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Brain control of the lower urinary tract.

The knowledge on neural pathways involved in micturition and continence has been expanded greatly the last ten years. The aim of the present review is to summarize results obtained from animal and human experiments and to discuss the pathophysiology of relevant urological dysfunction. Four specific parts of the mammalian neural system are important for the control of micturition and continence: 1) ganglion cells in the bladder wall and sympathetic chain (autonomic) and dorsal root chain (sensory); 2) motoneurons and sensory interneurons in the caudal spinal cord; 3) the caudal brainstem; and 4) the cortical and subcortical areas. The parts 1) to 3) comprise the basic components of the micturition reflex and are interconnected via peripheral nerves and central fiber tracts. Normally, we are continent for urine continuously, except for the necessary emptying of the bladder five to eight times a day. Specific lesions of the neural pathways can result in distinct types of urological dysfunction: hypoactivity or hyperactivity of the micturition or continence pathways, and a loss of control of the beginning of micturition.

Animals↗

Walter Heiligenberg: the jamming avoidance response and beyond.

Walter Heiligenberg (1938-1994) was an exceptionally gifted behavioral physiologist who made enormous contributions to the analysis of behavior and to our understanding of how the brain initiates and controls species-typical behavioral patterns. He was distinguished by his rigorous analytical approach used in both behavioral studies and neuroethological investigations. Among his most significant contributions to neuroethology are a detailed analysis of the computational rules governing the jamming avoidance response in weakly electric fish and the elucidation of the principal neural pathway involved in neural control of this behavior. Based on his work, the jamming avoidance response is perhaps the best-understood vertebrate behavior pattern in terms of the underlying neural substrate. In addition to this pioneering work, Heiligenberg stimulated research in a significant number of other areas of ethology and neuroethology, including: the quantitative assessment of aggressivity in cichlid fish; the ethological analysis of the stimulus-response relationship in the chirping behavior of crickets; the exploration of the neural and endocrine basis of communicatory behavior in weakly electric fish; the study of cellular mechanisms of neuronal plasticity in the adult fish brain; and the phylogenetic analysis of electric fishes using a combination of morphology, electrophysiology, and mitochondrial sequence data.

Animals↗

[Freezing of gait is a symptom of Parkinson disease].

One could distinguish between "off freezing", which is a symptom tightly bound to L-dopa dosage and titration, and is clinically bound to wearing off, and, on the contrary, "on freezing" which does not respond to therapy modifications or to different drug's titration. On freezing seems to be related to frontal-basal ganglia-pontine neural pathway disruption. This neural disruption may be related with altered perception of extra and peri-personal space which are two major problems of these patients. We demonstrate in a group of patients with "on freezing" evident defect of attention, focus capability, of set-shifting properties, and of alteration in body/space relationship. We discuss on results obtained by specific training of physiotherapy with an review on literature.

Antiparkinson Agents↗

Taste responses in neurons in the nucleus of the solitary tract that do and do not project to the parabrachial pons.

1. Mechanisms of neural coding of gustatory stimuli were studied in the nucleus of the solitary tract (NTS), the first relay in the neural pathway for gustation, in anesthetized rats. Taste-responsive NTS units were identified as "relay" or "nonrelay" based on the electrophysiological response to electrical pulses delivered to the parabrachial nucleus of the pons (PbN), the second relay in the neural pathway for gustation. Coding mechanisms in each group were analyzed separately. 2. Taste responses to sapid solutions of NaCl (0.1 M), HCl (0.01 M), quinine HCl (0.01 M), sucrose (0.5 M) and Na-saccharin (0.004 M) were recorded in single units in the NTS. After gustatory stimulation, electrophysiological responses to electrical stimulation of the taste-responsive part of the ipsilateral PbN were recorded. A 0.2-ms pulse was delivered at 75-250 microA at a rates of 1, 25, 50 and 100 pps through a bipolar stainless steel electrode. An antidromic response was defined as a time-locked spike that occurred at a fixed latency after PbN stimulation that followed high stimulation frequencies. A collision test also was performed. 3. Of 42 taste-responsive NTS units, 19 (45%) were relay units, 22 (52%) were nonrelay and 1 unit was activated orthodromically by PbN stimulation. Latencies of evoked spikes ranged from 1.75 to 4.0 ms 2.1 +/- 0.2 ms (mean +/- SE, median, 1.75 ms). 4. Examination of general response characteristics revealed few differences among relay and nonrelay units.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Adrenocortical responses following sciatic nerve stimulation in rats with partial hypothalamic deafferentations.

Studies from this laboratory have demonstrated that the adrenocortical response following sciatic nerve stimulation is completely inhibited in rats with hypothalamic islands, indicating that this response depends entirely on the activation of afferent neural pathways to the hypothalamus. With the purpose of identifying the site of entry of these neural pathways into the mediobasal hypothalamus the effects of partial hypothalamic deafferentations were studied. It was found that in rats with posterior or posterolateral deafferentation the adrenocortical responses were similar to those obtained in intact rats, while anterior and anterolateral deafferentation resulted in a reduction of 62.3 and 53.3%, respectively. These results would indicate that the sciatic impulses which activate the adrenocortical response involve neural afferents which enter the mediobasal hypothalamus by an anterior pathway.

Adrenal Cortex↗

Neurophysiologic study of beta-thalassemia patients.

Neurophysiologic investigations were performed in 34 Chinese patients with beta-thalassemia major maintained on long-term desferrioxamine treatment to look for subclinical toxicity in the auditory, visual, peripheral, or central neural pathways. In the auditory pathway study, four patients (12%) had mild sensorineural hearing impairment. Two patients (6%) had increased P 100 latencies in the visual evoked potential study, and nine patients (26%) had abnormal electroretinogram results. All had normal electrooculograms. Ophthalmoscopic examination was abnormal in three patients (9%), and three (9%) had a visual field defect. In the peripheral or central nervous pathways, seven patients (21%) had sensory neuropathy, of which three cases were probably related to diabetes mellitus. All had normal motor conduction velocities. Four patients (12%) had increased cortical latencies of median or posterior tibial somatosensory evoked potential. Abnormalities in multiple neural pathways were seen in four patients (12%). There was a significant association between subclinical toxicity to the peripheral or central nervous systems and serum ferritin level (P < .03) and the presence of diabetes mellitus (P < .002). There was no significant relationship between the age, dosage, or duration of desferrioxamine used and the increased risk of neurotoxicity to the auditory, visual, peripheral, or central nervous systems. There was also no association between the risk of neurotoxicity and the serum zinc, copper, or fructosamine levels.

Adolescent↗

Neuroendocrine mechanism mediating fasting-induced suppression of luteinizing hormone secretion in female rats.

Forty-eight hours fasting profoundly suppresses LH secretion in female rats. The following neural pathway mediating fasting-induced suppression of LH secretion has been suggested by a series of experiment: a signal associated with fasting emanating from the upper digestive tract reaches the A2 region in the medulla oblongata via afferent vagal nerve so as to activate the noradrenergic pathway projecting to the hypothalamic paraventricular nucleus (PVN); this results in an increased corticotropin-releasing hormone release to suppress LHRH release and then LH release. The PVN and A2 region of the medulla oblongata are the estrogen feedback sites to activate the above-mentioned neural pathway. The estrogen feedback action on the PVN and A2 region is considered to be due to an increased expression of estrogen receptors in these nuclei after 48-h fasting. The response of gonadal axis during fasting could be due to the changes in some nutrients, such as glucose and free-fatty acids. In this context, malnutrition could be a kind of stress accompanied by an increased feeding behavior and decreased gonadal activity.

Animals↗

Electromyelography, a useful test for evaluation of the sacral spinal cord.

Bradley was the first to describe an accurate and objective test for the evaluation of the integrity of the sacral spinal cord involved with micturition. Measurements of the latency time from an electrical stimulation of the proximal urethra and its response, the contraction of the anal sphincter, was found to be approximately 70 msec. The neural pathways involved with this reflex include the afferent pelvic nerves and the efferent pudendal nerves. Prolonged latency times signify damage to this sacral arc. This testing, which Bradley termed electromyelography, can help to diagnose, in a more definitive fashion, some abnormalities of micturition. We report on 3 patients with varied lesions of the sacral neural pathways and their urodynamic evaluation, including cystometry, sphincter electromyography and measurements of latency times of evoked responses of the anal sphincter. All 3 cases showed prolonged latency times with 1 reverting to normal after improvement of the underlying disorder. The usefulness of electromyelography and its ease of implementation are stressed. Measurements of evoked response may be an important addiction in the evaluation of complicated neurourological problems.

Adult↗

Knife cuts lateral but not dorsal to the hypothalamic paraventricular nucleus abolish gonadal responses to photoperiod in female hamsters (Mesocricetus auratus).

Horizontal and parasagittal knife cuts in the hypothalamus of female hamsters (Mesocricetus auratus) were employed to investigate the neural pathways that mediate gonadal responses to photoperiod. Bilateral horizontal knife cuts placed dorsal to the paraventricular nucleus (PVN) did not prevent short-day-induced acyclicity and uterine regression. On the other hand, regardless of photoperiod, animals with bilateral parasagittal knife cuts placed lateral to the PVN continued to exhibit regular 4-day estrous cycles and stimulated uteri. Thus, parasagittal cuts prevented the effects of short days on reproductive physiology. This finding suggests that the lateral efferent projections from the PVN represent an important component of the neural pathway mediating reproductive photoperiodism in female hamsters.

Animals↗

Ednrb2 orients cell migration towards the dorsolateral neural crest pathway and promotes melanocyte differentiation.

Endothelin receptors B (Ednrb) are involved in the development of the enteric and melanocytic lineages, which originate from neural crest cells (NCCs). In mice, trunk NCCs and their derivatives express only one Ednrb. In quail, trunk NCCs express two Ednrb: Ednrb and Ednrb2. Quail Ednrb is expressed in NCCs migrating along the ventral pathway, which gives rise to the peripheral nervous system, including enteric ganglia. Ednrb2 is upregulated in NCCs before these cells enter the dorsolateral pathway. The NCCs migrating along the dorsolateral pathway are melanocyte precursors. We analyzed the in vitro differentiation and in ovo migration of mouse embryonic stem (ES) cells expressing and not expressing Ednrb2. We generated a series of transfected ES cell lines expressing Ednrb2. This receptor, like Ednrb, oriented genuine ES cells towards melanocyte lineage differentiation in vitro. The in ovo migration of Ednrb2-expressing ES cells was massively oriented towards the dorsolateral pathway, unlike that of WT or Ednrb-expressing ES cells. Thus, Ednrb2 is involved in melanoblast differentiation and migration.

Animals↗

Neuroanatomical approaches of the tectum-reticular pathways and immunohistochemical evidence for serotonin-positive perikarya on neuronal substrates of the superior colliculus and periaqueductal gray matter involved in the elaboration of the defensive behavior and fear-induced analgesia.

Deep layers of the superior colliculus, the dorsal periaqueductal gray matter and the inferior colliculus are midbrain structures involved in the generation of defensive behavior and fear-induced anti-nociception. Local injections of the GABA(A) antagonist bicuculline into these structures have been used to produce this defense reaction. Serotonin is thought to be the main neurotransmitter to modulate such defense reaction in mammals. This study is the first attempt to employ immunohistochemical techniques to locate serotonergic cells in the same midbrain sites from where defense reaction is evoked by chemical stimulation with bicuculline. The blockade of GABA(A) receptors in the neural substrates of the dorsal mesencephalon was followed by vigorous defensive reactions and increased nociceptive thresholds. Light microscopy immunocytochemistry with streptavidin method was used for the localization of the putative cells of defensive behavior with antibodies to serotonin in the rat's midbrain. Neurons positive to serotonin were found in the midbrain sites where defensive reactions were evoked by microinjection of bicuculline. Serotonin was localized to somata and projections of the neural networks of the mesencephalic tectum. Immunohistochemical studies showed that the sites in which neuronal perikarya positive to serotonin were identified in intermediate and deep layers of the superior colliculus, and in the dorsal and ventral columns of the periaqueductal gray matter are the same which were activated during the generation of defense behaviors, such as alertness, freezing, and escape reactions, induced by bicuculline. These findings support the contention that serotonin and GABAergic neurons may act in concert in the modulation of defense reaction in the midbrain tectum. Our neuroanatomical findings indicate a direct neural pathway connecting the dorsal midbrain and monoaminergic nuclei of the descending pain inhibitory system, with profuse synaptic terminals mainly in the pontine reticular formation, gigantocellularis nucleus, and nucleus raphe magnus. The midbrain tectum-gigantocellularis complex and midbrain tectum-nucleus raphe magnus neural pathways may provide an alternative output allowing the organization of the fear-induced anti-nociception by mesencephalic networks.

Aggression↗

Neuronal pathways from foot pad afferents to hindlimb motoneurons in the low spinalized cats.

Experiments were performed on 16 adult spinalized (L2) cats. Postsynaptic potentials (PSPs) produced by electrical stimulation of afferent nerves innervating foot pads were recorded from hindlimb motoneurons innervating the following hindlimb muscles: the posterior biceps and semitendinosus (PBSt), anterior biceps and semimembranosus (ABSm), lateral gastrocnemius and soleus (LGS), medial gastrocnemius (MG), plantaris (P1), tibialis anterior (TA), popliteus (Pop), flexor digitorum longus and flexor hallucis longus (FDHL) and peroneus longus (Per.l). The rate of occurrence of different types of PSPs (EPSPs, IPSPs and mixed PSPs), the size of the PSPs and their central latencies were analyzed for each group of motoneurons to identify the neural pathways from the afferents innervating foot pads to hindlimb motoneurons. The rates of occurrence of different types of PSPs did not depend on the foot pad stimulated in PBSt, ABSm and LGS motoneurons, but for other groups of motoneurons their rates of occurrence depended on the foot pad stimulated. It was often noted that the size of PSPs in the same motoneurons differed according to the foot pad stimulated. Measurements of the central latencies of the PSPs indicated that the shortest neural pathways for EPSPs and IPSPs were disynaptic (central latencies < 1.8 ms). The functional role of neuronal pathways from afferent nerves innervating foot pads to hindlimb motoneurons could be to maintain stability of the foot during different postural and motor activities.

Animals↗

Connections of the dorsomedial part of the nucleus intercollicularis in a male non-songbird, the Grey partridge: a tract-tracing study.

Vocal control systems have been poorly investigated in non-songbirds. In this study we describe descending neural pathways to the dorsomedial portion of the nucleus intercollicularis (ICo) in a galliform (male Grey partridges) by means of the DiI in vitro tracing technique. The simple and sex-dimorphic vocalizations of partridges, which have a critical role in sexual selection, favour this species as a model system for the study of vocal control mechanisms. Our data demonstrate that the ICo, an important site mediating the activation of vocal behavior in all birds, receives afferents from several important higher centers: the nucleus pretectalis, the tuberoinfundibular hypothalamic region, the dorsal thalamus, the preoptic region and the paleostriatal region. Efferent connections of the ICo were directed mainly to the hypothalamic area. This complex neural pathway is consistent with a major role of ICo in male courtship and vocal performance control.

Animals↗

Altered carbachol-induced contractile responses of rat jejunal smooth muscle following local myenteric plexus ablation.

Alterations in smooth muscle responsiveness and neural pathways in adjacent tissue may occur after local myenteric denervation. The in vitro contractile responses of both longitudinal and circular muscle to the mixed muscarinic and nicotinic cholinergic agonist carbachol were determined 15, 30, and 45 days after localized myenteric plexus ablation. Denervated longitudinal muscle exhibited decreased responsiveness to carbachol at all times examined. Denervated circulated muscle was initially supersensitive, but with time became subsensitive. These changes probably reflect the loss of the nicotinic (neuronal) component of the action of carbachol. Muscle orad to the site of denervation appeared subsensitive, while muscle caudad to the lesion was supersensitive (circular) or unaffected (longitudinal). These results suggest that there are changes in ascending and descending neural pathways. Alterations in the cholinergic responsiveness of intestinal smooth muscle, both at and beyond the site of myenteric plexus ablation, may result in altered intestinal motility that could lead to functional obstruction.

Animals↗

Waiting periods versus early innervation: the development of axonal connections in the zebra finch song system.

This study examines the development of two neural pathways within the zebra finch forebrain that function respectively in the juvenile acquisition and the adult production of learned song. In the adult male zebra finch forebrain, the song nuclei L-MAN and HVc both innervate nucleus RA; L-MAN plays a crucial role in juvenile song acquisition but, unlike HVc and RA, is not essential for adult song production. Previous studies have shown that HVc axons arrive at the dorsal border of RA as early as posthatch day 15 (day 15), and only enter the male RA after days 25-30, but never enter the female RA. The present study examines the development of axonal projections from L-MAN to RA and finds that, in contrast to HVc axons, L-MAN terminals are present within the male and female RA by day 15, and persist there throughout adult life. Unlike RA-projecting HVc neurons, HVc neurons projecting to area X innervate this target by day 20. Like L-MAN, area X plays a transient role in song acquisition. These results suggest that in the zebra finch forebrain, neural pathways essential to juvenile song learning develop before those needed for adult song production.

Animals↗

Gastric mucosal hyperemia due to acid backdiffusion depends on splanchnic nerve activity.

Acid backdiffusion through a disrupted gastric mucosal barrier leads to an increase in gastric mucosal blood flow (MBF). This response involves afferent neurons that pass through the celiac ganglion. The present study examined the neural pathways that underlie the rise in MBF caused by gastric perfusion with 15% ethanol in 0.15 N HCl. MBF was measured by the hydrogen gas clearance technique in urethan-anesthetized rats. Mucosal hyperemia due to acid backdiffusion was not changed by acute bilateral subdiaphragmatic vagotomy but was blocked by acute removal of the celiac-superior mesenteric ganglion complex or acute bilateral transection of the greater splanchnic nerves. Hexamethonium (85 mumol/kg iv) also attenuated the rise in MBF due to acid backdiffusion, whereas guanethidine (0.225 mmol/kg sc) had no effect. None of the procedures and drug treatments altered basal MBF to a significant extent. Transection of the splanchnic nerves, hexamethonium, and guanethidine lowered mean arterial blood pressure, but hypotension as such did not significantly influence the hyperemic response under study. Taken together, the previous and present data indicate that the rise in MBF caused by acid backdiffusion depends on the integrity of afferent and efferent neural pathways that run in the splanchnic nerves and through the celiac ganglion. The efferent pathway involves ganglionic transmission through nicotinic acetylcholine receptors but is independent of noradrenergic neurons.

Animals↗

Vasovagal syncope and skeletal muscle vasodilatation: the continuing conundrum.

During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypotension, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed since vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In both cases, there is no bradycardia but hypotension during the syncopal attacks. The major site of the vasodilation is in skeletal muscle and muscle sympathetic nerve activity is suppressed just prior to and during vasovagal attacks, indicating that sympathetic withdrawal contributes to the dilation. However, the skeletal muscle vasodilation seen during syncope is greater than that caused by sympathetic withdrawal alone, and it is absent in limbs that have undergone surgical sympathectomy, or local anesthetic nerve block. These observations suggest a role for neurally mediated "active" vasodilation during syncope. The afferent neural pathways that evoke the profound vasodilation during vasovagal attacks remain the subject of debate. The neural pathways responsible for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, beta-adrenergic, and nitroxidergic (nitric oxide) vasodilator mechanisms are not essential to observe the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.

Adrenergic Fibers↗