tolerant cells to block afferent sensitization pathways differs from the mechanism of tolerance to picryl chloride, reported by others, where efferent pathways are blocked.

Animals↗
PubMed1997

Effect of pulmonary lymphatic obstruction on rabbit urine flow.

1. The effects of pulmonary lymphatic obstruction on urine flow, sodium and potassium excretion were examined on anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic obstruction was produced by raising the pressure in a pouch created from the right external jugular vein. The experiments were performed on two groups of rabbits (non-hydrated and hydrated). 2. Pulmonary lymphatic obstruction caused a significant increase in urine flow in both groups of rabbits. After release of the obstruction, the urine flow returned to basal values. Urine flow (ml (10 min)-1) for both groups was initial control, 5.3 +/- 0.9; lymphatic obstruction, 8.9 +/- 1.0; final control, 6.2 +/- 0.7 (means +/- S.E.M.; n = 21, P < 0.025). 3. The increase in urine flow was not accompanied by significant changes in concentration of sodium and potassium in urine. Sodium excretion increased significantly only in the hydrated rabbits. 4. The increase in urine flow was abolished by bilateral cervical vagotomy and by renal nerve sectioning. Cooling the cervical vagi to 8 degrees C also abolished the response. 5. Pulmonary lymphatic obstruction did not produce any significant change in heart rate, mean arterial blood pressure, mean right atrial pressure and peak airway pressure. 6. These findings suggest that obstructing the lymph drainage from the lung results in a reflex increase in urine flow. The afferent pathway for this reflex resides in the myelinated fibres of the vagi and the efferent pathway in the renal nerves. The rapidly adapting receptors of the airways are likely to be the receptors involved.

Animals↗
PubMed2006

Reorganization of CA3 area of the mouse hippocampus after pilocarpine induced temporal lobe epilepsy with special reference to the CA3-septum pathway.

We showed that when CA3 pyramidal neurons in the caudal 80% of the dorsal hippocampus had almost disappeared completely, the efferent pathway of CA3 was rarely detectable. We used the mouse pilocarpine model of temporal lobe epilepsy (TLE), and injected iontophoretically the anterograde tracer phaseolus vulgaris leucoagglutinin (PHA-L) into gliotic CA3, medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei, or the retrograde tracer cholera toxin B subunit (CTB) into gliotic CA3 area of hippocampus. In the afferent pathway, the number of neurons projecting to CA3 from medial septum and the nucleus of diagonal band of Broca, median raphe, and lateral supramammillary nuclei increased significantly. In the hippocampus, where CA3 pyramidal neurons were partially lost, calbindin, calretinin, parvalbumin immunopositive back-projection neurons from CA1-CA3 area were observed. Sprouting of Schaffer collaterals with increased number of large boutons in both sides of CA1 area, particularly in the stratum pyramidale, was found. When CA3 pyramidal neurons in caudal 80% of the dorsal hippocampus have almost disappeared completely, surviving CA3 neurons in the rostral 20% of the dorsal hippocampus may play an important role in transmitting hyperactivity of granule cells to surviving CA1 neurons or to dorsal part of the lateral septum. We concluded that reorganization of CA3 area with its downstream or upstream nuclei may be involved in the occurrence of epilepsy.

Animals↗
PubMed1984

Discrete lesions of the cerebellar cortex abolish the classically conditioned nictitating membrane response of the rabbit.

The classically conditioned nictitating membrane response (NMR) of the rabbit is useful for analyses of brain structures and pathways involved in mammalian associative learning. Lesions of the entire cerebellum, its nuclei or its efferent pathway abolish conditioned NMR learning and prevent its reacquisition. Until now it has not been clear whether the cerebellar cortex is an essential part of the circuitry for NMR conditioning. Here we report that small lesions of the cerebellar cortex in the hemispheral portion of lobule VI, with sparing of the underlying nuclei, abolish the ipsilateral conditioned NMR and prevent it from being reacquired.

Animals↗
PubMed1999

Deafening alters neuron turnover within the telencephalic motor pathway for song control in adult zebra finches.

In the telencephalon of adult songbirds, projection neurons are lost and replaced within the efferent pathway controlling learned vocal behavior. We examined the potential role of auditory experience in regulating the addition and long-term survival of vocal control neurons in adult male zebra finches. Deafened and control birds were injected with the cell birth marker [(3)H]thymidine and then killed 1 or 4 months later. At the 1 month survival time, the number of [(3)H]-labeled neurons present in the high vocal center (HVC) was 70% lower in deafened birds compared with controls. This was true for all [(3)H]-labeled HVC neurons, as well as the subset that projected to the robust nucleus of the archistriatum. Over the next 3 months, two-thirds of the [(3)H]-labeled HVC neurons in control birds were lost, presumably through cell death. Surprisingly, deafened birds showed no loss over this interval. The total number of HVC neurons did not differ between control and deafened birds at either survival time. Nuclear diameters of [(3)H]-labeled HVC neurons decreased with cell age in both control and deafened birds, a process that may relate to the eventual death and replacement of these cells. These results suggest that experience influences the addition and also the longer-term fate of neurons formed in adulthood. We propose that auditory deprivation decreases the incorporation of new neurons and prolongs their life span. Alterations in the neuronal replacement cycle may relate to the gradual deterioration in song that occurs after deafening in adult zebra finches.

Animals↗
PubMed2004

Trigeminocardiac reflex. A clinical phenomenon or a new physiological entity?

The trigemino-cardiac reflex (TCR) is defined as the sudden onset of parasympathetic dysrhythmia, sympathetic hypotension, apnea or gastric hypermotility during stimulation of any of the sensory branches of the trigeminal nerve. The sensory nerve endings of the trigeminal nerve send neuronal signals via the Gasserian ganglion to the sensory nucleus of the trigeminal nerve, forming the afferent pathway of the reflex arc. This afferent pathway continues along the short internuncial nerve fibers in the reticular formatio to connect with the efferent pathway in the motor nucleus of the vagus nerve. Clinically, the trigemino-cardiac reflex has been reported to occur during craniofacial surgery, balloon-compression rhizolysis of the trigeminal ganglion, and tumor resection in the cerebellopontine angle. Apart from the few clinical reports, the physiological function of this brainstem-reflex has not yet been fully explored. From experimental findings, it may be suggested that the trigemino-cardiac reflex represents an expression of a central neurogenic reflex leading to rapid cerebrovascular vasodilatation generated from excitation of oxygen-sensitive neurons in the rostral ventrolateral medulla oblongata. By this physiological response, the adjustments of the systemic and cerebral circulations are initiated to divert blood to the brain or to increase blood flow within it. As it is generally accepted that the diving reflex and ischemic tolerance appear to involve at least partially similar physiological mechanisms, the existence of such endogenous neuroprotective strategies may extend the actually known clinical appearance of the TCR and include the prevention of other potentially brain injury states as well. This may be in line with the suggestion that the TCR is a physiological, but not a pathophysiological entity.

Afferent Pathways↗
PubMed2005

Direct pyrogenic input from prostaglandin EP3 receptor-expressing preoptic neurons to the dorsomedial hypothalamus.

Fever is induced by a neuronal mechanism in the brain. Prostaglandin (PG) E2 acts as a pyrogenic mediator in the preoptic area (POA) probably through the EP3 subtype of PGE receptor expressed on GABAergic neurons, and this PGE2 action triggers neuronal pathways for sympathetic thermogenesis in peripheral effector organs including brown adipose tissue (BAT). To explore pyrogenic efferent pathways from the POA, we determined projection targets of EP3 receptor-expressing POA neurons with a special focus on rat hypothalamic regions including the dorsomedial hypothalamic nucleus (DMH), which is known as a center for autonomic responses to stress. Among injections of cholera toxin b-subunit (CTb), a retrograde tracer, into hypothalamic regions at the rostrocaudal level of the DMH, injections into the DMH, lateral hypothalamic area (LH) and dorsal hypothalamic area (DH) resulted in EP3 receptor immunolabelling in substantial populations of CTb-labeled neurons in the POA. Bilateral microinjections of muscimol, a GABA(A) receptor agonist, into the DMH and a ventral region of the DH, but not those into the LH, inhibited thermogenic (BAT sympathetic nerve activity, BAT temperature, core body temperature and expired CO2) and cardiovascular (arterial pressure and heart rate) responses to an intra-POA PGE2 microinjection. Further immunohistochemical observations revealed a close association of POA-derived GABAergic axon swellings with DMH neurons projecting to the medullary raphe regions where sympathetic premotor neurons for febrile and thermoregulatory responses are localized. These results suggest that a direct projection of EP3 receptor-expressing POA neurons to the DMH/DH region mediates febrile responses via a GABAergic mechanism.

Adipose Tissue, Brown↗
PubMed1981

[The neurological organisation of vesico-sphincter function (author's transl)].

On the basis of fundamental data drawn from urodynamic study of vesico-sphincter function, the authors begin by a review of the various mechanisms of vesico-sphincter coordination. They then study the neurological control of vesico-sphincter automatic activity. The review of the general organisation of the nervous system is certainly of great value to urologists who are not familiar with neuro-urological problems. This is followed by a more specific study of the neuro-anatomy of the nerve centres and pathways involved in vesico-sphincter automatic activity. Then a review of the reflex centres and their efferent pathways. This is followed finally by a study of integrated reflexes which offers the possibility of an approach to the alternation of phases of filling and micturition, then vesico-sphincter coordination during the phase of filling and the phase of micturition.

Animals↗