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PubMed2003

Forebrain neurons with collateral projections to both the interstitial nucleus of the posterior limb of the anterior commissure and the nucleus of the solitary tract in the rat.

The interstitial nucleus of the posterior limb of the anterior commissure (IPAC) receives inputs from several autonomic/limbic regions in the forebrain, including the agranular insular cortex, bed nucleus of the stria terminalis, the amygdaloid complex, and the lateral hypothalamic area. We sought to identify the distribution of afferent sources to the IPAC and to determine whether these IPAC projection fibers issue collaterals to the nucleus of the solitary tract (NTS), the principal relay of primary visceral afferents. Two fluorescent tracers, FluoroGold and FluoroRed, were centered stereotaxically on the IPAC and the NTS on chloral hydrate-anesthetized Sprague-Dawley rats. Although the majority of IPAC and NTS afferents were spatially segregated, small but substantial numbers of dually labeled neurons (three to four cells/section) were observed in the dorsal bank of the posterior agranular insular cortex, exclusively in layer V. Collateral projection neurons were also found in the posterior part of the lateral hypothalamic area (two to six cells/section). The branching projections identified here may represent a potential link between affective or motivated behavior and viscerosensory processing.

Amygdala↗
PubMed1998

Rostroventrolateral medulla neurons preferentially project to target-specified sympathetic preganglionic neurons.

The rostroventrolateral medulla is a key site for the regulation of vasomotor tone. Sympatho-excitatory neurons project from this region to contact sympathetic preganglionic neurons located in the intermediolateral nucleus of the thoracic and lumbat spinal cord. Functional studies show that stimulation of specific sites in the ventral medulla lead to selective activation of different vascular effectors. The present study was designed to determine the anatomical basis for this selectivity in vasomotor control. Anterograde and retrograde tracing methods were utilized to determine if the descending rostral ventrolateral projection is topographically organized such that neurons in particular locations within the nucleus project preferentially and contact a specific group of sympathetic preganglionic neurons. For this purpose spinally-projecting neurons at 15 sites from three separate rostrocaudal locations within the rostroventrolateral medulla in nine rats were anterogradely labelled with biotin dextran amine. The spinal cord was examined for axon terminals having close apposition to two groups of sympathetic preganglionic neurons, those projecting to the superior cervical ganglion and those to the adrenal medulla which were retrogradely labelled with cholera B chain-conjugated horseradish peroxidase. Areas of close apposition between retrogradely-labelled dendrites, cell bodies and anterogradely-labelled axons were found. Axons descending from the more rostral part of the rostroventrolateral medulla produced the highest density of close appositions to sympathetic preganglionic neurons in both target-specific populations. Caudal rostroventrolateral medulla injection sites gave rise to a less dense distribution of axons and terminals around the spinal sympathetic nuclei. This study has demonstrated that spinally-projecting neurons in the rostroventrolateral medulla are both topographically and viscerotopically organized. It is suggested that such an arrangement provides the means for selective and differential control of autonomic effectors and in particular those involved in cardiovascular regulation.

Animals↗
PubMed1999

Neural connections of the pontine reticular formation, which connects reciprocally with the nucleus prepositus hypoglossi in the rat.

The pontine reticular formation connected with the nucleus prepositus hypoglossi was studied in the rat using anterograde and retrograde tracer techniques. The area reciprocally connected with the nucleus prepositus hypoglossi was evident in the pontine reticular formation of the rat. The region had intensive reciprocal connections with the ipsilateral subthalamic region, the contralateral pontine reticular formation and the nucleus prepositus hypoglossi. Furthermore, it was confirmed that the region received cholinergic projections mainly from the pedunculopontine tegmental nucleus and the laterodorsal tegmental nucleus, and aminergic projections from the dopaminergic cell groups A13 and A11, noradrenergic cell groups A7, A6 and A5, and the serotoninergic B9 cell group. This region in the rat was considered to be the preoculomotor structure in the function of horizontal gaze corresponding to the paramedian pontine reticular formation in other animals.

Animals↗
PubMed1999

Evidence for cholinergic regulation of basal norepinephrine release in the rat olfactory bulb.

The effects of locally infused cholinergic agonists on extracellular levels of norepinephrine in the olfactory bulb of anesthetized rats were determined using in vivo microdialysis coupled with high-performance liquid chromatography and electrochemical detection. Using chronically implanted microdialysis probes, the basal norepinephrine level in the olfactory bulb was 0.55 pg/10 microl dialysate. Local infusion of K+ (30 mM) or the norepinephrine re-uptake inhibitor desipramine (1 microM) through the dialysis probe significantly increased basal norepinephrine levels. Focal activation of noradrenergic locus coeruleus neurons, the sole source of norepinephrine innervation of the olfactory bulb, increased norepinephrine levels by 247% of control. Local infusion of the acetylcholinesterase inhibitor soman (0.4 mM) into the olfactory bulb increased basal norepinephrine levels by 134% of control, suggesting that endogenously released acetylcholine modulates norepinephrine release. Intrabulbar infusion of acetylcholine (40 mM) or nicotine (40 mM) increased norepinephrine levels (317% and 178% of control, respectively), while infusion of the muscarinic receptor agonist pilocarpine (40 mM) reduced norepinephrine levels (54% of control). These results demonstrate that basal norepinephrine release in the olfactory bulb is potently modulated by stimulation of local cholinergic receptors. Nicotinic receptors stimulate, and muscarinic receptors inhibit, norepinephrine release from locus coeruleus terminals.

Animals↗
PubMed2003

Nerve sparing radical hysterectomy: latest developments and historical perspective.

Autonomic nerve damage during surgery is thought to play a crucial role in the aetiology of bladder dysfunction, sexual dysfunction and colorectal motility disorders which are seen in patients after radical hysterectomy. In order to prevent these complications, Japanese gynaecologists introduced a surgical technique with preservation of the pelvic autonomic nerves in the 1960s. In the 1980s the first English paper was published. Since then several surgical approaches have been described, i.e. liposuction, electrical stimulation to locate nerves intra-operatively and laparoscopically assisted techniques. Recently, more attention is being paid to the importance of sparing the sympathetic hypogastric nerve. All authors report results on small cohorts of patients. The incidence of urinary dysfunction seems very low after nerve sparing. Sparing the autonomic nerves during radical hysterectomy seems feasible and safe in both Japanese and Western patients. Literature review does not provide strong clues for a compromised radicality and cure due to nerve sparing. Future larger clinical trials will have to decide whether the technique of nerve sparing radical hysterectomy could be implemented as a standard treatment for cervical cancer patients.

Autonomic Pathways↗
PubMed2003

Vesical dysfunctions after radical hysterectomy for cervical cancer: a critical review.

Functional disorders of the lower urinary tract are the most common long-term complications following radical surgery for cancer of the uterine cervix (8-80%). These disturbances were associated to the partial interruption of the autonomic fibers innervating the bladder during the resection of anterior, lateral and posterior parametrium and vaginal cuff. The pathophysiology of these changes is actually debated. The nature of the surgical damage appears to be a decentralization rather than a complete denervation and bladder dysfunctions may be either the unmasking of intrinsic detrusor activity, characterized by a loss of beta-adrenergic innervation and a consequent alfa-adrenergic hyperinnervation or the influence of remaining sympathetic innervation. No data on long-term bladder function in patients who underwent class 4 radical hysterectomy have been reported. In our experience on long-term vesical function in 38 patients with locally advanced cervical cancer treated with neoadjuvant chemotherapy and 4 Piver type radical hysterectomy, urinary symptoms were reported in 11 patients (29%), while a normal urodynamic finding was recorded in only nine patients (24%). The most common bladder dysfunction was the storage dysfunction (47%). The voiding dysfunction was present in one patient (3%) and stress urinary incontinence in 20 patients (53%). The parametrial and vaginal resections were compared among the urodynamic diagnosis The size of lateral parametria measured on the giant sections did not differ among the groups of urodynamic diagnosis, while the length of vagina removed was significantly longer in patients with detrusor dysfunctions (storage and voiding dysfunctions) than in patients with normal diagnosis or genuine stress incontinence.

Autonomic Pathways↗
PubMed2000

Autonomic regulation of cystatin S gene expression in rat submandibular glands.

Innervation of rat submandibular and parotid glands by the autonomic nervous system regulates saliva volume, its rate of secretion and its composition. The autonomic nervous system also plays a regulatory role in the differentiation and growth of salivary glands, and in the expression of specific sets of genes. Rat cystatin S, a member of family 2 of the cysteine proteinase inhibitor superfamily, is expressed in submandibular and parotid glands of human and rat. In the rat, cystatin S gene expression is tissue- and cell type-specific, is temporally regulated during postnatal development, and not observed in adult animals. The beta-adrenergic agonist isoproterenol (IPR) induces hypertrophic and hyperplastic enlargements of rat salivary glands and the expression of a number of genes including cystatin S. Sympathectomy reduces, but does not completely block, IPR-induced expression of the cystatin S gene in submandibular glands of adult female rats, indicating the participation of sympathetic factor(s) in its regulation. Bilateral parasympathectomy also reduces IPR-induced cystatin S gene expression, suggesting a role of the parasympathetic nervous system in its regulation. Experiments described in this paper suggest that similar factor(s) arising from both the sympathetic and parasympathetic branches of the autonomic nervous system simultaneously participate in IPR-induced cystatin S gene expression in submandibular glands.

Animals↗
PubMed2002

Reflex choroidal blood flow responses of the eyeball following somatic sensory stimulation in rats.

The effect of cutaneous mechanical stimulation on choroidal blood flow (ChBF) of the eyeball measured using a laser Doppler flowmeter was examined in anesthetized rats. Noxious pinching stimulation of a forepaw for 20 s produced increases in ChBF and mean arterial blood pressure (MAP), whereas brushing of a forelimb produced no changes in either parameter. After spinal transection at the fourth thoracic (T4) level, forepaw pinching stimulation did not produce any MAP changes in 9 of 11 spinalized rats. In these nine spinalized animals, pinching stimulation of a forepaw produced no significant responses in ChBF. After the cutting of cervical sympathetic trunks in five spinal rats, forepaw pinching showed no effect on MAP, but produced an increase in ChBF, which was abolished by an intravenous (i.v.) injection of 1-(2-trifluoromethylphenyl) imidazole (TRIM), a selective inhibitor of neuronal nitric oxide synthase (nNOS). In another four spinalized rats, whose cervical sympathetic trunks were intact and the superior salivary nucleus (SSN) was destroyed, forepaw pinching showed no effect on MAP, but produced a decrease in ChBF, which was abolished by an i.v. injection of phentolamine, an alpha-adrenoceptor antagonist. The present experiment shows that somatic afferent stimulation can produce reflex responses of the ChBF of the eyeball, either a vasodilative response using parasympathetic efferent fibers or a vasoconstrictive response using sympathetic efferent fibers, independent of systemic blood pressure. It was also shown that the somatically induced vasodilative response was due to a release of nitric oxide (NO) from parasympathetic nerves and the vasoconstrictive response was due to a release of noradrenaline from sympathetic nerves.

Adrenergic alpha-Antagonists↗
PubMed2000

Muscle reflex control of sympathetic nerve activity in heart failure: the role of exercise conditioning.

Muscle reflex control of sympathetic nerve activity has been an area of considerable investigation. During exercise, the capacity of the peripheral vasculature to dilate far exceeds the maximal attainable levels of cardiac output. The activation of sympathetic nervous system and engagement of the myogenic reflex serve as the controlling influence between the heart and the muscle vasculature to maintain blood pressure (BP). Two basic theories of neural control have evolved. The first termed "central command", suggests that a volitional signal emanating from central motor areas leads to increased sympathetic activation during exercise. According to the second theory the stimulation of mechanical and chemical afferents in exercising muscle lead to engagement of the "exercise pressor reflex". Some earlier studies suggested that group III muscle afferent fibers are predominantly mechanically sensitive whereas unmyelinated group IV muscle afferents respond to chemical stimuli. In recent years new evidence is emerging which challenges the concept of functional differentiation of muscle afferents as well as the classic description of muscle "mechano" and "metabo" receptors. Studies measuring concentrations of interstitial substances during exercise suggest that K(+) and phosphate, but not H(+) and lactate, may be important muscle afferent stimulants. The role of adenosine as a muscle afferent stimulant remains an area of debate. There is strong evidence that sympathetic vasoconstriction due to muscle reflex engagement plays an important role in restricting blood flow to the exercising muscle. In heart failure (HF), exercise leads to premature fatigue and accumulation of muscle metabolites resulting in a greater degree of muscle reflex engagement and in the process further decreasing the muscle blood flow. Conditioning leads to an increased ability of the muscle to maintain aerobic metabolism, lower interstitial accumulation of metabolites, less muscle reflex engagement and a smaller sympathetic response. Beneficial effects of physical conditioning may be mediated by a direct reduction of muscle metaboreflex activity or via reduction of metabolic signals activating these receptors. In this review, we will discuss concepts of flow and reflex engagement in normal human subjects and then contrast these findings with those seen in heart failure (HF). We will then examine the effects of exercise conditioning on these parameters in normal subjects and those with congestive heart failure (CHF).

Autonomic Pathways↗
PubMed2001

Circadian rhythms of autonomic parameters during mental and physical activity.

The structure of circadian rhythms of autonomic parameters was monitored during working week in subjects occupied by physical and mental work. Differences in the rhythm structure depended on the work type and schedule, as well as on the subject age. Hard physical work was associated with biphasic changes in the autonomic nervous system functioning with dominating sympathetic and parasympathetic components in the beginning and at the end of the working week, respectively. Intensive physical work caused rhythm synchronization: the acrophases were shifted to 14.00 and the amplitude of daily oscillations was high. Mental activity with individual working schedule resulted in chronic desynchronization most pronounced in subjects over 30.

Adult↗
PubMed2003

Rostral ventrolateral medulla C1 neurons and cardiovascular regulation.

1. The rostral ventrolateral medulla (RVLM) is essential for the normal control of arterial pressure. This region of the brainstem is heterogeneous, and contains spinally projecting neurons that contain phenylethanolamine-N-methyltransferase (C1 neurons) and non-C1 neurons. 2. The availability of a toxin, a dopamine-beta-hydroxylase antibody conjugated to saporin, that can selectively destroy C1 neurons within the RVLM allows for the study of cardiovascular regulation in rats following depletion of the C1 neuronal population. 3. C1 neurons are not essential for the maintenance of resting blood pressure in anesthetized rats, but do contribute to many cardiovascular responses mediated through the RVLM. 4. The depressor response elicited by clonidine injected into the RVLM is dependent upon C1 neurons. 5. Studies in rats with selective toxin-induced destruction of RVLM C1 neurons demonstrate that C1 neurons contribute importantly to cardiovascular regulation.

Animals↗
PubMed2003

The gigantocellular depressor area revisited.

1. In studies conducted with Dr Donald Reis we described a functionally distinct region of the rat medullary reticular formation that we called the Gigantocellular Depressor Area (GiDA). The GiDA was defined as a region from which vasodepressor and sympathoinhibitory responses were evoked by nanoinjections of glutamate. We later showed that cells in the GiDA project to autonomic nuclei in the medulla, brainstem, and spinal cord, including the intermediolateral cell column. We also showed that kainic acid lesions of the GiDA induce hypertension and block the baroreceptor reflex evoked by electrical stimulation of the aortic depressor nerve. The present studies describe the effects of muscimol nanoinjections into the GiDA. 2. Nanoinjections of muscimol were made in the GiDA of anesthetized rats and changes in arterial pressure, heart rate, and responses to aortic depressor nerve stimulation were measured. 3. Bilateral nanoinjections of muscimol into the GiDA evoke an increase in arterial pressure and lead to fulminating hypertension. Unilateral injections of muscimol into the GiDA block the baroreflex response evoked by electrical stimulation of the ipsilateral aortic depressor nerve. However, these unilateral injections of muscimol into the GiDA evoked profound falls in arterial pressure to nearly spinal levels. In spite of this fall in blood pressure, heart rate also decreased significantly and there was not a compensatory tachycardia. Both the arterial pressure and baroreceptor responses required several hours to recover following the muscimol injections. 4. Although these data are consistent with the proposal that the GiDA is critical for the baroreflex. the opposing effects on blood pressure of unilateral and bilateral injections of muscimol are difficult to reconcile with ourcurrent models of central sympathetic regulation.

Animals↗
PubMed2003

Effect of endothelin on vasomotor and respiratory neurons in the rostral ventrolateral medulla in rats.

1. We have previously shown that intracisternal administration of endothelin-1 (ET-1) elicited cardiorespiratory responses acting on the ventral surface of the medulla oblongata (VSM) subjacent to the rostral ventrolateral medulla (RVLM). In this study, we examined whether vasomotor and respiratory neurons in RVLM participate in above-mentioned responses and whether those neurons respond to direct iontophoretic application of ET-1 and/or an ET-A receptor antagonist, FR139317. 2. Unit activity of vasomotor, respiratory, or nociceptive neurons in RVLM was recorded together with arterial blood pressure (AP) and heart rate (HR) in urethaneanesthetized Sprague-Dawley rats. 3. Intracisternal administration or topical application of ET-1 (0.1-1 pmol) to VSM caused excitation of the majority of vasomotor neurons (15/18) and respiratory neurons (10/11) but not in nociceptive neurons (0/7). Changes in neuronal activity were in similar time course with corresponding changes in AP and HR. Iontophoretic application of ET-1 to the vicinity of recording neuron caused excitation in 19 of 21 vasomotor neurons without affecting AP nor HR. Remaining two neurons were insensitive to ET-1. FR139317 did not affect basal activity of the vasomotor neurons but inhibited ET-1-evoked excitation. Twenty-four of 40 respiratory neurons were excited and 13 were inhibited by iontophoretic application of ET-1. Five of ET-1-excited respiratory neurons were inhibited by FR139317 alone while six of ET-1-inhibited neurons were not affected by FR139317 alone. In both cases, FR139317 inhibited the effect of simultaneously applied ET-1. Iontophoretic application of ET-1 excited only one out of 10 nociceptive neurons so far tested. 4. These results support the view that intracisternally administered ET-1 alters activity of vasomotor and respiratory neurons in the RVLM, at least in part by acting directly on neurons themselves and hence causes systemic cardiorespiratory changes. Majority of vasomotor and respiratory neurons should express ET-A receptors and some respiratory neurons are under tonic excitatory control by ET-1.

Action Potentials↗
PubMed2003

Brainstem in multiple system atrophy: clinicopathological correlations.

1. Multiple system atrophy (MSA) is a sporadic neurodegenerative disorder that manifests with parkinsonism, cerebellar ataxia, and autonomic failure in various combinations. 2. Orthostatic hypotension, neurogenic bladder, laryngeal stridor and sleep apnea, and rapid eye movement (REM) sleep behavior disorder are prominent manifestations of MSA. 3. In MSA, there is severe depletion of catecholaminergic neurons of the C1 and A1 areas in the ventrolateral medulla, and this may contribute to orthostatic hypotension and endocrine disturbances in this disorder, respectively. 4. Loss of corticotrophin-releasing factor (CRF) neurons in the pontine micturition area may contribute to neurogenic bladder dysfunction. 5. Respiratory abnormalities may reflect loss of cholinergic neurons in the arcuate nucleus of the ventral medulla. 6. Loss of cholinergic mesopontine neurons, in the setting of loss of locus ceruleus neurons and preservation of rostral raphe neurons, may contribute to REM sleep abnormalities in MSA.

Autonomic Pathways↗
PubMed1997

Natriuretic peptide immunoreactivity in nerve structures and Purkinje fibres of human, pig and sheep hearts.

Atrial natriuretic peptide is a well-described peptide in cardiac Purkinje fibres and has been shown to interfere with the autonomic regulation in the heart of various species, including man. Recently, we detected immunoreactivity for the peptide in intracardial ganglionic cells and nerve fibre varicosities of bovine hearts, by the use of a modified immunostaining technique that induced an improved detection of natriuretic peptides. These findings raised the question as to whether natriuretic peptides are detectable in these tissues in man and other species. The conduction system from human, pig and sheep hearts was dissected processed with antisera against atrial natriuretic peptide and the closely related brain natriuretic peptide. Immunostaining for the brain natriuretic peptide was detected in some Purkinje fibres in all of these species. Interestingly, in pig, sheep and human hearts, some ganglionic cells and nerve fibres showed atrial natriuretic peptide immunoreactivity, particularly in the soma of human ganglionic cells. This is the first study showing immunoreactivity for the atrial natriuretic peptide in nerve structures and for the brain natriuretic peptide in Purkinje fibres of the human heart. The results give a morphological correlate for the documented effects of atrial natriuretic peptide on the heart autonomic nervous system and for the presumable effects of brain natriuretic peptide in the conduction system of man.

Adult↗