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PubMed2000

Effect of acupuncture-like stimulation on cortical cerebral blood flow in anesthetized rats.

The effect of acupuncture-like stimulation of various areas (cheek, forepaw, upper arm, chest, back, lower leg, hindpaw, perineum) on cortical cerebral blood flow (CBF) was examined in anesthetized rats. An acupuncture needle (diameter, 340 microm) was inserted into the skin and underlying muscles at a depth of about 5 mm and twisted to the right and left once a second for 1 min. CBF of the cortex was measured using a laser Doppler flowmeter. Stimulation of the cheek, forepaw, upper arm and hindpaw produced significant increases in CBF, but stimulation of the chest, back, lower leg and perineum did not produce significant responses. Stimulation of the cheek, forepaw, and hindpaw produced an increase in mean arterial pressure (MAP), while stimulation of the back produced a decrease in MAP. Stimulation of the upper arm, chest, lower leg and perineum did not produce a significant MAP response. After spinal transection at the 1st to 2nd thoracic level, the blood pressure response to stimulation of the cheek and forepaw was suppressed, whereas an increase in CBF still took place. The increase in CBF induced by forepaw stimulation was abolished by severance of the somatic nerves at the brachial plexus. Forepaw stimulation enhanced the activity of the radial, ulnar and median nerves. Furthermore, in the present study, passing of an electric current through acupuncture needles showed that excitation of group III (Adelta) and group IV (C) afferent fibers in the somatic nerve was capable of producing an increase in CBF, whereas excitation of group I (Aalpha) and group II (Abeta) fibers was ineffective. The increase in CBF induced by forepaw stimulation was almost abolished by intravenous administration of muscarinic and nicotinic cholinergic blocking agents (atropine 5 mg/kg and mecamylamine 20 mg/kg), and by bilateral lesions in the nucleus basalis of Meynert. Acupuncture-like stimulation of a forepaw increased acetylcholine release in the cerebral cortex. We concluded that the increase in CBF, independent of systemic blood pressure, elicited by acupuncture stimulation is a reflex response in which the afferent nerve pathway is composed of somatic group III and IV afferent nerves, and efferent nerve pathway includes intrinsic cholinergic vasodilators originating in the nucleus basalis of Meynert.

Acetylcholine↗
PubMed1990

Quantitative noninvasive electrophysiological evaluation of the activity of the cutaneous division of the sympathetic nervous system.

The functional status of the cutaneous division of the orthosympathetic nervous system was indirectly and non-invasively assessed by monitoring the skin electrical relative resistance variations (SERV). The advantages of our recording system of second generation were (1) simultaneous recording on two or four channels of the evoked electrodermal response to psychic or to sensorial stimulus; (2) self-balancing system which allows the recording of the relative variation of the electric parameter, i.e. its variation with time; (3) precise determination of the amplitude (omega/s, mu F/s) of the evoked response; (4) reference of the latency time (LT) of the evoked response to the length of the anatomical pathway of the signal giving the autonomic conduction velocity (ACV). Decrease in diabetic autonomic neuropathy of both spontaneous and evoked electrodermal activities suggested their relationship with cutaneous sympathetic activity.

Acoustic Stimulation↗
PubMed2006

Update on the relationship between sexual dysfunction and lower urinary tract symptoms/benign prostatic hyperplasia.

PURPOSE OF REVIEW: Lower urinary tract symptoms (LUTS) associated with benign prostatic hyperplasia (BPH) is a condition that commonly affects older men and is often associated with sexual dysfunction. Recent evidence of an association between LUTS/BPH and sexual dysfunction will be reviewed, as well as the effects of pharmacological treatment options for symptomatic LUTS/BPH on sexual function. RECENT FINDINGS: Large-scale epidemiological studies conducted worldwide have provided strong evidence for an association between LUTS, erectile dysfunction and ejaculatory dysfunction. In multivariate analyses controlling for age, comorbidities, and lifestyle factors, LUTS have been clearly demonstrated to be an independent risk factor for erectile and ejaculatory dysfunction. Various pathophysiological mechanisms have been proposed for the association between LUTS and male sexual dysfunction. These include autonomic hyperactivity, alterations in Rho/Rho kinase pathway, endothelial (nitric oxide synthase/nitric oxide) dysfunction, pelvic ischemia, and age-related hormone imbalances. Owing to the link between LUTS/BPH and male sexual dysfunction, patients presenting with one of these conditions should be routinely screened for the other condition. In addition, because medical and surgical treatments for LUTS/BPH are commonly associated with sexual side effects, patients with LUTS/BPH should be monitored for treatment-related sexual outcomes. SUMMARY: LUTS/BPH is an independent risk factor for sexual dysfunction in aging men. Further studies are needed to define the mechanism(s) underlying the link between LUTS/BPH and male sexual dysfunction. Additional studies of combination therapy for LUTS/BPH, sexual dysfunction, and other age-associated comorbidities are needed to establish new approaches to the optimal management of these conditions in aging men.

Adrenergic alpha-Antagonists↗
PubMed1993

Reversible lesions of the nucleus of the solitary tract attenuate the memory-modulating effects of posttraining epinephrine.

Rats implanted with cannula tips placed above the nucleus of the solitary tract (NTS) were trained to obtain food pellets placed in 2 arms of a Y maze and then given a footshock in 1 arm of the maze. The rats then received bilateral injections of lidocaine or buffer into the NTS and peripheral injections of saline or epinephrine (0.01 or 0.05 mg/kg ip). Two tests were given 24 and 48 hr after training to assess retention in the presence and absence of contextual cues (the stainless steel floor) associated with the footshock training trial. Epinephrine (0.05 mg/kg) produced a significant enhancement in retention, which was attenuated by injections of lidocaine into the NTS. These findings indicate that the NTS is involved in mediating the memory-modulating effects of peripheral epinephrine and that such effects are initiated at least in part by activation of vagal afferents projecting to the NTS.

Afferent Pathways↗
PubMed1996

Long-term inhibition of NO synthase induces cardiac hypertrophy with a decrease in adrenergic innervation.

Data concerning the effect of NO on the function and structure of the heart are controversial. We have studied two main questions: (i) Does the heart muscle reflect the hypertension induced by long-term inhibition of NO synthase? (ii) Since the arginine-NO pathway is also operative in the autonomic nervous system, the second goal was to ascertain the possible changes of the adrenergic nervous system in the heart after long-term NO synthase inhibition. Wistar rats were administered L-NAME in drinking water (50 mg/kg bw/day) for 8 weeks. Systolic blood pressure and heart rate were monitored weekly. The heart/body weight ratio were determined at the end of experiment. The adrenergic nerve terminals visualized by histochemistry were counted according to Haug's point counting method. Blood pressure increased significantly in L-NAME-treated rats. No changes were found in the heart rate. Heart/body weight ratio increased markedly. Surprisingly, the density of adrenergic nerve terminals did not alter accordingly. The density of adrenergic nerve terminals in the left ventricle and septum decreased but no significant changes were found in the left atrium and the right ventricle. Hypertension due to NO deficiency induced cardiac hypertrophy that was characterized by a decline in the density of adrenergic innervation of the overloaded left ventricle and septum.

Adrenergic Fibers↗
PubMed2005

Nerve growth factor-tyrosine kinase A pathway is involved in thermoregulation and adaptation to stress: studies on patients with hereditary sensory and autonomic neuropathy type IV.

Hereditary sensory and autonomic neuropathy type IV (HSAN IV) is caused by mutations in the tyrosin kinase A (TrkA) gene, encoding for the high-affinity receptor of nerve growth factor (NGF). The NGF-TrkA system is expressed in many endocrine glands. We hypothesized that HSAN IV represents a natural model for impaired NGF effect on the neuroendocrine system in humans. We have documented the clinical outcome of 31 HSAN IV patients in a single medical center, and investigated their basal endocrine system status. The endocrine system response to thirst was compared between six patients and six healthy children. High rates of mortality (22%) and severe morbidity (30%) have been found in HSAN IV patients. Hypothermia was noted in 40% of the patients and unexplained fever was observed in 56%. Subnormal adrenal function was demonstrated in six (30%) of the patients studied. Furthermore, we found lower plasma norepinephrine (NE) levels in six HSAN IV patients compared with a control group after the thirst test. Our findings emphasize the importance of NGF-TrkA pathway in the physiology of the neuroendocrine system and its response to stress. Inadequate response to stress might contribute to the observed significant mortality, morbidity, and temperature instability in HSAN IV patients.

Body Temperature Regulation↗
PubMed2001

The R22X mutation of the SDHD gene in hereditary paraganglioma abolishes the enzymatic activity of complex II in the mitochondrial respiratory chain and activates the hypoxia pathway.

Hereditary paragangliomas are usually benign tumors of the autonomic nervous system that are composed of cells derived from the primitive neural crest. Even though three genes (SDHD, SDHC, and SDHB), which encode three protein subunits of cytochrome b of complex II in the mitochondrial respiratory chain, have been identified, the molecular mechanisms leading to tumorigenesis are unknown. We studied a family in which the father and his eldest son had bilateral neck paragangliomas, whereas the second son had a left carotid-body paraganglioma and an ectopic mediastinal pheochromocytoma. A nonsense mutation (R22X) in the SDHD gene was found in these three affected subjects. Loss of heterozygosity was observed for the maternal chromosome 11q21-q25 within the tumor but not in peripheral leukocytes. Assessment of the activity of respiratory-chain enzymes showed a complete and selective loss of complex II enzymatic activity in the inherited pheochromocytoma, that was not detected in six sporadic pheochromocytomas. In situ hybridization and immunohistochemistry experiments showed a high level of expression of markers of the angiogenic pathway. Real-time quantitative reverse transcriptase (RT)-PCR measurements confirmed that vascular endothelial growth factor and endothelial PAS domain protein 1 mRNA levels were significantly higher (three- and sixfold, respectively) than those observed in three sporadic benign pheochromocytomas. Thus, inactivation of the SDHD gene in hereditary paraganglioma is associated with a complete loss of mitochondrial complex II activity and with a high expression of angiogenic factors.

Adult↗
PubMed2003

Vestibular nucleus projections to the Edinger-Westphal and anteromedian nuclei of rabbits.

The Edinger-Westphal nucleus (EW), anteromedian nucleus (AM) and adjacent neurons in the ventral tegmental area (VTA) are sources of preganglionic parasympathetic innervation of intraocular smooth muscle, including blood vessels, pupillary muscle and the ciliary body in mammals. They also have central connections that are believed to affect parasympathetic outflow indirectly. This study utilized anterograde transport of biotinylated dextran amine and Phaseolus vulgaris leucoagglutinin to demonstrate direct projections from the vestibular nuclei to the Edinger-Westphal and anteromedian nuclei in rabbits. The rabbit AM and adjacent VTA contain moderate to intensely choline acetyltransferase (ChAT)-immunopositive neurons. The rabbit EW, by contrast, is nearly devoid of ChAT-immunopositive neurons. Vestibular nucleus projections to these regions originate from all levels of the superior, medial and lateral vestibular nuclei, but do show topographic organization. The densest terminations were observed in AM and the ventral and central aspects of EW. The projections to AM terminate in both ipsilaterally and in a narrow paramedian region. Predominantly ipsilateral terminations were observed in VTA. Terminations on ChAT-positive cells in AM and VTA were verified in three rabbits. It is suggested that projections to some intensely ChAT-positive AM and VTA neurons may be a substrate for vestibular influences on lens accommodation, pupillary constriction and regulation of intraocular circulation during changes in posture and gravitoinertial challenges. The projections to ChAT-negative (and weakly immunoreactive) cells in AM, VTA and EW, on the other hand, are likely to contribute vestibular signals to a variety of motor responses via descending pathways.

Animals↗
PubMed1993

Effects of ponalrestat, an aldose reductase inhibitor, on neutrophil killing of Escherichia coli and autonomic function in patients with diabetes mellitus.

In diabetic subjects, polyol pathway activity might inhibit neutrophil function and cause nerve damage. The effects of ponalrestat, an aldose reductase inhibitor, were assessed on neutrophil intracellular killing of Escherichia coli and on autonomic function in diabetic subjects in a randomized double-blind, placebo-controlled, crossover trial. We studied 31 diabetic subjects with autonomic dysfunction and 21 age- and sex-matched control subjects. During two 12-wk treatment periods, the diabetic subjects took either 600 mg of ponalrestat or matching placebo once daily. Neutrophil killing of E. coli was measured by a microbiological assay technique. Kmax by neutrophils from the diabetic subjects was lower than in the control group (Kmax of diabetic subjects 54.5 +/- 26.4 vs. control subjects 67.3 +/- 16.3, P = 0.045). Ponalrestat significantly increased bacterial killing in the diabetic subjects (Kmax of ponalrestat 75.1 +/- 16.5 vs. placebo 58.2 +/- 20.8, P = 0.003) so that there was no longer any significant difference in Kmax between the control subjects and the diabetic subjects on active treatment. Ponalrestat had no significant effect on a range of standard cardiovascular autonomic nerve function tests. We conclude that neutrophil killing of E. coli is impaired in diabetic subjects with autonomic dysfunction. This is restored to normal by ponalrestat.

Aldehyde Reductase↗
PubMed1992

Projections of anterior hypothalamic neurones to the dorsal and ventral periaqueductal grey in the rat.

Projections of neurones in the rostral hypothalamus to the periaqueductal grey matter (PAG) of the rat were investigated using retrograde tracing of red and green fluorescent latex microspheres. Microspheres were injected into one of 4 PAG sub-divisions, namely the dorsal, dorsolateral, ventral and ventrolateral parts. The patterns of retrogradely labelled neurones in the hypothalamus from each of the 4 PAG sub-divisions were found to differ and these are described. The precise nature of projections of neurones in the anterior hypothalamic area (AHA) was investigated and it was found that neurones within a circumscribed area of AHA, the lateral area of the anterior hypothalamus (LAAH), projected predominantly to the dorsolateral PAG while neurones in immediately adjacent areas projected to either dorsolateral or ventrolateral aspects of the PAG. Double retrograde tracing studies, where the two different colour beads were injected into different subdivisions of the PAG, gave rise to very few double labelled hypothalamic neurones, indicating that neurones in the hypothalamus project to only one sub-division of the PAG. The functional significance of these pathways is discussed in relation to mechanisms of autonomic and sensory control.

Animals↗
PubMed2001

Excitatory stimulation of neurons in the arcuate nucleus inhibits gastric acid secretion via vagal pathways in anesthetized rats.

It is well established that autonomic control of gastrointestinal function is modulated by central autonomic neurotransmission. In this context it has been shown that gastrointestinal motility and secretion can be modulated by exogenous neuropeptides microinjected into the paraventricular nucleus of the hypothalamus (PVN). Furthermore, there is considerable evidence suggesting that neurons projecting from the arcuate nucleus (Arc) to the PVN may be the source of endogenous neuropeptide release in the PVN. This poses the question whether stimulation of neurons in the arcuate nucleus, e.g. by an excitatory amino acid, alters gastrointestinal function. In the present study, we investigated the effect of an excitatory amino acid, kainate, microinjected into the arcuate nucleus on gastric acid secretion in urethane-anesthetized rats. Kainate (140 pmol/rat) bilaterally microinjected into the Arc induced an significant inhibition of pentagastrin (PG) stimulated (16 mg/kg per h) gastric acid secretion throughout an observation period of 120 min after microinjection. Microinjection of kainate into hypothalamic areas outside the arcuate nucleus did not modify gastric secretion. Bilateral cervical vagotomy blocked the effect of kainate injected into the Arc on PG-stimulated gastric acid secretion. These data show that gastric secretory function can be modulated by stimulation of neuronal activity in the Arc via efferent vagal pathways. The results suggest that the arcuate nucleus is a forebrain area involved in the CNS regulation of gastrointestinal function.

Anesthetics, Intravenous↗