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PubMed2005

Fos activation in hypothalamic neurons during cold or warm exposure: projections to periaqueductal gray matter.

The hypothalamus, especially the preoptic area, plays a crucial role in thermoregulation, and our previous studies showed that the periaqueductal gray matter is important for transmitting efferent signals to thermoregulatory effectors in rats. Neurons responsible for skin vasodilation are located in the lateral portion of the rostral periaqueductal gray matter, and neurons that mediate non-shivering thermogenesis are located in the ventrolateral part of the caudal periaqueductal gray matter. We investigated the distribution of neurons in the rat hypothalamus that are activated by exposure to neutral (26 degrees C), warm (33 degrees C), or cold (10 degrees C) ambient temperature and project to the rostral periaqueductal gray matter or caudal periaqueductal gray matter, by using the immunohistochemical analysis of Fos and a retrograde tracer, cholera toxin-b. When cholera toxin-b was injected into the rostral periaqueductal gray matter, many double-labeled cells were observed in the median preoptic nucleus in warm-exposed rats, but few were seen in cold-exposed rats. On the other hand, when cholera toxin-b was injected into the caudal periaqueductal gray matter, many double-labeled cells were seen in a cell group extending from the dorsomedial nucleus through the dorsal hypothalamic area in cold-exposed rats but few were seen in warm-exposed rats. These results suggest that the rostral periaqueductal gray matter receives input from the median preoptic nucleus neurons activated by warm exposure, and the caudal periaqueductal gray matter receives input from neurons in the dorsomedial nucleus/dorsal hypothalamic area region activated by cold exposure. These efferent pathways provide a substrate for thermoregulatory skin vasomotor response and non-shivering thermogenesis, respectively.

Animals↗
PubMed1995

The mechanism responsible for hypertension in a patient with Guillain-Barré syndrome.

We report a case of hypertension associated with Guillain-Barré syndrome. In this case, the circadian variation of blood pressure was interrupted. Examination of neurohumoral factors revealed a hyperactive sympathetic nervous system and an increase in plasma renin activity. Clonidine, which acts centrally to inhibit sympathetic outflow, did not suppress serum norepinephrine or epinephrine. These observations suggest that autonomous hyperactivity of the efferent pathway of the sympathetic nervous system may cause the sustained hypertension throughout the day in this case.

Adult↗
PubMed1985

Cholecystokinin-induced excitation in the substantia nigra: evidence for peripheral and central components.

Cholecystokinin (CCK), one of the most common brain peptides, coexists with dopamine (DA) in neurons of the medial substantia nigra (SN). CCK has been shown to excite these neurons following either direct iontophoretic or systemic administration suggesting that peripherally administered CCK may cross the blood brain barrier to act directly on nigral DA cells. However, biochemical evidence suggests that CCK does not cross the blood brain barrier, and several studies have shown that the behavioral and the satiety-inducing effects of peripherally administered CCK are abolished by vagotomy. In order to test for vagal mediation of the nigral response to systemically administered CCK, we examined the effects of a series of lesions to the vagal pathways on CCK-induced excitation in the SN. Neither acute thoracic nor chronic subdiaphragmatic vagotomies had any effect on the excitatory response of nigral DA neurons to systemically administered CCK. High cervical spinal cord transections were similarly without effect. In contrast, lesions of either vagal fibers in the medulla or of the efferent pathways from the nucleus tractus solitarii, the primary sensory nucleus of the vagus, produced significant attenuations of the nigral effects of systemically administered CCK. However, neither lesion blocked effects of CCK completely. We suggest that peripherally administered CCK has two components to its excitatory action in the SN; a component probably mediated through CCK receptors in the nucleus tractus solitarii and a direct action on DA neurons.

Animals↗
PubMed1993

Differential responses of barosensitive neurons of rostral ventrolateral medulla to hypoxia in rats.

We examined the responses to hypoxia of 48 spontaneously active barosensitive neurons of the rostral ventrolateral medulla (RVL) of anesthetized rats. Twenty-nine projected to the spinal cord while 19 did not. All spinal barosensitive neurons increased their discharges in advance of an elevation of arterial pressure in the presence or absence of arterial chemoreceptors. In contrast, 18/19 of the non-spinal barosensitive neurons were not excited by hypoxia. The results indicate that barosensitive RVL neurons consist of two populations differing in efferent pathway and responsivity to hypoxia and that the spinal barosensitive RVL neurons are functionally discrete and selectively sensitive to hypoxia.

Animals↗
PubMed1990

Enhanced sympathetic mediation of chronotropic baroreflexes in old Sprague-Dawley rats.

We compared reflex heart rate responses elicited during intravenous infusions of phenylephrine or sodium nitroprusside in conscious 4- and 24-month-old male Sprague-Dawley rats to determine whether baroreflex regulation changes with age. Underlying neural mechanisms were assessed by repeating baroreflex tests following cholinergic blockade with methylatropine or beta-adrenergic blockade with propranolol. Basal blood pressures always tended to be higher, while corresponding heart rates were lower, in old than in young rats. Reflex bradycardia (but not tachycardia) was initially weaker in 24-month-old rats as were reductions in both reflex bradycardia and tachycardia after cholinergic blockade. On the other hand, the reduction in reflex tachycardia following beta-adrenergic blockade in old rats was more pronounced and almost equal to that produced by combined cholinergic and beta-adrenergic blockade. From these results we conclude that with old age in male Sprague-Dawley rats, just as has been shown previously in Fischer 344 rats, predominant efferent pathways for regulating heart rate reflexes are also altered to become almost exclusively beta-adrenergic or sympathetic.

Aging↗
PubMed1986

Reflex activation of the lower oesophageal sphincter in the cat induced by stimulation of the splanchnic afferent fibres.

Reflex responses of the lower oesophageal sphincter (l.o.s.) to electrical stimulation of the splanchnic afferent fibres were recorded by electromyographic and manometric techniques. Repetitive stimulation of the central end of a splanchnic nerve induced a long latency excitation of the l.o.s., i.e. bursts of spike potentials concomitant with repetitive phasic contractions. Experiments involving nerve sections showed that the efferent pathways of this reflex were served either by stellate sympathetic and/or splanchnic fibres, or by vagal fibres. These responses were abolished following the administration of atropine. These results show that the splanchnic afferent fibres are involved in l.o.s. reflex motor responses through the activation of the sympathetic and parasympathetic efferent supply to the sphincter.

Animals↗
PubMed1976

Effects of atropine, injected into a lateral cerebral ventricle of the rabbit, on fevers due to intravenous leucocyte pyrogen and hypothalamic and intraventricular injections of prostaglandin E1.

1. Cholinergic synapses in the hypothalamus may transmit information in those thermoregulatory pathways which function to raise body temperature. The effect of atropine, administered intracranially, on the febrile response to intravenous leucocyte pyrogen or intracranial prostaglandin E1 was therefore examined in conscious rabbits. 2. In rabbits exposed to a thermoneutral environment, micro-injections of PGE1, into the anterior hypothalamus, intraventricular injections of PGE1, and intravenous injection so leucocyte pyrogen all caused fever accompanied by vasoconstriction in the ears and reduced respiratory rate. Intraventricular injection of 200 mug atropine during such fevers attenuated their development. This was due to the activation of heat loss mechanisms through vasodilatation in the ears and an increase in the frequency of respiration. This suggests a similarity in the pattern of neuronal activity evoked by PGE1 and leucocyte pyrogen, at least at the site(s) where atropine directly or indirectly exerted its effect and in the efferent pathways from this site. 3. In rabbits exposed to a cold environment, intraventricular injection of PGE1 caused fever through the activation of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shivering accompanied by increased O2 consumption. Intraventricular injection of atropine during the development of fever caused an inhibition of shievering and a decrease in O2 consumption so that temperature ceased to rise and returned to normal. 4. During fever, reversal by atropine of the increased heat conservation of rabbits in a neutral environment, and of their increased heat production in a cold environment adds further support to the concept that cholinergic synapses provide an important link in central temperature-rasising pathways.

Animals↗
PubMed1999

Cough, cough receptors, and asthma in children.

This review discusses current general concepts on cough and the relationship between cough, cough receptor sensitivity, and asthma in children. It presents models of the relationship between cough and bronchoconstriction, and proposes a new model outlining the relationship between cough receptor sensitivity, airway hyperresponsiveness, and the clinical issues of cough, wheeze, and dyspnea in children with and without asthma. Cough is very common in children, with a prevalence of 15-20%. Those with non-specific cough (dry cough in the absence of identifiable respiratory illness) are often treated with a variety of drugs, in particular, medications for asthma and gastroesophageal reflux. However, there is little evidence to use these medications for the sole symptom of cough in children. Clinical studies on cough need to be interpreted in light of inherent methodological problems in studying cough. These methodological problems include the nonrepeatable nature of questions on cough, the unreliability of subjective measurements of cough, the lack of objective measurements to quantify cough severity, and the period effect (spontaneous resolution of cough). Although cough can be troublesome, cough serves as an important function for maintaining normal health of the respiratory system. The importance of cough in maintaining respiratory health is reflected in the development of lung atelactasis/collapse from retained secretions and recurrent pneumonia in clinical situations where the cough reflex is ineffective. The cough reflex is complex and still poorly understood. In this article the simplified cough pathway is presented and involves cough receptors, mediators of sensory nerves and the afferent pathway, the vagus nerve, the cough centre, efferent pathway, and cough effectors.

Adolescent↗
PubMed1994

Transmitter mechanisms in vagal afferent-induced reduction of lower oesophageal sphincter (LOS) pressure in the rat.

The extrinsic neural pathways and transmitter mechanisms involved in neural influences controlling lower oesophageal sphincter (LOS) pressure have been evaluated in three groups of experiments in urethane anaesthetized rats. A miniature perfused sleeve/sidehole catheter measured gastric, LOS and oesophageal pressures. Group 1: Vago-vagal and vago-spinal reflex pathways were activated simultaneously via the central nervous system by stimulation of the central cut end of the left vagus. This caused a prolonged drop in LOS pressure with a rapid onset and a slow return to baseline. Subsequent right (bilateral) vagotomy in these animals increased basal LOSP (P < 0.001). Central vagal stimulation-induced reduction of LOSP was not significantly changed in amplitude but was shorter in duration (P < 0.01) than before bilateral vagotomy. IV administration of the 5-HT3 receptor antagonist granisetron (50 micrograms/kg), after bilateral vagotomy had no effect on the response to central vagal stimulation. The nitric oxide (NO) synthase inhibitor L-nitroarginine methyl ester (L-NAME) (100 mg/kg) reduced the depth of relaxation (P < 0.01) and temporarily increased basal LOSP. Propranolol (1.5 mg/kg, i.v.) subsequently increased basal LOSP (P < 0.01), but had no further effect on the vagal stimulation-induced reduction in LOSP. Alpha adrenergic blockade with phentolamine (1 mg/kg, i.v.) decreased basal LOSP (P < 0.01), and nearly abolished the response to vagal stimulation (P < 0.01). Group 2: Both alpha 1- and alpha 2-adrenoceptors were shown to be involved by the combined use of the more selective antagonists yohimbine (1 mg/kg, i.v.) and prazosin (200 micrograms/kg) in place of phentolamine. Group 3: To observe neurotransmitter mechanisms in the vago-vagal pathway, central left vagal stimulation was performed after left vagotomy, and subsequently after blockade of sympathetic motor pathways with guanethidine (5 mg/kg), leaving intact efferent pathways in the right vagus. Guanethidine increased basal LOSP (P < 0.01), and reduced the duration of vagal-induced LOS relaxation (P < 0.05). Depth of relaxation was unchanged. Subsequently, granisetron and L-NAME had no significant effects. Finally, additional right vagotomy abolished the remaining response. Our data indicate the existence of vago-spinal and vago-vagal inhibitory reflex pathways to the rat LOS. The inhibitory vago-spinal pathway is mainly alpha-adrenergic, and has a minor NO-mediated component, but no 5-HT3 receptor-mediated mechanism. In the vago-vagal pathway, no significant involvement of NO-mediated or 5-HT3 receptor-mediated effects was observed. Other non-adrenergic inhibitory mechanisms were, however, apparent.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1982

Various transmitters as filters in transferring information in an identified neural network of gastropods.

1. The motor and interneurones in the identified neural network regulating the cardio-renal system of Helix pomatia L. produced differing effects with ACh, 5HT, DA and OP. They were less sensitive to glutamate. 2. On the double action interneuron the sensitivity to the neurotransmitters was modified by the source of input and the sequence of their application. 3. The interneuron V21 uses ACh and 5HT as neurotransmitters. Seven afferent excitatory pathways terminate on interneuron V21. 4. The efferent pathways of interneuron V21 can be selectively blocked by haloperidol and ergotamine. 5. The peptide-like factor released spontaneously following haloperidol and ergotamine treatment block the cholinergic and aminergic pathways onto interneuron V21, while the amino acid mechanism remains unaltered.

Animals↗
PubMed1976

Neurogenic influences on blood pressure and vascular tone from peripheral receptors during muscular contraction.

In anesthetized dogs, contraction of the muscles of the thigh was elicited either by applying electrodes in the muscles or by stimulation of the spinal ventral roots. The carotid sinuses were isolated; the vagi and the depressor nerves cut. Rhythmic muscular contraction caused hypotension and vasodilatation; tetanic contraction caused hypertension and vasoconstriction. These responses are of reflexogenic origin: the afferent pathway is in the somatic nerves, the efferent pathway in the sympathetic nerves.

Animals↗
PubMedDate not supplied

Reflex-induced acceleration of mucociliary activity in rabbit after exposure to cigarette smoke.

Short-term exposure to cigarette smoke is known to accelerate mucociliary (m.c.) activity in the rabbit maxillary sinus and to increase m.c. clearance from the lung. Several components of cigarette smoke stimulate sensory C-fibre endings in the airways. Some of these fibres contain the neuropeptide substance P (SP), and release of SP after stimulation of C-fibre endings is thought to accelerate m.c. activity. The purpose of the present investigation was to study possible mechanisms responsible for the increase of m.c. activity in the rabbit maxillary sinus after exposure to cigarette smoke. When delivered once a minute, 2.5 ml smoke puffs each accelerated the m.c. activity, the maximal increase being 34.7 +/- 2.4%, with a latency of 3.7 +/- 0.5 s. The response to cigarette smoke was suppressed in rabbits pretreated with atropine, an SP antagonist [(D-Pro2, D-Trp7,9)SP], capsaicin or hexamethonium. A response, albeit reduced, elicited in atropinized rabbits indicated a non-cholinergic component. The atropine-resistant acceleration was abolished by the SP antagonist. Together the results suggest that cigarette smoke accelerates m.c. activity through a reflex involving sensory SP containing C-fibres (afferent pathway) and cholinergic (probably parasympathetic) effector neurones (efferent pathway). Hence, the effect of cigarette smoke on the m.c. system reflects the joint release of both SP and acetylcholine. This dual mechanism may be of importance in the regulation of m.c. activity.

Acetylcholine↗
PubMed1985

[Efferent connections of the caudate nucleus of the cat studied using retrograde axonal transport of horseradish peroxidase].

The origin of descending efferent pathways from the caudate nucleus was studied by retrograde axonal transport of horseradish peroxidase. Widespread topically organized projections were observed to the paleostriatum and the substantia nigra and less numerous to the thalamus. The main source of these projections were small and medium-size cells. A particular role of the subthalamic nucleus in the descending efferent system of the caudate nucleus is pointed out: this nucleus besides projections to the caudate nucleus itself possesses direct connections with principal output structures of the latter--the the paleostriatum and substantia nigra.

Animals↗
PubMed1982

The brain-islet axis: the nervous control of the endocrine pancreas.

The central nervous system exerts a control on the endocrine pancreas and can modulate the basic feed-back loop linking the concentration of the main energy substrates in blood with islet cell functions. Thus, the elementary glucose-insulin system can be modulated under physiological conditions by both the long-recognized entero-insular axis and by a brain-islet axis, particularly when insulin release occurs in anticipation of meals. Experimental stimulation or section of afferent nerves to the pancreas have demonstrated the existence of this nervous control. Changes in islet cell secretion during stress illustrate this influence under clinical conditions. A variety of experimental data suggest intervention of the brain-islet axis under the physiological circumstances: 1) Manipulation of certain hypothalamic centres followed by modification of feeding behaviour and of islet secretion. 2) Input to the brain is both humoral (carried by arterial carotid blood or the cerebrospinal fluid) and nervous, of sensory and visceral origins. Changes in these afferent pathways may influence islet secretion via the efferent pathways of the vagus and splanchnic nerves. 3) Besides acetylcholine and catecholamines, peptide neurotransmitters are likely to be involved in the transmission of these nervous inputs to islet cells. 4) Furthermore, hypothalamic factor (s) may also modify the endocrine pancreatic secretions.

Adrenergic Fibers↗
PubMed1980

Endorphin-parasympathetic interactions in spinal shock.

We have recently shown that the opiate antagonist naloxone can partially reverse the hypotension which accompanies spinal cord transection, through actions on opiate receptors in the central nervous system. In the present studies we demonstrate that either vagotomy or atropine prevents the ability of naloxone to reduce the hypotension caused by spinal transection in the rat and cat. Since the peripherally acting methyl-atropine blocks the cardiovascular effects of centrally administered naloxone in this model, these findings imply an interaction between endorphin systems and central parasympathetic centers in spinal shock. This interaction results in a depression of cardiovascular function which is mediated through cholinergic vagal efferent pathways. Furthermore, the fact that naloxone reduces the hypotension following spinal transection, along with the role of the parasympathetic system in this process, appears to question the classic conception that such hypotension results entirely from interruption of descending sympathetic pressor pathways. Finally, the beneficial cardiovascular effects of naloxone in spinal shock may have important therapeutic implications in the management of spinal cord injury.

Animals↗
PubMed1975

Interactions between vagus nerve stimulation and pentagastrin or secretin on the guinea pig gallbladder.

In guinea pigs, anaesthetised with urethane, stimulation of the peripheral cut end of the cervical vagus activates cholinergic excitatory and non-adrenergic inhibitory fibres to the gallbladder. Central vagal stimulation reflexly contracts the gallbladder by an efferent pathway in the vagus and also activates an adrenergic, non-vagal inhibitory pathway to the gallbladder. Injections of pentagastrin (12-33 mug kg-1 s.c.) or secretin (0.1-0.2 U kg-1 i.a.), doses which produce no effect on gallbladder tone when administered alone, significantly increase the contractions evoked by vagal stimulation.

Animals↗
PubMed1987

The central efferent mechanism of brown adipose tissue thermogenesis induced by preoptic cooling.

This study was performed to investigate central efferent mechanisms for brown adipose tissue thermogenesis. In unanesthetized rats, the effects of local anesthesia of the ventromedial hypothalamus, anterior hypothalamus, and lateral hypothalamus were observed on the brown adipose tissue thermogenesis induced by preoptic cooling. Rats had a thermode, thermocouple, and bilateral injection cannulae chronically implanted in the hypothalamus and a thermocouple beneath the interscapular brown adipose tissue. The experiments were done at an ambient temperature of 24-25 degrees C. Preoptic cooling increased brown adipose tissue and colonic temperatures without shivering. Injecting lidocaine bilaterally into the ventromedial hypothalamus during preoptic cooling reduced brown adipose tissue temperature (Tbat). The mean maximum decrease of Tbat was 0.51 +/- 0.26 degrees C and occurred 5-8 min after lidocaine injection. When lidocaine was injected into the anterior hypothalamus, Tbat increased. The mean maximum increase of Tbat was 0.85 +/- 0.29 degrees C and occurred 4-9 min after lidocaine injection. In the lateral hypothalamus, lidocaine had no effect on Tbat. Tbat was not influenced by injection of saline into the ventromedial, anterior, or lateral hypothalamus. The efferent pathway from preoptic to brown adipose tissue may thus traverse the medial part of hypothalamus. The ventromedial hypothalamus facilitates and anterior hypothalamus inhibits brown adipose tissue thermogenesis induced by preoptic cooling.

Adipose Tissue, Brown↗
PubMed1976

Telencephalic projections in two teleost species.

The efferent pathways of the telencephalon were investigated in the percomorph Eugerres and the berycomorph Holocentrus. One telencephalic hemisphere was resected by suction and the animals were perfused 7-35 days thereafter. The brains were processed according to a modification (Method 7 in Ebbesson, '70) of the Fink-Heimer ('67) technique for selective silver impregnation of degenerating axons and terminals. Some fibers emerging from the lesioned telencephalic hemisphere terminate upon the contralateral hemisphere. The large bulk of efferent fibers, however, descends into the ipsilateral diencephalon and gives off the so-called strio-tectal bundle (STB) as well as the medial forebrain bundle (MFB). The remaining contingent eventually splits into the so-called strio-lobar bundle (SLB) and the lateral forebrain (LFB), but, previous to splitting, it contributes most of the telencephalic projection to the optic tectum in Eugerres, and gives abundant terminals to the ipsilateral nucleus rotundus or prethalamicus in both Eugerres and Holocentrus. The STB conveys all telencephalo-tectal fibers in Holocentrus, and some of them in Eugerres. Telencephalic efferents teminate ipsilaterally in the middle level of the tectum's stratum griseum centrale; in Holocentrus there is also a small projection to the stratum opticum. The MFB terminates at the caudal hypothalamus and gives terminals all along its course. The LFB also gives terminals all along its course and terminates upon a nucleus located between the midline and the corpus glomerulosum. The SLB spreads out and terminates in the inferior lobe of the hypothalamus.

Animals↗