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PubMed1999

Chronic hypoglycemia and diabetes impair counterregulation induced by localized 2-deoxy-glucose perfusion of the ventromedial hypothalamus in rats.

Previous studies have demonstrated that the ventromedial hypothalamus (VMH) plays a critical role in sensing and responding to systemic hypoglycemia. To evaluate the mechanisms of defective counterregulation caused by iatrogenic hypoglycemia and diabetes per se, we delivered 2-deoxy-glucose (2-DG) via microdialysis into the VMH to produce localized cellular glucopenia in the absence of systemic hypoglycemia. Three groups of awake chronically catheterized rats were studied: 1) nondiabetic (with a mean daily glucose [MDG] of 6.9 mmol/l) BB control rats (n = 5); 2) chronically hypoglycemic nondiabetic (3-4 weeks, with an MDG of 2.7 mmol/l) BB rats (n = 5); and 3) moderately hyperglycemic insulin-treated diabetic (with an MDG of 12.4 mmol/l) BB rats (n = 8). In hypoglycemic rats, both glucagon and catecholamine responses to VMH glucopenia were markedly (77-93%) suppressed. In diabetic rats, VMH 2-DG perfusion was totally ineffective in stimulating glucagon release. The epinephrine response, but not the norepinephrine response, was also diminished by 38% in the diabetic group. We conclude that impaired counterregulation after chronic hypoglycemia may result from alterations of the VMH or its efferent pathways. In diabetes, the capacity of VMH glucopenia to activate the sympathoadrenal system is only modestly diminished; however, the communication between the VMH and the alpha-cell is totally interrupted.

Animals↗
PubMed1986

Auditory field reduction in human following head trauma.

We measured the tonal auditory threshold for 500, 2000 and 4000 Hz, and made BAER recordings for both ears with unfiltered 125 dB SPL clicks, with 40 subjects between 18 and 23 years of age, 20 subjects having suffered minor cranial trauma during the preceding 48 hours and 20 being control subjects matched for age and sex. Compared to the control group, trauma patients showed a significantly higher auditory threshold: 19 dB SPL at 500 Hz, 9 dB SPL at 2000 and 4000 Hz. This threshold rise was bilateral. The head trauma patients showed, on average, one significantly earlier BAER wave I than did controls. This alteration was likewise bilateral. The latencies of waves II, III and V, the I-III, III-V, and I-V intervals, and the interaural wave latency and interval differences are comparable for trauma patients and control subjects. One to eight months after cranial trauma, 7 subjects manifested one sign of the subjective cranial trauma syndrome. Auditory threshold and BAER wave I earliness were not any greater for these subjects. Trauma patients seemed to show a reduction of the auditory field. They were hypersensitive to high stimulus intensities (shortening of BAER wave I) and less sensitive to low intensities (rise in tonal auditory threshold). This auditory alteration was bilateral. It can thus be thought that the trauma acts on the central nervous system to affect the operation of the cochlea via efferent pathways.

Adolescent↗
PubMed1977

New approach of the cardio-vascular depressive mechanism during lateral hypothalamic stimulation.

Paraventricular nucleus stimulation acts directly on the alpha- and beta-adrenoreceptors in heart and arterioles, eliciting arterial hypotension and cardiac chronotropism and inotropism decrease. Efferent pathways follow sympathetic nervous fibres through the medulla and the thoraco-lumbar ganglionic chain. The role of the alpha- and beta-adrenoreceptors in these depressive reactions is discussed.

Adrenergic alpha-Antagonists↗
PubMed1987

Baroreceptor mechanisms in rat.

Baroreflex control of cardiovascular parameters was studied in control, atropine- and guanethidine-treated rats. Baroreceptor activity was tested by the relationship between the increase in blood pressure produced by a phenylephrine administration (bolus ov infusion) and the induced bradycardia. No differences were observed in basal arterial blood pressure and heart rate between treated- and control rats. Baroreceptor sensitivity was lower in atropine- or guanethidine-treated rats than in control animals. Baroreceptor activity has two components: a first, rapid, predominantly parasympathetic and a second, slower, that is mediated by both parasympathetic and sympathetic efferent pathways.

Animals↗
PubMed2004

Treatment of hemiballismus with stereotactic pallidotomy. Case report and review of the literature.

Hemiballismus is a relatively rare movement disorder that is characterized by uncontrolled, random, large-amplitude movements of the limbs. It is usually caused by a vascular lesion that involves the contralateral subthalamic nucleus (STN) (also known as the nucleus hypothalamicus or corpus luysi) and its afferent and efferent pathways. The authors present a case of medically intractable hemiballismus in a 70-year-old woman who was successfully treated with stereotactic posteroventral pallidotomy. In agreement with the data reported earlier by other groups, the microrecording performed during the pallidotomy showed a decreased rate of firing of the pallidal neurons, supporting the theory of impaired excitatory input from the STN to the internal part of the globus pallidus. Stereotactic pallidotomy may be the procedure of choice in the treatment of medically intractable hemiballismus. Intraoperative microrecording significantly improves the precision of the stereotactic targeting and should be considered a standard part of the pallidotomy protocol.

Action Potentials↗
PubMed2005

Monitoring of facial muscle motor evoked potentials during microvascular decompression for hemifacial spasm: evidence of changes in motor neuron excitability.

OBJECT: Hemifacial spasm (HFS) is thought to be due to a hyperactive facial motor nucleus consequent to chronic neurovascular contact. The lateral spread (LS) response is presumed to reflect changes in facial motor neuron excitability. Facial muscle motor evoked potentials (MEPs) use the same efferent pathway as LS, therefore the authors speculated that these potentials should reflect differences consistent with changes at the facial motor nucleus level. METHODS: Monitoring of LS and bilateral facial MEP was performed in 10 consecutive patients undergoing MVD for HFS. Ipsilateral facial MEPs were monitored in 17 patients undergoing MVD for trigeminal neuralgia (TN). Latency, amplitude, and duration of the MEPs were compared before and after MVD. Following MVD the duration of ipsilateral MEPs decreased from 17.6 +/- 1.2 to 7.6 +/- 0.7 msec and their amplitude decreased from 269.9 +/- 66.3 to 76.5 +/- 26.2 microV (p < or = 0.01). These changes were consequent to the abolition of LS in eight of 10 patients and an approximately 50% reduction in two patients. The relationship between the reduction in MEPs and changes in LS was significant (p < 0.01). Control facial muscle MEPs (nonspastic side in patients with HFS and in those with TN) did not change significantly during the MVD procedure. Spasms were alleviated in nine of 10 patients, and there was no indication of facial nerve damage intraoperatively or postoperatively. CONCLUSIONS: Facial muscle MEPs represent a novel tool for studying the neurophysiological mechanisms of HFS in particular and monitoring the facial nerve in general. Data in this study support the hypothesis that the development of HFS and its alleviation with MVD are related to changes in facial motor nucleus activity.

Case-Control Studies↗
PubMed1999

Glutamatergic aspects of schizophrenia.

Almost all the neurons in the brain are influenced by the excitatory amino acid glutamate. Glutamatergic neurotransmission has been associated functionally with a number of physiological processes and with certain pathophysiological processes, including schizophrenia. Imaging studies provide indirect evidence that glutamate may be involved in schizophrenia. Positron emission tomography scanning has shown a correlation between positive symptoms of schizophrenia and abnormalities of glucose metabolism in components of the limbic system with the highest concentration of glutamate receptors. Studies with ketamine, an anaesthetic that antagonises the N-methyl-D-aspartate (NMDA) glutamate receptor, show an exacerbation or worsening of positive symptoms when this drug is administered to patients with schizophrenia. Regional cerebral blood flow studies with ketamine show that the drug produces increased blood flow in the anterior cingulate cortex, the area where high concentrations of NMDA receptors exist and where alterations in glucose metabolism seem to occur in people with schizophrenia. Diminished glutamatergic neurotransmission in the hippocampal glutamate-mediated efferent pathways and cerebral dysfunction in the hippocampus and its target areas, particularly the anterior cingulate cortex, may underlie some of the clinical manifestations of schizophrenia.

Cerebrovascular Circulation↗
PubMed1999

Calcium binding proteins immunohistochemistry and identification of neurons in the mammalian pineal gland of the African giant rat: Cricetomys gambianus.

The presence of true neurons in the rodent pineal gland is still a matter of controversy. In this work, by using immunohistochemistry with five antibodies against calcium-binding proteins (calbindin-D28k, calretinin, calmodulin, neurocalcin and S-100 beta) and Cricetomys gambianus, a rodent belonging to Muridae family living in Africa, we were able to illustrate the presence of neurons in the pineal gland. Anti-calbindin-D28k and anti-calretinin labelled neurons belonging to two neural ganglia. One ganglion was localized in the anterior part of the gland near the pineal stalk and the other one in the posterior portion of the organ. Immunoreactive neurons are medium in size (15-20 microns) and have long thick processes running towards the stalk. Calretinin and calbindin-D28k positive neurons stained with different intensities. Thin processes were detected by anti-calretinin whereas thick processes were preferentially calbindin-D28k positive. Neurocalcin labelled a few smaller neurons and many thin processes within the ganglion. Calmodulin could not be detected immunochemically. Within the ganglia many astrocytic processes were S-100 beta positive. The afferent and the efferent pathways of the pineal ganglia remain to be elucidated.

Animals↗
PubMed1976

Interactions between narcotic analgesics and benzodiazepine derivatives on behavior in the mouse.

Interactions between the benzodiazepine derivatives, diazepam and oxazepam, and the narcotic analgesics, morphine and methadone, were evaluated on locomotor activity and in the tail-flick and hot-plate tests for analgesia in the mouse. The dose-related stimulation of locomotor activity by morphine was reduced by diazepam and oxazepam at doses which alone had no effect on locomotor activity. However, only oxazepam reduced the dose-related stimulation of locomotor activity by methadone. The observed decreases produced by diazepam and oxazepam were comparable in magnitude to those produced by naloxone. Stimulation of locomotor activity by d-amphetamine was not affected by either diazepam or oxazepam. Dose-response curves for locomotor activity were also determined with morphine and methadone administered intraventricularly. As before, diazepam and naloxone given i.p. decreased the stimulation of locomotor activity produced by morphine, but only naloxone affected methadone-stimulated locomotor activity. Neither diazepam, oxazepam nor naloxone reduced the brain or plasma levels of 3H-morphine or 3H-methadone. In contrast to the results on locomotor activity, neither of these benzodiazepines significantly modified the dose-response curves of morphine or methadone in either test for analgesia. The mechanisms involved in the observed interactions on locomotor activity may be related to the influences of benzodiazepines and narcotic analgesics on motor efferent pathways summating in such a manner as to interfere with the ability of the mice to locomote. The present results demonstrate that prominent interactions occur between members of the benzodiazepine and narcotic analgesic classes; these interactions are dependent upon both the specific combination of drugs administered and upon the test procedure.

Analgesics, Opioid↗
PubMed2000

Multiple sites of action in the inhibitory effect of nociceptin on the micturition reflex.

PURPOSE: Nociceptin, the endogenous peptide ligand for the opioid receptor-like1 (ORL1) receptors, exerts a naloxone-resistant suppressant effect on micturition reflex after intravenous administration. This work aims to elucidate the mechanism and the site of action of the inhibitory effect of nociceptin on the micturition reflex. MATERIALS AND METHODS: The bladder of urethane-anesthetized rats was cannulated through the dome (cystometries) or the urethra in isovolumetric conditions (distension-induced reflex contractions, DIRCs). In this latter model, the effect of the application of nociceptin onto the serosal surface of the urinary bladder was determined. The effect of intravenous, intrathecal and intracerebroventricular administration of nociceptin on ongoing cystometries at two different infusion rates (50 and 250 microL/min.) was assessed. The effect of the intravenous administration of nociceptin on cystometries was also studied in capsaicin-pretreated animals. RESULTS: When cystometric recordings were obtained at a low infusion-rate (50 microL/min.), the intravenous administration of nociceptin (10 to 100 nmol./kg.) induced a dose-dependent reduction in the micturition frequency associated to an increase of the pressure threshold for activating the micturition reflex, whereas the amplitude of micturition contractions was unaffected. These effects faded within 60 minutes. The intracerebroventricular administration of nociceptin (0.3 nmol./rat) produced urodynamic changes similar to those observed after the intravenous route and, in addition, also reduced the amplitude of micturition contractions. The intrathecal administration of nociceptin up to 1 nmol./rat was ineffective. Capsaicin pretreatment (164 micromol./kg., s.c. 5 to 6 days before) significantly reduced the micturition frequency as compared with controls. In capsaicin pretreated animals intravenous nociceptin was ineffective. When cystometries were recorded at a high infusion-rate (250 microL/min.) either intravenous (100 nmol./kg.), i.t. (1 nmol./rat) nociceptin or capsaicin pretreatment had no effect. In contrast, intracerebroventricular nociceptin (0.3 and 1 nmol./rat) inhibited the micturition reflex by reducing both the frequency and the amplitude of micturition contractions: these effect were not modified by naloxone (0.5 micromol./kg., i.v.). The topical application of nociceptin (5 and 50 nmol./rat) caused a dose-dependent inhibition of DIRCs. CONCLUSION: Nociceptin inhibits the micturition reflex at a peripheral and at a supraspinal site. The effects observed after the intravenous administration of nociceptin indicate that the functional integrity of capsaicin-sensitive bladder afferents is required for exerting its inhibitory activity at the peripheral level. In contrast, the supraspinal effect of nociceptin involves both the afferent and the efferent pathways of the micturition reflex, possibly through a direct effect on ORL1 receptors located in the pontine micturition center.

Animals↗
PubMed1999

Influence of continuous, isobaric rectal distention on smooth muscle tone and cardiovascular activation in healthy volunteers.

UNLABELLED: Interactions between visceral, intestinal stimulation and autonomic cardiovascular function have received increasing attention over the last years. The aim of the study was to investigate the effect of long-term continuous rectal distention on rectal tone and cardiovascular function at the threshold for first sensation of distention and moderate urge to defecate compared to a resting period without distention. Continuous isobaric rectal distention was performed in 13 healthy volunteers with a ten minute pressure tracking procedure at each subject's predetermined individual threshold for either moderate urge or first sensation, separated by a ten minute resting period. Rectal volume, heart rate, systolic and diastolic blood pressure were determined continuously. RESULTS: Rectal tone decreased significantly over time at the threshold for moderate urge and first sensation. Cardiovascular measures remained stable over the distention procedures, except for a significant increase in systolic blood pressure at the threshold for moderate urge. DISCUSSION: The previously reported rectal accommodation response to rectal distention was confirmed. The increase in systolic blood pressure is most likely mediated through sympathetic efferent pathways.

Adaptation, Physiological↗
PubMed2000

Inhibition of the carotid baroreflex by urinary bladder distension.

OBJECTIVE: The cardiovascular responses to urinary bladder distension include a rise in arterial blood pressure, an increase in vascular resistance and heart rate, which are abolished by sectioning the pelvic and hypogastric nerves. There are indications in the literature that inputs from the arterial baroreceptors and urinary bladder converge at the same autonomic efferent pathways. Recent data provided evidence of a partial inhibitory action of the carotid baroreflex on the reflex cardiovascular responses evoked by bladder distension. In this study, we investigate the influence of urinary bladder distention upon cardiovascular responses elicited by carotid baroreceptor stimulation. METHODS: Wistar Rats were anaesthetised with alpha-choloralose (80 mg/kg, i.p.) supplemented as necessary. The carotid sinus was stimulated randomly with different volumes of saline (0.5-2.0 ml). The ureters were ligated and the bladder was cannulated. Arterial blood pressure (BP), ECG, heart rate (HR), and bladder pressure (BLP) were monitored. Baroreceptor stimulation was undertaken on two levels of BLP (2 and 20 cmH2O). The cardiovascular response to baroreceptor activation was assessed as the maximal variation of BP, HR and R-R interval for different volumes of saline injected. RESULTS: Our results showed that in all tests baroreceptor stimulation evoked a decrease in BP and HR but the magnitude of these responses was significantly different for each volume of saline and for two levels of BLP. The effectiveness and reproducibility of responses to these stimuli were confirmed by injecting a fixed volume of saline into the carotid sinus of two animals at two levels of BLP. In five animals, the variation in BP increased as the magnitude of the stimulus to the baroreceptor increased. However, the response was reduced with increased BLP. The fitted regression line was calculated for all the tests (n = 82; s = 8.2; Yint = 0.62 for BLP = 2 cmH2O; s = 9.5; Yint = 2.9; r = 0.69 for BLP = 20 cmH2O). Similar effects were observed and similar patterns of regression lines were obtained with regard to HR changes (n = 48; s = 13.3; Yint = 2.7; r = 0.82 for BLP = 2 cmH2O; s = 15.8; Yint = 0.89; r = 0.76 for BLP = 20 cmH2O) and interval changes (n = 48; s = 7.1; Yint = 4.3; r = 0.78 for BLP = 2 cmH2O; s = 8.5; Yint = 0.2; r = 0.76 for BLP = 20 cm H2O). CONCLUSIONS: These data suggest that the cardiovascular responses evoked by carotid baroreceptor stimulation are significantly different when the urinary bladder is empty or full with the response diminishing as the urinary bladder is distended.

Animals↗
PubMed2000

[Importance of the stapedial reflex in the diagnosis of several pathologies].

The stapedius muscle plays an important role in auditory physiology. Its function may be assessed using a test named impedancemetry, where its reflex is measured. For the stapedial reflex to function, it is necessary that the middle ear and the afferent and efferent pathways are intact. Several pathologies of the middle and internal ear, as well as other otoneurological disorders and systemic illnesses, may change the physiology of the stapedius muscle. This review has incorporated various bibliographic sources with the objective to show the modifications of the stapedial reflex in several types of pathology. It reveals that the research of the stapedial reflex as well as its interpretation constitute a very important diagnostic supplement in the clinical audiology.

Acoustic Impedance Tests↗
PubMedDate not supplied

[Otoacoustic emissions--a step closer to understanding cochlear function].

INTRODUCTION: Otoacoustic emission is a phenomenon that may occur in a large group of normal-hearing subjects. Ear is an organ which collects and treats sounds from the surrounding environment, and nerve fibres transmit the perceived information to the brain in terms of nerve signals. However, ear can also produce a sound (otoacoustic-emission), which can be recorded using very sensitive microphones placed in the ear canal. OTOACOUSTIC EMISSION: Otoacoustic emissions may be spontaneous (SOAE) or may be a response to given auditory stimuli: transiently evoked otoacoustic emissions (TEOAE) and distortion product otoacoustic emissions (DPOAE). Applications of otoacoustic emissions in clinical and experimental medicine are various. Hearing screening program of newborns aims to identify infants with permanent bilateral hearing loss in the first days after birth. Screening programs are based on recordings of transiently evoked otoacoustic emissions (TEOAE) in the first step, and then (if it is necessary) brainstem evoked response audiometry. Transiently evoked otoacoustic emissions may also be used for differential diagnosis of cochlear and retrocochlear disorder. UTILIZATION: In cases of substantial retrocochlear pathological findings without cochlear involvement, transiently evoked otoacoustic emissions should be recordable because outer hair cell function is unaffected. It is possible to detect ototoxic effects of drugs before hearing loss can be detected by other methods (pure-tone audiometry). In a similar way, using otoacoustic emissions, it is possible to detect noise induced damages of the outer hair cells. Otoacoustic emissions provide a unique means for assessing the integrity of the medial efferent pathway. Further research into the properties of various types of otoacoustic emissions would contribute to understanding of cochlear function, and in particular, the relative roles of inner and outer hair cells. Evoked otoacoustic emissions are directly related to outer hair cell function and may be somewhat independent of inner hair cells. At present, there is insufficient evidence to indicate whether inner and outer hair cell disorders can exist separately, and if they can, whether they are so strongly correlated that statistically the distinction is meaningless. Applications of otoacoustic emissions in clinical practice is an important route in furthering our understanding.

Cochlea↗
PubMed2001

Anisocoria and middle cerebral artery saccular (berry) aneurysm in a rhesus macaque (Macaca mulatta).

A 27-year-old female rhesus macaque (Macaca mulatta) developed anisocoria. The left pupil was dilated and unresponsive to light. The macaque was euthanized because of unrelated reasons and the body was submitted for necropsy. On gross examination, a berry aneurysm of the right middle cerebral artery causing marked compression of the right optic tract was found. Arteriosclerotic changes were observed microscopically in the right middle cerebral and in the internal carotid arteries. The left iris was markedly degenerated, with atrophy of the constrictor muscle. Compression of the right optic tract may cause homonimus hemianopsia. A dilated and unresponsive left pupil indicated a lesion in the ipsilateral parasympathetic efferent pathway. In the absence of appreciable lesions of the left oculomotor nerve, the most likely cause of mydriasis was the iridic lesion. Intracranial aneurysms are common in humans (2 to 5%), but not in other species. Only about 10% of unruptured aneurysms are associated with neurologic deficits related to mechanical compression, such as visual deficits or anisocoria. Meticulous investigation of the ocular vascular and neural pathways led us to conclude that the anisocoria was unrelated to the aneurysm. To our knowledge, this report represents the first documented case of a naturally occurring intracranial aneurysm in nonhuman primates.

Animals↗
PubMed2002

[Protective effects of paraventricular nucleus stimulation and vasopressin on gastric ischemia-reperfusion injury in rats].

The effects of paraventricular nucleus (PVN) stimulation and vasopressin on gastric ischemia-reperfusion injury (GI-RI) were investigated in male SD rats of which the celiac artery was clamped for 30 min and reperfused for 1 h by removal of the clamp. The results were as follows. Both electrical and chemical stimulation of the PVN obviously attenuated the GI-RI. Bilateral electrolytic lesion of the nucleus tractus solitarius (NTS) or microinjection of AVP-V(1) receptor antagonist into the NTS could eliminate the protective effect of electrical stimulation of the PVN on GI-RI. Hypophysectomy did not influence the effect of electrical stimulation of the PVN. Both vagotomy and sympathectomy could increase the effect of stimulating PVN on GI-RI. Microinjection of arginine-vasopressin (AVP) into the PVN also attenuated the effect on GI-RI. These results suggest that the PVN and AVP participate in the regulation of GI-RI and play an important role in protection against GI-RI. This protective effect of PVN on GI-RI might be mediated by activation of AVP-ergic neurons in the PVN, which release AVP from the descending projection fibers and activate the AVP-V(1) receptors on the NTS neurons. The vagus and sympathetic nerves are involved in the efferent pathway exerting their effects on GI-RI. Hypophysis does not seem to be involved in the protective effect of PVN stimulation.

Afferent Pathways↗
PubMed2002

Vocal control neuron incorporation decreases with age in the adult zebra finch.

In adult male zebra finches, high vocal center (HVC) neurons continuously die and are replaced. Many of these cells are projection neurons that form part of the efferent pathway controlling learned song production. Although it is known that HVC receives new neurons well into adulthood, it is unknown whether this occurs at a constant rate or declines with adult age. We used [3H]thymidine to label new HVC neurons in male zebra finches that were 3-36 months of age. Birds were killed 4 months after 3H injections to measure the long-term incorporation of new HVC neurons. HVC neurons projecting to the robust nucleus of the archistriatum (HVC-RA) were retrogradely labeled with Fluoro-Gold 4 d before death. We found a dramatic age-related decline in the number of 3H-labeled HVC-RA neurons present 4 months after cell birth dating. A similar decline in new HVC neurons was found as soon as 1 month after their formation. These results indicate that the production or early survival of adult-formed neurons decreases with age. HVC volume and total neuron number did not change with bird age, suggesting that the age-related decrease in new neuron addition was balanced by increased survivorship of neurons incorporated previously. Reliance of song structure on auditory feedback also wanes with age. We propose that with aging, fewer new cells are added as the numbers of functionally appropriate cells increase, a process that may be linked to age-related increases in motor program stability.

Aging↗