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At least 613 records · Page 34Linked to original sources

PubMed1997

Effects of angiotensinogen antisense oligonucleotides on fluid intake in response to different dipsogenic stimuli in the rat.

The role of centrally synthesised angiotensinogen in neural mechanisms subserving water drinking in rats was investigated by injecting antisense oligonucleotides complementary to rat angiotensinogen mRNA into the brain with the aim of inhibiting cerebral angiotensinogen synthesis. Phosphorothioate antisense oligonucleotides (18 mer) encompassing the translation start codon were injected into the lateral ventricle of rats and their responses to a number of dipsogenic stimuli tested. These were: intracerebroventricular (i.c.v.) renin, i.c.v. angiotensin II, i.c.v. carbachol, subcutaneous isoproterenol, intravenous hypertonic saline, water deprivation for 24 h or subcutaneous injection of polyethylene glycol. Antisense treatment significantly reduced (by approximately 50%) the volume of water drunk in response to i.c.v. injection of renin or subcutaneous isoproterenol, but did not reduce water intake elicited by the other dipsogenic stimuli. The i.c.v. administration of mismatch, scrambled or sense oligonucleotides did not inhibit water intake. These data suggest that centrally produced angiotensinogen may have a role in neural pathways subserving isoproterenol-induced drinking.

Angiotensinogen↗

PubMed1975

Complete inhibition of adrenocortical responses following sciatic nerve stimulation in rats with hypothalamic islands.

Previous studies from this laboratory have demonstrated that in rats with hypothalamic islands the adrenocortical response to photic and acoustic stimulation was partially inhibited indicating that they were at least to a certain degree neurally mediated, though ether stress produced normal adrenocortical responses. With the purpose of determining to what extent afferent somatosensory connections to the hypothalamus participate in the activation of adrenocortical responses following sciatic nerve stimulation, the effects of this stimulus applied through chronically implanted electrodes were studied on the plasma corticosterone levels in pentobarbital anaesthetized intact animals and in rats with hypothalamic islands. Ether stress or sciatic nerve stimulation for 2 min in intact rats produced a rise of plasma corticosterone to 32.1 plus or minus 1.2 and 32.1 plus or minus 1.8 mug/100 ml, respectively. However, in animals with hypothalamic islands the corresponding values were 29.2 plus or minus 1.8 and 12.4 plus or minus 0.8 mug/100 ml, respectively. The latter value was not significantly different from the basal corticosterone levels (13.0 plus or minus 1.2 mug/100 ml) found in rats 15 min after pentobarbital anaesthesia, the time when the sciatic stimulus was applied. The present data indicate that the adrenocortical discharge following sciatic nerve stimulation is completely inhibited by hypothalamic deafferentation and therefore depends entirely on the activation of the afferent neural pathways to the hypothalamus.

Adrenal Cortex↗

PubMed2003

Neurotological findings in a patient with narrow internal auditory canal: a case report.

We report neurotological findings in a patient with unilateral narrow internal auditory canal, as confirmed by computed tomography. The patient presented no auditory brainstem response on the affected side. Vestibular tests including vestibular-evoked myogenic potentials (VEMP) and caloric test revealed normal function of both inferior and superior vestibular neural pathways.

Acoustic Stimulation↗

PubMed1979

Neurogenic gastroduodenal ulceration and bleeding associated with spinal cord injuries.

Twenty-four of 576 consecutive patients with spinal cord injuries developed acute gastroduodenal ulceration and hemorrhage. Twenty-two were males and two were females: 88% were 12 to 25 years old. Seventeen patients sustained injuries to the spinal cord in sports and recreation related activities. Twenty-three patients had lesions of the spinal cord above the sympathetic outflow. Twenty patients developed gastroduodenal perforation or bleeding within 4 weeks following the injury. Ten patients developed perforation of gastric or duodenal ulcer and "shoulder tip" pain was a symptom of perforation in six patients. Six patients of seven who had gastroscopy and upper GI series were found at laparotomy to have ulcers. Gastric (nine) and duodenal (seven) ulcers were evenly distributed. There were no deaths due to gastroduodenal hemorrhage in the present series. A single cause for the pathogenesis of gastroduodenal ulceration and hemorrhage cannot be pinpointed. However, ischemia of gastric mucosa produced in various ways and altered equilibrium between the parasympathetic and sympathetic neural pathways following trauma to the spinal cord seem to be important in initiating the process.

Acute Disease↗

PubMed1999

Noxious stimulation of emesis.

This review will focus on the mechanisms of emesis initiated or inhibited from receptors located in the periphery or activated by a peripherally released humoral factor. Excitatory and inhibitory receptors have been found in the thorax. Nausea and vomiting sometimes occur after coronary artery occlusion or with vasovagal syncope, and the receptors of this emetic response are probably tension receptors of the left ventricle. The thorax is also source of antiemetic receptors. Vagal section above the level of the heart causes an intractable vomiting syndrome and central cervical vagal stimulation inhibits vomiting. In addition, respiratory maneuvers that decrease activation of pulmonary afferents enhance the sensitivity to motion sickness. Therefore, pulmonary vagal afferent fibers may tonically inhibit retching and vomiting. Abdominal stimulation by irritants or toxins can activate nausea and vomiting through mechano- or chemoreceptors. Mechanoreceptors have been found in the stomach, jejunum and ileum, but the location of these receptors in the gut wall or the type of mechanical stimuli most effective in exciting these receptors is unknown. The chemoreceptors have a similar distribution and are probably located in the mucosa and respond to a variety of noxious agents, eg, CuSO4. CuSO4-induced vomiting is mediated by peripheral 5-HT4 receptors. Two clinically relevant toxic stimuli, x-irradiation and chemotherapeutic agents, have been found to activate vomiting through 5-HT3 receptors in the digestive tract. Regardless of the stimulus, the afferent neural pathways mediating emesis from the abdomen may be the same. The noxious stimulus may cause release of serotonin from enterochromaffin cells of the digestive tract, which activates visceral afferents. The vagus nerves mediate responses from the stomach and proximal small intestine and the splanchnic nerves and spinal cord mediate responses from the entire small intestine. Emesis-related afferents from the periphery terminate primarily in the nucleus tractus solitarius and area postrema. The area postrema contains the chemoreceptive trigger zone that can be activated by endogenous agents released into the circulation from the periphery. The role of peripheral receptors or peripherally released agents in the etiology of cyclic vomiting is unknown, but multiple pathways have been identified that can form a brain-gut interaction to provide a possible mechanism of cyclic vomiting.

Adult↗

PubMed1987

Cholecystectomy alters the hormonal response of the sphincter of Oddi.

We have previously described a cholecysto-sphincter of Oddi reflex whereby sphincter of Oddi (SO) motility is mediated in part by the degree of gallbladder distension. Therefore, we tested the hypothesis that cholecystectomy alters the response of the SO to endogenous and exogenous hormonal stimulation. Eight months after sham laparotomy (n = 8) or cholecystectomy (n = 10), prairie dogs were anesthetized with alpha-chloralose. The common bile duct was cannulated distally with a side-hole, pressure-monitored catheter perfused with degassed water at 0.15 ml/min. The duodenum was cannulated distal to the SO to allow perfusion of the proximal 30 cm of intestine with 20 mmol/L sodium oleate at 0.4 ml/min. In animals undergoing sham laparotomy the gallbladder was cannulated, aspirated, and kept empty throughout the experiment. SO phasic wave frequency (F), amplitude (A), and baseline pressure were measured for 60 minutes before and during intraduodenal (ID) perfusion of sodium oleate and then for 60 minutes before and 30 minutes during intravenous (IV) infusion of cholecystokinin-octapeptide (CCK-OP) at 10 ng/kg/min. A SO motility index (MI) (MI = F X A) was calculated for each 10-minute period. Common duct diameter and resting SO motility were unaltered 8 months after cholecystectomy. In animals that had sham laparotomy ID infusion of sodium oleate reduced SO MI by 46% (p = 0.06) and 75% (p less than 0.05) at 30 and 60 minutes, respectively, whereas in animals that had cholecystectomy the reduction in SO MI was only 6% and 25% (p less than 0.05) during the same periods. In animals that had sham laparotomy IV CCK-OP increased the SO MI by 175% (p less than 0.05), but in the animals that had cholecystectomy IV CCK-OP increased SO MI by only 60% (no significance). These findings indicate that after cholecystectomy resting SO motility is unaltered, but the response to ID sodium oleate and to IV cholecystokinin is blunted. We suggest that cholecystectomy alters neural pathways that mediate the normal response of the SO to endogenous and exogenous hormonal stimulation.

Ampulla of Vater↗

PubMed2003

Projection neurons originating from thermo- and hygrosensory glomeruli in the antennal lobe of the cockroach.

Most insects are equipped with specialized thermo- and hygroreceptors to locate a permissible range of ambient temperature and distant water sources, respectively. In the cockroach, Periplaneta americana, cold, moist, and dry receptor cells in the antennae send axons to particular sets of two or three glomeruli in the dorsocentral part of the antennal lobe (primary olfactory center), designated DC1-3 glomeruli. However, it is not known how thermo- and hygrosensory signals from these glomeruli are represented in higher-order centers, the protocerebrum, in any insect species. With the use of intracellular recording and staining techniques, we identified a new class of interneurons with dendrites almost exclusively in the DC1, DC2, or DC3 glomeruli and axons projecting to the protocerebrum in the cockroach. Remarkably, terminals of all these projection neurons (PNs) covered almost identical areas in the lateral protocerebrum (LP), although their termination areas outside the LP differed from neuron to neuron. The termination areas within the LP were distinct from, but close to, those of uniglomerular and macroglomerular PNs that transmitted signals concerning general odors and female sex pheromones, respectively. PNs originating from DC1, DC2, and DC3 glomeruli exhibited excitatory responses to cold, moist, and dry stimuli, respectively, probably due to excitatory synaptic input from cold, moist, and dry receptor cells, respectively, whereas their responses were often modulated by olfactory stimuli. These findings suggested that dorsocentral PNs participate in neural pathways that lead to behavioral responses to temperature or humidity changes.

Animals↗

PubMed2000

Estrogen-induced remodeling of hypothalamic neural circuitry.

For decades, sexual behavior has been a valuable model system for behavioral neuroscientists studying the neural basis of motivated behaviors. One striking example of a change in motivation is the binary switch in sexual receptivity that occurs during the estrous cycle in female rats. Investigations of the neural basis of this change in behavior have fundamentally advanced our understanding of both behaviorally relevant neural pathways and basic mechanisms of steroid action in the brain. These advances have made this behavioral model system a staple of neuroendocrinology. A challenge that remains before us, given our current understanding of the circuitry and chemistry, is to develop a coherent model of how neural plasticity in the hypothalamus contributes to the dependence of this behavior on motivational state. This review will focus on the ventromedial nucleus of the hypothalamus, especially its ventrolateral subdivision. First, the anatomical, neurochemical, and functional aspects of the macro- and microcircuitry of this brain region will be discussed, followed by a discussion of the likely mechanisms of estrogen action within the ventrolateral VMH. Then, the evidence for estrogen-induced neural plasticity will be considered, including a comparison with the effects of estrogen on synaptic organization in other brain regions. Finally, a working model of neural plasticity within the ventrolateral VMH microcircuitry will be presented as a starting point for future experiments to verify or, more likely, revise and expand.

Animals↗

PubMed1980

Stimulation-dependent changes in synaptic effects on unit activity of medial preoptic nucleus neurones in rats.

Stimulation-dependent changes in synaptic effects were observed in medial preoptic nucleus neurones during stimulation of the amygdala or pyriform cortex in anaesthetized female rats. The changes occurred after 35--240 triple pulse stimuli repeated at 0.89 Hz. Median eminence stimulation did not produce any synaptic change. These data show the existence of synaptic plasticity in the neural pathway from the amygdala and pyriform cortex to the medial preoptic nucleus.

Amygdala↗

PubMed1996

Vagus nerve mediates the increase in estrogen receptors in the hypothalamic paraventricular nucleus and nucleus of the solitary tract during fasting in ovariectomized rats.

The effect of total subdiaphragmatic vagotomy on estrogen-receptor immunoreactivity (ERIR) in the paraventricular nucleus (PVN) and nucleus of the solitary tract (NTS) was examined in fasted ovariectomized rats to clarify the peripheral inputs mediating fasting-induced increase in ERIR in these two nuclei. Vagotomy abolished the effect of 48-h fasting on the expression of ER in these two areas. The result indicates that the neural signal(s) that increase the expression of ER in the PVN and A2 region of the NTS following 48-h fasting is transmitted through the vagus. The involvement of the vagus in the fasting-induced increase in ER in the PVN and A2 region may also be the same neural pathway involved in the suppression of pulsatile luteinizing hormone secretion in fasted female rats.

Animals↗

PubMed1994

Putative pathways involved in cardiovascular responses evoked from the caudal pressor area.

1. The caudal pressor area (CPA) is a recently identified site within the ventrolateral medulla which is involved in cardiovascular regulation. CPA chemical stimulation by L-glutamate produces an increase in arterial blood pressure (ABP) while its inhibition by GABA or glycine evokes marked hypotension. In the present study, we sought to determine the potential neural pathways underlying these responses. 2. In urethane-anesthetized, paralyzed, artificially ventilated rats, CPA inhibition by bilateral microinjection of the inhibitory amino acid glycine (Gly, 100 nmol 200 nl-1 site-1) produced an average decrease of -38 +/- 4.3 mmHg in ABP (N = 6). Ten min after bilateral microinjection of the broad-spectrum glutamate antagonist kynurenic acid (KYN, 2 nmol 200 nl-1 site-1) into the caudal ventrolateral medulla (CVLM) depressor responses to CPA inhibition were virtually abolished (-3 +/- 1.7 mmHg, P < 0.05). Similar microinjection of KYN into the rostral ventrolateral medulla (RVLM) or into the CPA itself did not modify depressor responses to CPA inhibition by glycine. 3. CPA stimulation by bilateral microinjection of the excitatory amino acid L-glutamate (L-glu, 50 nmol 200 nl-1 site-1) produced an increase in ABP (+43 +/- 5.4 mmHg, N = 6). Bilateral microinjection of the GABAA antagonist bicuculline methiodide (BIC, 200 pmol 200 nl-1 site-1) into the CVLM markedly reduced pressor responses to CPA stimulation (+6 +/- 2.7 mmHg, P < 0.05). Similar application of BIC into the RVLM or CPA did not modify pressor responses to CPA stimulation by glutamic acid.

Animals↗

PubMed1990

The response of nucleus preopticus neurosecretory cells to ovarian pressure in the frog, Rana tigrina.

Intraovarian pressure (IOP) of 5, 15, and 25 mm Hg was administered in the frog, Rana tigrina, and the response of the nucleus preopticus (NPO) pars magnocellularis was investigated with aldehyde fuchsin (AF) stain and immunocytochemical method using neurophysin (NP) antisera. The 5 mm Hg IOP treatment resulted in cell and cell nuclear hypertrophy (P less than 0.001); discrete signs of de novo synthesis of AF-positive and NP-immunoreactive material in the perikarya and remarkable increases in the number and size of "Herring bodies" in the processes were observed. Stimulatory response after 15 mm Hg IOP treatment was characterized by dramatic augmentation of the AF-positive and NP-immunoreactive material in the processes; the engorged and coalescing Herring bodies totally predominated the lateral preoptic area. IOP of 25 mm Hg resulted in extensive loss of secretory material; the processes revealed the presence of vacuoles indicative of the rapid anterograde transport of the neurosecretory material. Furthermore, the application of IOP seemed to promote the transport of NP-immunoreactive material toward the anterior preoptic area and amygdala pars medialis and the release of secretory material into the cerebrospinal fluid. No changes were observed in the NPO when treatment was preceded by the transection of ipsilateral dorsal spinal nerve roots or the spinal cord. The results suggest the existence of an afferent neural pathway from the ovary capable of conducting the stretch signals to the NPO and triggering the synthesis and release of neurohypophysial hormones.

Animals↗

PubMed1984

A study of the contribution of hippocampal-accumbens-subpallidal projections to locomotor activity.

Locomotor activity recorded in an automated open-field apparatus was increased substantially by unilateral injections of carbachol, a cholinergic agonist, into the dentate gyrus of the hippocampus. Hyperactivity elicited in this way was reduced significantly when glutamate antagonists were injected into the ipsilateral nucleus accumbens. Injecting gamma-aminobutyric acid into the ipsilateral subpallidal region also reduced the hyperactivity from injections of carbachol into the dentate gyrus. When these compounds were injected into the contralateral accumbens and subpallidal region, respectively, there was little or no reduction in the carbachol-elicited locomotor activity. These observations suggest that neural pathways fom hippocampus to accumbens to subpallidal region may contribute to locomotor activity.

Animals↗

PubMed1989

Different interhemispheric transfer of kanji and kana writing evidenced by a case with left unilateral agraphia without apraxia.

Recent neuropsychological studies have revealed that the processing of kanji (the Japanese morphograms) and kana (the Japanese syllabograms) involves different intrahemispheric mechanisms. We describe a patient showing left unilateral agraphia without apraxia for kanji, but not for kana, who was diagnosed by magnetic resonance imaging as having a lesion of the posterior body of the corpus callosum. This patient indicates that different neural pathways are used for kanji and kana not only intrahemispherically, but also interhemispherically.

Aged↗

PubMed1982

Is a retrosplenial (cingulate) pathway involved in the mediation of high frequency hippocampal rhythmical slow activity (theta)?

In previous experiments we demonstrated that in rats there are two kinds of hippocampal rhythmical slow activity patterns (RSA or theta) as defined by the dominating EEG frequencies. RSA with a frequency of 6-8 Hz appeared during exploratory behavior (locomotion), whereas stimulation of the dorsomedial hypothalamus (DMH) elicited RSA with frequencies of 8-12 Hz. To determine the neural pathways involved in the mediation of these two types of RSA, local injections of tetracaine were made either in the medial septum or in the cingulate cortex in order to reversibly interrupt the functional activity of these loci. Blockade of the medial septum suppressed the 6-8 Hz 'walking-associated' RSA in the hippocampal EEG, but had no effect on the 8-12 Hz DMH-driven RSA. On the other hand, a tetracaine injection into the cingulate cortex selectively blocked the high-frequency RSA elicited by DMH stimulation, but had no effect on the 6-8 Hz 'walking-associated' RSA. Both effects disappeared between 30 and 90 min after tetracaine injection. We conclude that the DMH-driven RSA is mediated by the cingulum and/or fibers traveling through the cingulate cortex (retrosplenial region) and thus, that this type of RSA operates without septal involvement.

Animals↗

PubMed1996

Carbamazepine inhibits the potentiation by adenosine analogues of agonist induced inositolphosphate formation in hippocampal astrocyte cultures.

Carbamazepine (CBZ) resembles lithium in its beneficial effects in therapy and prophylaxis of affective disorders. Since lithium is presumed to act via an attenuation of the inositolphosphate/Ca(2+)-second messenger system, it is of particular interest whether or not CBZ might also have inhibitory effects on this type of signal transduction. CBZ is an antagonist of adenosine A1-receptor subtypes. We show here that activation of adenosine A1-receptors potentiates the phenylephrine induced formation of inositolphosphates in hippocampal astrocytes and that this potentiating effect is inhibited by CBZ at a therapeutically relevant concentration. These results indicate that CBZ can by antagonism of adenosine A1-receptors inhibit the inositolphosphate/Ca(2+)-signalling in neural pathways regulated by adenosine.

Adenosine↗

PubMed1989

Quantitative [14C]2-deoxyglucose study of a functional dissociation between anterior and posterior cingulate cortices in mice.

We have previously shown that lesion of the posterior cingulate cortex (CCP) but not of the anterior cingulate cortex (CCA), produced learning and memory deficits. As a first evaluation of the functional anatomical basis of this dissociation, we used the quantitative [14C]2-deoxyglucose method and electrical brain stimulation to determine the functional connections of the CCA and CCP in mice. CCP stimulation (but not CCA stimulation) produced significant metabolic increases in the hippocampal formation and in the subicular complex. This result is consistent with the hypothesis that learning and memory deficits following CCP lesion may be due to the disruption of functional neural pathways between the CCP and hippocampal structures.

Animals↗

PubMed2002

Correlation between the fighting rates of REM sleep-deprived rats and susceptibility to the 'wild running' of audiogenic seizures.

Sleep-deprived rats exhibit defensive fighting as well as explosive flights very similar to the wild-running of audiogenic seizures. In order to determine why sleep deprivation is a common factor that facilitates both panic and convulsive manifestations, the present study was undertaken to investigate whether rats that display sleep deprivation-induced fighting (SDIF) are the same as those that are susceptible to audiogenic wild-running (WR). Twenty-eight male adult Wistar rats were divided into two groups assigned to two experimental schemes. In the first, 18 subjects were submitted to REM-sleep deprivation for 5 days and had their SDIF evaluated in social grouping. After 1 week for recovery, their susceptibility to WR was tested in an acoustic stimulation trial (104 dB, 200 Hz, 60 s). Rats that did not present WR received a lactate infusion and were tested again by acoustic stimulation 40 min later. In the second experimental scheme, 10 subjects were initially evaluated for WR susceptibility and the number of SDIF was recorded in social grouping after 1 week. Three categories of WR-susceptibility were determined: WR-sensitive rats, intermediate WR-sensitive rats and WR-insensitive rats. The number of SDIF in each category was significantly different and there was a high positive correlation (r=0.89; Spearman test) between the number of SDIF and the level of WR-susceptibility. We conclude that the reasons why sleep deprivation exerts facilitatory effects on both panic and convulsive manifestations are due to overlappings of neural pathways responsible for both behavioral patterns and for the property of sleep deprivation to increase neuronal excitability.

Acoustic Stimulation↗