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PubMed1978

Effects of chronic deafferentation on adrenergic ganglion cells and small intensely fluorescent cells.

To determine the reaction of adrenergic ganglion cells and small intensely fluorescent (SIF) cells to chronic deafferentation, catecholamine fluorescence of the major pelvic ganglion (MPG) of the rat has been studied following section of the hypogastric nerve, pelvic nerve and sympathetic trunk. Only minor changes occurred following section of the hypogastric nerve; the fluorescence surrounding a few adrenergic ganglion cells became brighter. In contrast, pelvic neurectomy resulted in the appearance of numerous varicose fibres and an increase in the fluorescent intensity of fibres enclosing many ganglion cells. Varicose fibres seem to originate from adrenergic ganglion cells and SIF cells. In many instances, nests of SIF cells gave rise to radially oriented fibres. Removal of the sympathetic trunk appeared to have no effect on the MPG. It is suggested that the appearance of varicose fibres from SIF cells following deafferentation may be due to collateral sprouting of these cells or to the increased fluorescence of pre-existing processes.

Adrenergic Fibers↗
PubMed1988

Sympathetic nervous influence on the internal anal sphincter and rectum in man.

The effect of sympathetic nerve block and efferent stimulation of the sympathetic nerves on anorectal motility was studied in 21 patients undergoing operation for rectal carcinoma. Anal pressure and rectal volume were simultaneously recorded before and after epidural anaesthesia and during nerve stimulation. Efferent electrical stimulation of the presacral hypogastric nerves (HGN) elicited a contraction of the internal anal sphincter (IAS) in 13 out of 15 patients. The contraction was preceded by a relaxation in seven patients. In the rectum stimulation of the HGN caused variable responses. A weak contraction was the most frequent response. Efferent stimulation of the periarterial lumbar colonic nerves (LCN) elicited a clear-cut contraction of the IAS, while rectal motor responses were only occasionally observed. Epidural anaesthesia encompassing the thoraco-lumbar region (EDA), when used to block the sympathetic discharge to the IAS and the rectum, caused a reduction of anal pressure (28 +/- 11%) and an increased rectal tone. The results imply that the human IAS receives a sympathetic excitatory innervation via both the HGN and the LCN. Furthermore, it appears that the HGN convey inhibitory fibres to the IAS. The rectal responses to EDA and sympathetic nerve stimulation also indicate the presence of both excitatory and inhibitory neurones in the sympathetic nerve supply to the rectum in man.

Aged↗
PubMedDate not supplied

Neural mechanisms of autonomic responses elicited by somatic sensory stimulation.

All evidence introduced here indicates that, in anesthetized animals in which emotional factors have been eliminated, somatic afferent nerve stimulation can regulate various visceral functions by responses that are reflex in nature. One conclusion emerging from the evidence presented is that the effects of somatic afferent stimulation are dependent upon the particular organs and on the spinal afferent segments. When the central nervous system is intact, the responses are sometimes general, as seen in cerebral cortical blood flow, heart rate, and adrenal medullary hormonal secretion and splenic immune function, whereas sometimes they have a strong segmental organization, as seen in gastric motility and urinary vesical contractility (Fig. 8). Needless to say, in the spinalized preparation all responses are strongly segmental. The contribution of the sympathetic and parasympathetic efferent nerves to the somato-visceral reflexes depends on the organs. It is difficult for us to state specifically or to generalize upon which autonomic component, the sympathetic or parasympathetic, will dominate as the efferent path in these reflexes, because this depends on the individual organ, the site being stimulated, and the nature or mode of the stimulation. The somatically-induced reflex responses of autonomic, hormonal and immune functions demonstrated in anesthetized animals, as have been discussed herein, appear to function even during conscious states. We need further studies to evaluate the physiological meaning of these somato-autonomic reflex responses. The analysis of neural mechanisms of these reflex responses seems to be very important for clinical application to regulate visceral function by physical treatment.

Animals↗
PubMed1991

The cause of increased pupillary light reflex latencies in diabetic patients: the relationship between pupillary light reflex and visual evoked potential latencies.

In 42 diabetic patients the relationship between the latency of the pupillary light reflex and the pattern reversal visual evoked potential (P100) was examined. Fifty-five percent of diabetic patients had pupillary light reflex latencies above the normal range. In 19% the visual evoked potentials were prolonged when compared to the normal range. Latencies of pupillary light reflexes and VEPs showed no correlation. There was a minimal correlation between the presence of retinopathy and prolongation of both the pupillary light reflex and the visual evoked response latency (kappa coefficients respectively: 0.31, P less than 0.01 and 0.36, P less than 0.02). The presence of an increased pupillary light reflex latency was positively correlated with a reduced respiratory sinus arrhythmia (kappa coefficient: 0.58, P less than 0.0001). Increased VEP latencies showed no correlation with signs of cardiovascular autonomic neuropathy. We conclude that the afferent optic pathway can be affected in diabetic patients. However, prolongation of pupillary light reflex latency in diabetic patients is primarily due to an efferent pupillary defect and represents parasympathetic dysfunction.

Adult↗
PubMed1988

Central nervous system effects of corticotropin-releasing factor on gastrointestinal transit in the rat.

Corticotropin-releasing factor (CRF) administered into the lateral cerebral ventricle significantly inhibited gastric emptying and small bowel transit, but most markedly increased large bowel transit in a dose-related fashion in freely moving rats. Inhibition of gastric emptying induced by central administration of CRF was completely abolished by pretreatment of the animals with either the ganglionic blocking agent chlorisondamine or the opioid antagonist naloxone, or by noradrenergic blockade with bretylium, but not by truncal vagotomy. Either chlorisondamine, naloxone, or vagotomy--but not bretylium--reversed the inhibitory effect of central CRF on small bowel transit. Chlorisondamine or vagotomy, but neither bretylium nor naloxone, abolished the stimulatory effect of central CRF on large bowel transit. Neither hypophysectomy nor adrenalectomy altered the gastrointestinal motor responses induced by central administration of CRF. Intraperitoneal administration of CRF also significantly inhibited gastric emptying and stimulated large bowel transit but did not alter small bowel transit. These peripheral effects of CRF were not prevented by blockade of autonomic efferents with bretylium or chlorisondamine. It is concluded that (a) CRF acts within the central nervous system to delay gastric emptying, to inhibit small bowel transit, and to increase large bowel transit in freely moving rats and (b) CRF exerts these biological actions by modulation of the autonomic nervous system and, in part, by opioid pathways.

Animals↗
PubMed1981

Organization of the sacral parasympathetic reflex pathways to the urinary bladder and large intestine.

Electrophysiological and horseradish peroxidase (HRP) techniques have provided new insights into the organization of the sacral parasympathetic reflex pathways to the large intestine and urinary bladder. The innervation of the two organs arises from separate groups of sacral preganglionic cells: (1) a dorsal band of cells in laminae V and VI providing an input to the intestine; and (2) a lateral band of cells in lamina VII providing an input to the bladder. These two groups of cells were separated by an interband region containing tract cells and interneurons. Neurons in the interband region received a visceral afferent input and exhibited firing correlated with the activity of intestine and urinary bladder. It seems reasonable therefore to consider the interband region as a third component of the sacral parasympathetic nucleus. Anterograde transport of HRP revealed that visceral afferents from the intestine and bladder projected into the parasympathetic nucleus. Most of the projections were collaterals from afferent axons in Lissauer's tract that passed in lamina I laterally and medially around the dorsal horn. These afferent collaterals were located in close proximity to preganglionic perikarya and dendrites in laminae I, V and VI. The proximity of visceral afferents and efferents in the sacral cord probably reflects the existence of polysynaptic rather than monosynaptic connections since electrophysiological studies revealed that both the defecation and micturition reflexes occurred with very long central delays (45-70 msec). The reflex pathways mediating defecation and micturition in cats with an intact neuraxis were markedly different. Defecation was dependent upon a spinal reflex with unmyelinated (C-fiber) peripheral afferent and efferent limbs. On the other hand, micturition was mediated by a spinobulbospinal pathway with myelinated peripheral afferent (A-fiber) and efferent axons (B-fiber). Transection of the spinal cord at T12-L2 blocked the micturition reflex but only transiently depressed the defecation reflex. In chronic spinal cats the micturition reflex recovered 1-2 weeks after spinalization; however, in these animals bladder-to-bladder micturition reflexes were elicited by C-fiber rather than A-fiber afferents. The C-fiber afferent-evoked reflex was weak or undetectable in animals with an intact neuraxis. Transection of the spinal cord also changed the micturition reflex in neonatal kittens (age 5-28 days). In neonates with an intact neuraxis bladder-to-bladder reflexes occurred via a long latency spinobulbospinal pathway (325-430 msec). The long latency is attributable to the slow conduction velocity in immature unmyelinated peripheral and central axons. In chronic spinal kittens (3-7 days after spinalization) the long latency reflex was abolished and a shorter latency (90-150 msec) bladder reflex was unmasked. The emergence of this spinal pathway may reflect axonal sprouting and the formation of new reflex connections within the sacral parasympathetic nucleus.

Afferent Pathways↗
PubMed1994

Anal and rectal motility responses to distension of the urinary bladder in the cat.

The neural pathways and possible transmission mechanisms of the integrated autonomic nervous control of the urinary bladder and anorectum, were investigated in chloralose anaesthetized cats. Bladder distension and spontaneous detrusor contractions increased internal anal sphincter-tone, a response which was blocked by an alpha-adrenoceptor antagonist. Moreover, a nicotinic transmission step was present. Both the afferent and efferent limbs of the reflex were conveyed in the postganglionic hypogastric nerves and the preganglionic lumbar splanchnic nerves. Intact connection with the central nervous system was therefore essential. Contrasting to the specific reflex response in the internal anal sphincter, bladder distension also elicited a nociceptive vaso-pressor response. Rectal motility appeared to be unaffected by bladder distension.

Adrenal Glands↗
PubMed1993

Emotional memory systems in the brain.

The neural mechanisms of emotion and memory have long been thought to reside side by side, if not in overlapping structures, of the limbic system. However, the limbic system concept is no longer acceptable as an account of the neural basis of memory or emotion and is being replaced with specific circuit accounts of specific emotional and memory processes. Emotional memory, a special category of memory involving the implicit (probably unconscious) learning and storage of information about the emotional significance of events, is modeled in rodent experiments using aversive classical conditioning techniques. The neural system underlying emotional memory critically involves the amygdala and structures with which it is connected. Afferent inputs from sensory processing areas of the thalamus and cortex mediate emotional learning in situations involving specific sensory cues, whereas learning about the emotional significance of more general, contextual cues involves projections to the amygdala from the hippocampal formation. Within the amygdala, the lateral nucleus (AL) is the sensory interface and the central nucleus the linkage with motor systems involved in the control of species-typical emotional behaviors and autonomic responses. Studies of cellular mechanisms in these pathways have focused on the direct relay to the lateral amygdala from the auditory thalamus. These studies show that single cells in AL respond to both conditioned stimulus and unconditioned stimulus inputs, leading to the notion that AL might be a critical site of sensory-sensory integration in emotional learning. The thalamo-amygdala pathway also exhibits long-term potentiation, a form of synaptic plasticity that might underlie the emotional learning functions of the circuit. The thalamo-amygdala pathway contains and uses the amino acid glutamate in synaptic transmission, suggesting the possibility that an amino-acid mediated form of synaptic plasticity is involved in the emotional learning functions of the pathway. We are thus well on the way to a systems level and a cellular understanding of at least one form of emotional learning and memory.

Animals↗
PubMed1995

The quantitation of altered hepatic foci during multistage hepatocarcinogenesis in the rat: transforming growth factor alpha expression as a marker for the stage of progression.

The experimental three-stage hepatocarcinogenesis protocol of initiation, promotion, and progression, coupled with the analytical technique of stereology, permits quantitative analysis of the carcinogenic process, including the derivation of biologically based risk assessment models. The aberrant expression of the placental isozyme of glutathione S-transferase (PGST) is an efficient marker for initiated, preneoplastic, and neoplastic hepatocytes. Putatively initiated cells and their clonal progeny can be identified, enumerated, and their growth characteristics determined on the basis of their aberrant expression of this protein. A lack of suitable markers has made the identification and quantitation of hepatocytes in the early stage of progression more difficult. One characteristic of cells in the stage of progression is the evolution of relatively autonomous growth. The alteration of growth factor signalling pathways may provide one mechanism for this observation. The expression of transforming growth factor alpha (TGF alpha) is seen in many malignancies. The initiation-promotion-progression protocol has been used to induce progression in the rat liver. The focal expression of TGF alpha was found to correlate with areas of progression in rats subjected to this protocol. The ability to identify and quantitate cells in the stage of progression should facilitate application of the Moolgavkar-Venzon-Knudson model for assessing human risk from carcinogens active at each of these three stages. Validation of this model will require determination of the number and growth characteristics of hepatocytes in the stage of progression.

Animals↗
PubMed1987

Projections between the hypothalamus and the dorsal vagal complex in the cat: an HRP and autoradiographic study.

The hypothalamus is known to be intimately involved in the control of autonomic function. This study provides detailed information about pathways between the hypothalamus and the dorsal vagal complex in cat. Injection of horseradish peroxidase into the dorsomedial medulla produced retrograde neuronal labeling in the paraventricular nucleus of the hypothalamus. Injection of 3H-leucine into the paraventricular nucleus produced dense anterograde labeling in the dorsal motor nucleus of the vagus, and lighter labeling in the nucleus of the tractus solitarius, particularly in its medial subnucleus. The subnucleus gelatinous was virtually free of label, except in its medial and lateral portions. Anterograde labeling was distributed bilaterally, with an ipsilateral predominance. Injection of horseradish peroxidase into the area of the paraventricular nucleus produced retrograde neuronal labeling bilaterally in the nucleus of the tractus solitarius and the reticular formation ventrolateral to the dorsal vagal complex. anterograde terminal labeling overlapped the distribution of retrogradely labeled neurons. These findings are compared to those in rat, and discussed in relation to their functional implications.

Animals↗
PubMed2005

Non-cell autonomous RNA silencing.

In plants and in some animals, the effects of post-transcriptional RNA silencing can extend beyond its sites of initiation, owing to the movement of signal molecules. Although the mechanisms and channels involved are different, plant and animal silencing signals must have RNA components that account for the nucleotide sequence-specificity of their effects. Studies carried out in plants and Caenorhabditis elegans have revealed that non-cell autonomous silencing is operated through specialized, remarkably sophisticated pathways and serves important biological functions, including antiviral immunity and, perhaps, developmental patterning. Recent intriguing observations suggest that systemic RNA silencing pathways may also exist in higher vertebrates.

Animals↗
PubMed2005

Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response.

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.

Adaptation, Physiological↗