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[Central projections of the rat superior laryngeal nerve].

Laryngeal nerves contain the fibres that control the laryngeal function. On the rat, the studies on the functional components and the real origin of the fibres conveyed by the superior laryngeal nerve (SLN) are few. No one of such works were developed using biotinylated dextrane amines (BDA), a powerful tool for tracing neural pathways. The aim of our study was to identify by using BDA, in the rat, the nuclei of real origin of the fibres of the SLN, knowing in this way the functional components of this nerve. The study has been developed in 11 adult male Sprague-Dawley rats, applying the BDA into the damaged SLN. The results obtained in all the animals shown that the rat SLN carries efferent fibres originated within the ipsilateral nucleus ambiguous (NA) and dorsal nucleus of the vagus (DNV), and that afferent fibres reach the tractus solitari and the nucleus tractus solitari. So, in the rat, the SLN seems to convey efferent fibres from the NA and DNV and, probably, all the laryngeal afferent fibres.

Animals↗

PubMed2001

The role of substance P release in the lung with esophageal acid.

To investigate whether tachykinins are released in the airways by stimulating the esophagus, airway plasma extravasation induced by intraesophageal hydrochloric acid (HCl) in the presence or absence of the neutral endopeptidase (NEP) inhibitor phosphoramidon and the neurokinin-1-receptor antagonist FK888 was studied in anesthetized guinea pigs. Airway plasma extravasation also was studied in the presence of the NEP inhibitor in guinea pigs pretreated with capsaicin or bilateral vagotomy. Propranolol and atropine were used in all animals to block adrenergic and cholinergic nerve effects. Airway plasma leakage was evaluated by measuring extravasated Evans blue dye. One normal HCl infusion into the esophagus significantly increased plasma extravasation in the trachea. Phosphoramidon significantly potentiated plasma extravasation induced by HCl infusion into the esophagus in the trachea and main bronchi, and FK888 significantly inhibited extravasation in a dose-related manner. In capsaicin-treated animals, airway plasma extravasation was completely inhibited even in the presence of phosphoramidon. Tracheal plasma extravasation potentiated by phosphoramidon was significantly inhibited in the bilaterally vagotomized animals. These results suggest that locally acting substances are released by intraesophageal HCl stimulation that cause airway plasma extravasation. These substances are generated through activation of neural pathways, including some that traffic through the vagus nerves that link the esophagus or airways.

Animals↗

PubMed2000

Central integration of swallow and airway-protective reflexes.

The relationship between the timing of respiration and swallowing has been proven not to be random. Using pseudorabies virus (PRV) as a transsynaptic neural tracer, a basis for the central integration of swallowing and airway-protective reflexes can be located in the neural circuits projecting to swallowing-related muscles. The premotor neurons (PMNs) that constitute the swallowing central pattern generators, interneuronal networks able to initiate repetitive rhythmic muscle activity independent of sensory feedback, connect with multiple areas of the brainstem and other areas of the central nervous system. Those PMNs that project to muscles used in swallowing have been localized within the nucleus of the solitary tract (NTS) and its adjacent reticular formation, and they are synaptically linked both to peripheral afferents and to cortical swallowing areas. Bartha PRV, an attenuated vaccine strain of swine alpha-herpesvirus with a long postinjection survival rate and the ability to produce controlled infections that spread in a hierarchical manner within synaptically linked neurons, can specifically label neurons projecting to PMNs of a given circuit. Thus, it has been used to isolate two neuroanatomically distinct subnetworks of PMNs involved in the buccopharyngeal and esophageal phases of swallowing. Use of PRV as a neural tracer shows that during the buccopharyngeal phase of swallowing, vagal afferents from the pharynx and larynx and from the superior laryngeal nerve terminate in the intermediate and interstitial subnuclei of the NTS. Motoneurons projecting to the pharynx and larynx are located in the semicompact and loose formations of the nucleus ambiguus (NA). Neural tracing with PRV also shows that esophageal PMNs have direct synaptic contact with esophageal motoneurons in the compact formation of the NA. Moreover, esophageal PMNs are localized exclusively to the central subnucleus of the NTS, a site that also is the sole point of termination of esophageal vagal afferents. Using PRV, one can identify third-order (neurons projecting to PMNs) esophageal neurons in sites where pharyngeal PMNs have been noted. Injection of PRV into the esophagus and subsequent detection using immunofluorescence found a subpopulation of neurons in the intermediate and interstitial subnuclei of the NTS. This subpopulation projects to pharyngeal motoneurons and buccopharyngeal PMNs, and it is synaptically linked to esophageal PMNs. The synaptic link between buccopharyngeal and esophageal PMNs provides a potential anatomic substrate within the NTS for the central integration of esophageal peristalsis with the pharyngeal phase of swallowing and airway-protective reflexes. Human studies and animal models investigating esophagoglottal closure and pharyngo-upper esophageal sphincter (pharyngo-UES) contractile reflexes have located the neural pathways that mediate airway-protective reflexes. Similar studies and models using two PRV strains injected simultaneously into different swallowing and respiration-related muscle groups may identify synaptic connectivity between laryngeal, esophageal, and pharyngeal PMNs and, thus, may help to demonstrate the central integration of swallowing and airway-protective reflexes.

Deglutition↗

PubMed1988

Postprandial neurohormonal control of gastric emptying.

The delay in gastric emptying after a meal is thought to result from nutrient distention-induced release of peptides and neurotransmitters in the gut. The potential contribution of the brain and central neuropeptides to the postprandial regulation of gastric emptying has not been studied adequately. The purpose of this study was twofold: to examine the relative importance and pure central stimulation (sham feeding) or pure peripheral stimulation (duodenal feeding) on gastric emptying, and to determine whether relevant neuropeptides act in the brain to slow gastric emptying of a meal. Six mongrel dogs were prepared with esophageal fistulas, gastric fistulas, duodenal fistulas, and chronic lateral cerebroventricular guides. Gastric emptying of a 300 ml saline solution meal was measured by a phenol red dye dilution technique. Sham feeding of a blenderized meal through the esophageal fistula was used as a central cephalic stimulus. Intraduodenal oleic acid was used as a peripheral stimulus. Both sham feeding and intraduodenal oleic acid inhibited gastric emptying by 59 +/- 12 percent, 73 +/- 5 percent, respectively. In separate studies, we examined the effect on gastric emptying of a bolus injection into the lateral cerebral ventricle of graded doses of corticotropin-releasing factor (110 to 440 pmol/kg), cholecystokinin (16 to 128 pmol/kg), somatostatin-14 (55 pmol/kg), human calcitonin gene-related peptide (230 pmol/kg), and neuropeptide Y (62 to 250 pmol/kg). These peptides are known to affect satiety, gastric emptying, and gastric acid secretion. Of these, only neuropeptide Y and cholecystokinin had an effect on gastric emptying when administered into the lateral cerebral ventricle. Neuropeptide Y inhibited emptying by 28 +/- 8 percent and cholecystokinin accelerated emptying by 32 +/- 12 percent (p less than 0.05). Sham feeding inhibits gastric emptying to a similar degree as intraduodenal feeding, and of the neuropeptides tested, only neuropeptide Y inhibited gastric emptying when given into the brain. The central release of neuropeptides such as neuropeptide Y during a meal may trigger neural pathways that promote postprandial delay in gastric emptying. Central signals may be as important as peripheral signals in the postprandial control of gastric emptying. Further studies are needed to determine the mechanism by which sham feeding inhibits gastric emptying and whether central release of neuropeptide Y is involved.

Animals↗

PubMed2001

Regional cerebral blood flow effects of nicotine in overnight abstinent smokers.

BACKGROUND: Most people agree that dependence to tobacco is mediated by the effects of nicotine on the central nervous system, albeit the neural pathways involved are not clearly delineated. We investigated the effect of nasal nicotine spray on regional cerebral blood flow (rCBF) in a sample of habitual smokers, with H2 15O and positron emission tomography (PET). METHODS: Eighteen volunteer smokers were studied after 12 hours of smoking deprivation. Regional cerebral blood flow measures were obtained with PET and 50 mCi H2 15O in six consecutive scans. Nicotine spray and a placebo spray were administered in a single-blind design, preceded and followed by baseline studies. Images were coregistered and anatomically standardized. Square (9-mm side) regions of interest were placed in 10 preselected brain regions, bilaterally. The effects of the experimental condition and gender were tested with two-way repeated-measures analysis of variance in each of the regions studied. RESULTS: Nicotine reduced rCBF in the left anterior temporal cortex and in the right amygdala. Increases were noted in the right anterior thalamus. CONCLUSIONS: In habitual smokers after overnight abstinence, nicotine induced differing effects on regional blood flow relative to whole brain blood flow. Increases were observed in the thalamus, a region rich in nicotinic receptors, and reductions in limbic and paralimbic (amygdala, anterior temporal cortex) regions.

Adolescent↗

PubMed1999

Cardiac adaptivity to attention-demanding tasks in children with a pervasive developmental disorder not otherwise specified (PDD-NOS).

BACKGROUND: Decreases in heart rate variability (HRV) have been repeatedly demonstrated to be an index of effort allocation to attention-demanding tasks. Children with autistic-type problems in social interaction and in adapting to unfamiliar situations (DSM-IV: PDD-NOS) have been shown to have specific attention deficits. These children were hypothesized to exhibit less cardiac adaptivity to attention-demanding tasks. METHODS: Two groups of 18 children with PDD-NOS, judged to be hyperactive and nonhyperactive, were compared to 18 healthy children with respect to their performances on a visual attention task and the differences in HRV measured during periods of task performance and periods of rest. RESULTS: Compared to the control group, both clinical groups were found to have a stronger capacity limitation in processing high loads of information, and to be less capable of maintaining a stable task performance throughout the whole task. Both clinical groups showed significantly less decreases in HRV during the periods of task performance. The magnitude of rest-task differences in HRV was found to correlate significantly with a behavioral measure of resistance to unexpected changes in daily routines. CONCLUSIONS: Children with PDD-NOS are significantly less flexible in their autonomic adaptation to attention-demanding tasks. The findings are interpreted as reflecting a deficiency in the functional organization of those neural pathways that provide cortical control of the visceral efferents.

Adaptation, Physiological↗

PubMed2001

Activation of skeletal muscle afferents evokes release of glutamate in the subretrofacial nucleus (SRF) of cats.

The subretrofacial nucleus (SRF) is a region of the rostral ventrolateral medulla known to play a crucial role in sympathoexcitation. SRF neurons send direct projections to the intermediolateral cell columns of the spinal cord where they form synaptic contact with preganglionic sympathetic motor neurons. Activation of this neural pathway increases sympathetic outflow to the heart and blood vessels affecting cardiac function and vasomotor tone. Previous studies utilizing electrophysiological recording techniques and c-Fos expression have established that the activity of SRF neurons is increased during skeletal muscle contraction. However, the excitatory neurotransmitter mediating this increased activity remains in question. In the present study, static contraction of the triceps surae was induced by electrical stimulation of L7 and S1 ventral roots in anesthetized cats (n=12). Endogenous release of glutamate (Glu) from the SRF was recovered by microdialysis and measured by HPLC. Static muscle contraction for 4 min increased mean arterial pressure (MAP) 38+/-4 mmHg from a control level of 102+/-12 mmHg (P< 0.05). During muscle contraction the extracellular concentration of Glu recovered from the SRF increased from 623+/-117 to 1078+/-187 nM (P<0.05). To determine the effect of muscle contraction on Glu release in the absence of synaptic input from other reflexogenic areas, contraction was repeated following acute sinoaortic denervation and vagotomy. Following this denervation, muscle contraction increased MAP 41+/- 4 mmHg (P < 0.05) and Glu concentration from 635+/-246 to 1106+/-389 nM (P < 0.05). Muscle paralysis prevented the increases in MAP and Glu concentration during ventral root stimulation. These results suggest that: (i) Glu is released in the SRF during activation of contraction-sensitive skeletal muscle afferent fibers in the cat; and (ii) synaptic input from other reflexogenic areas appears to be ineffective in modulating the release of Glu in the SRF during static muscle contraction.

Animals↗

PubMed2001

Role of vagal afferent innervation in feeding and brain Fos expression produced by metabolic inhibitors.

Hepatic vagal afferent fibers have been implicated in the feeding responses initiated by administration of 2,5-anhydro-D-mannitol (2,5-AM; an inhibitor of hepatic metabolism) and methyl palmoxirate (MP; an inhibitor of fat metabolism). 2,5-AM and MP also increase brain Fos expression, an indicator of neural activity, which suggests that Fos expression can reveal the central neural pathways involved in the stimulation of feeding by these agents. To more closely test the hypothesis that brain Fos expression is related to the effects of 2,5-AM and MP on feeding, the vagus was lesioned by application of capsaicin, which destroys afferent fibers, directly to the cervical vagi. Perivagal capsaicin treatment blocked 2,5-AM-induced eating and attenuated MP-induced eating. Although perivagal capsaicin treatment attenuated MP-induced Fos expression, capsaicin treatment did not affect brain Fos expression produced by 2,5-AM. It is concluded that (1) brain Fos expression is not always related to the effects of 2,5-AM on feeding, (2) capsaicin-sensitive hepatic vagal afferent fibers carry the signal that stimulates feeding following 2,5-AM treatment, and (3) MP-induced feeding and brain Fos expression is mediated in part by capsaicin-sensitive fibers.

Animals↗

PubMed2002

Exposure to the estrogenic pollutant bisphenol A affects pain behavior induced by subcutaneous formalin injection in male and female rats.

We investigated the effects of perinatally administered bisphenol A (BPA), an environmental contaminant with estrogenic activity, on formalin-induced nociceptive responses. Male and female offspring of mother rats treated with BPA or oil were cross-fostered after birth to obtain three homogeneous groups: BPA-prenatal, receiving BPA via the placenta; BPA-postnatal, receiving BPA through suckling; OIL, control, from mothers receiving only peanut oil (vehicle). All groups underwent a pain test with s.c. formalin injection (50 microl, 10%) or were sham injected (pricking with a syringe needle) in the dorsal hind paw. They were immediately placed in an open field apparatus where pain responses (licking, flexing and paw-jerk) were recorded for 60 min. Corticosterone, testosterone and estradiol serum levels were determined in blood obtained at the end of the experiment. BPA-prenatal treatment induced an increase in licking duration in females and in flexing duration in both sexes in the first half of the test (0-30 min after formalin injection). BPA-postnatal treatment induced a decrease in paw-jerk frequency in males and females during the second part of the test (30-60 min after formalin injection). Plasma concentrations of corticosterone, estradiol and testosterone did not differ significantly between groups. These results indicate that exposure to BPA modified the activity of neural pathways and/or centers involved in nociception and pain in a sex-related and exposure-related manner.

Animals↗

PubMed2002

Simultaneous measurement of parasympathetic reflex vasodilator and arterial blood pressure responses in the cat.

We measured the changes in lower lip blood flow and systemic arterial blood pressure evoked by lingual nerve or trigeminal spinal nucleus (Vsp) stimulation to gain an insight into the brainstem integration of sympathetic and parasympathetic responses to nociceptive stimulation. We used artificially ventilated, cervically vago-sympathectomized cats deeply anesthetized with alpha-chloralose and urethane. A lip blood flow increase occurred in an intensity- and frequency-dependent manner following electrical stimulation of Vsp or lingual nerve regardless of whether systemic arterial blood pressure increased or decreased. In contrast, there was no apparent optimal frequency for the changes in systemic arterial blood pressure elicited by electrical stimulation of Vsp or lingual nerve. No relationship was found between the amplitude of the lip blood flow increase and that of the systemic arterial blood pressure change. Microinjection of lidocaine or kainic acid into the Vsp evoked, respectively, reversible and irreversible inhibition of the lip blood flow increase and systemic arterial blood pressure change evoked by lingual nerve stimulation. When microinjected unilaterally directly into the ipsilateral Vsp, the GABA agonist muscimol abolished both lingual nerve-evoked effects (increase in lip blood flow and changes in systemic arterial blood pressure) without changing basal systemic arterial blood pressure, suggesting the presence in the Vsp of GABA receptors serving to modulate both the parasympathetically mediated lip blood flow increase and the sympathetically mediated systemic arterial blood pressure change. Lidocaine microinjection into the salivatory nucleus caused a significant attenuation of the lingual nerve-induced blood flow increase, but had no effect on the lingual nerve-induced systemic arterial blood pressure change. Thus, the neural pathway mediating the lingual nerve-induced lip blood flow increase seems to be simple, requiring a minimum of four neurons: trigeminal afferent-Vsp-parasympathetic pre-ganglionic neurons with cell body located in the inferior salivatory nucleus-otic postganglionic neuron. On the other hand, the pathway underlying the evoked systemic arterial blood pressure changes, presumably mediated via altered sympathetic activity, seems to be more complicated and could be affected by more numerous factors.

Anesthetics, Local↗

PubMed2003

Further evidence for the interaction of mu- and delta-opioid receptors in the antinociceptive effects of the dual inhibitor of enkephalin catabolism, RB101(S). A spinal c-Fos protein study in the rat under carrageenin inflammation.

We have previously shown that RB101, a dual inhibitor of enkephalin-degrading enzymes, decreased carrageenin-evoked c-Fos protein expression at the spinal cord level in awake rats. Moreover, we have also shown that c-Fos expression is a useful marker of the possible direct or indirect interactions between neural pathways, such as opioid and cholecystokinin systems. We now investigated the respective roles of the three main types of opioid receptors (mu, delta, or kappa) and their possible interactions, in the depressive effects of RB101 in inflammatory nociceptive conditions induced by intraplantar carrageenin (6 mg/150 microl of saline). We used beta-funaltrexamine (beta-FNA), naltrindole (NTI), and nor-binaltorphimine (BNI) as specific antagonists for mu, delta- and kappa-opioid receptors, respectively. c-Fos protein-immunoreactivity (c-Fos-IR) was evaluated as the number of c-Fos-IR nuclei in the lumbar spinal cord 90 min after carrageenin. c-Fos-IR nuclei were preferentially located in the superficial (I-II) and deep (V-VI) laminae of segments L4-L5 (areas containing numerous neurons responding exclusively, or not, to nociceptive stimuli). RB101(S) (30 mg/kg, i.v.) significantly reduced the total number of carrageenin-evoked c-Fos-IR nuclei (30% reduction, P<0.01). This effect was completely blocked by beta-FNA (10 mg/kg, i.v.), or NTI (1 mg/kg, i.v.). In contrast, BNI (2.5 mg/kg, i.v.) did not reverse the reducing effects of RB101(S) on carrageenin-evoked c-Fos protein expression. These results suggest that functional interactions occur between mu- and delta-opioid receptors in enkephalin-induced antinociceptive effects.

Analgesics↗

PubMed1997

Identification of hypothalamic vasopressin and oxytocin neurons activated during the exercise pressor reflex in cats.

Blood pressure and heart rate reflexly increase during static muscle contraction in anesthetized cats. Previous studies have demonstrated that vasopressin (AVP) and oxytocin (OT) may act as neuromodulators to regulate cardiovascular responses elicited by contraction of skeletal muscle. In this study, we tested the hypothesis that neurons containing AVP and OT in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON) of the hypothalamus are activated during static muscle contraction. A laminectomy was performed to expose the spinal cord and the peripheral cut ends of L7 and S1 ventral roots were stimulated electrically to induce muscle contraction. Hypothalamic neurons activated during the muscle contraction were identified by Fos-like immunoreactivity (FLI). Static muscle contraction significantly increased FLI in the PVN and SON, compared with sham-operated cats. Double-staining of neurons in the PVN for AVP and OT showed that 22 +/- 4% of the AVP and 26 +/- 3% of the OT neurons in the PVN expressed FLI. In contrast, only 4 +/- 1% of the AVP and 3 +/- 1% of the OT neurons in the PVN were labeled with FLI in sham-operated animals. These results indicate that neurons in the PVN and SON of the hypothalamus were activated during static muscle contraction. Furthermore, as FLI was present in AVP and OT neurons, this suggests these neurons may constitute a part of the neural pathway involved in cardiovascular regulation during static muscle contraction.

Animals↗

PubMed1998

Methyl palmoxirate increases eating behavior and brain Fos-like immunoreactivity in rats.

Administration of methyl palmoxirate (MP), an inhibitor of fatty acid oxidation, stimulates eating behavior in rats. Fos immunohistochemistry was used to determine neural pathways that may play a role in the eating response to MP. The number of cells showing Fos-like immunoreactivity (Fos-li) was quantified by computerized image analysis. MP treatment, at a dose that increased food intake (10 mg/kg, p.o.), induced Fos expression in the nucleus of the solitary tract, area postrema, lateral parabrachial nucleus, central lateral nucleus of the amygdala, dorsal lateral bed nucleus of the stria terminalis, and the paraventricular nucleus of the hypothalamus. The results suggest that MP activates an afferent pathway projecting from the hindbrain to the forebrain, which may be involved in the eating response after MP treatment.

Animals↗

PubMed1998

Herpes virus-mediated preproenkephalin gene transfer to the amygdala is antinociceptive.

To evaluate the role of the amygdala in pain modulation and opioid-mediated antinociception, a recombinant, replication-defective herpes virus carrying the human preproenkephalin cDNA was injected bilaterally into the rat amygdala. Four days after gene delivery nociceptive behavior was assessed by the formalin test. Rats infected with the virus expressing preproenkephalin showed a selective, naloxone-reversible abolition of phase 2 flinching behavior compared to rats infected with a control virus. The results implicate the amygdala in the control of pain and in opioid analgesia and demonstrate the use of recombinant herpes viruses as tools for studying gene function in specific neural pathways of the central nervous system.

Amygdala↗

PubMed1999

Fos expression in the cat brainstem after unilateral vestibular neurectomy.

Immediate early genes are generally expressed in response to sensory stimulation or deprivation and can be used for mapping brain functional activity and studying the molecular events underlying CNS plasticity. We immunohistochemically investigated Fos protein induction in the cat brainstem after unilateral vestibular neurectomy (UVN), with special reference to the vestibular nuclei (VN) and related structures. Fos-like immunoreactivity was analyzed at 2, 8, and 24 h, and 1 and 3 weeks after UVN. Data from these subgroups of cats were quantified in light microscopy and compared to those recorded in control and sham-operated animals submitted to anesthesia and anesthesia plus surgery, respectively. Results showed a very low level of Fos expression in the control and sham conditions. By contrast, Fos was consistently induced in the UVN cats. Asymmetrical labeling was found in the medial, inferior, and superior VN (ipsilateral predominance) and in the prepositus hypoglossi (PH) nuclei and the beta subnuclei of the inferior olive (betaIO) (contralateral predominance). Symmetrical staining was observed in the autonomic, tegmentum pontine, pontine gray, locus coeruleus and other reticular-related nuclei. As a rule, Fos expression peaked early (2 h) and declined progressively. However, some brainstem structures including the ipsilateral inferior VN and the bilateral pontine gray nuclei displayed a second peak of Fos expression (24 h-1 week). By comparing these data to the behavioral recovery process, we conclude that the early Fos expression likely reflects the activation of neural pathways in response to UVN whereas the delayed Fos expression might underlie long-term plastic changes involved in the recovery process.

Animals↗

PubMed1999

The caudal subnucleus caudalis (medullary dorsal horn) acts as an interneuronal relay site in craniofacial nociceptive reflex activity.

We have recently documented that bilateral increases in electromyographic (EMG) activity of digastric (DIG) and masseter (MASS) muscles can be evoked by injection into the rat's temporomandibular joint (TMJ) region of the small-fiber excitant and inflammatory irritant mustard oil and that this increased jaw muscle activity can be significantly reduced by extensive lesions of the trigeminal subnucleus caudalis (Vc). This study was carried out in 34 anaesthetized rats to test whether neurones in the caudal Vc are indeed of critical importance in these craniofacial nociceptive reflexes. The effects of micro-injection of the cellular neurotoxic chemical ibotenic acid in histologically confirmed sites of the caudal brainstem on the mustard oil-evoked EMG activity of ipsilateral and contralateral DIG and MASS were tested. Ibotenic acid micro-injection in the left caudal Vc significantly reduced the increased EMG activity of all four muscles evoked by mustard oil injection into the left TMJ region whereas mustard oil injection into the right TMJ region in these same rats still readily evoked an increase in EMG activity. In other groups of rats, ibotenic acid micro-injection into the rostral Vc, the C2 segment or the reticular formation at the obex level did not produce any significant reduction in the reflexly evoked EMG activity. These findings suggest that neurones in the caudal Vc may be critical elements in neural pathways underlying the reflex responses evoked in jaw muscles by noxious stimulation of the TMJ region.

Animals↗

PubMed1999

Modulation of vestibular function by nociceptin/orphanin FQ: an in vivo and in vitro study.

The effects of nociceptin (orphanin FQ) on medial vestibular nucleus (MVN) neurons in vitro, and on vestibulo-ocular reflex (VOR) function in vivo, were investigated in order to determine the role of 'opioid-like orphan' (ORL1) receptors in modulating vestibular reflex function in the rat. Nociceptin (100 nM-1 microM) potently inhibited the spontaneous discharge of the majority (86%) of MVN neurons tested in the rat dorsal brainstem slice preparation in vitro. This inhibition was dose-dependent and persisted after blockade of synaptic transmission in low Ca2+/Co2+ medium. The inhibitory effects were insensitive to the opioid antagonist naloxone, but were effectively antagonised by the selective ORL1 receptor antagonist, [Phe1Psi(CH2-NH)Gly2]Nociceptin(1-13)NH2. The majority of MVN neurons ( approximately 70%) were inhibited by both nociceptin and the delta-opioid receptor agonist, [D-ala2, D-leu5]-enkephalin (DADLE), while a minority of cells (approximately 30%) were selectively responsive either to DADLE or to nociceptin, but not both. Co-application of nociceptin and DADLE to neurons that were responsive to both agonists, resulted in an inhibitory response that was the same as or less than the inhibition evoked by either agonist alone. Intracellular whole-cell patch clamp recordings from identified Type A and Type B MVN cells showed that both these cell types are responsive to nociceptin, which induced membrane hyperpolarisation and decrease in input resistance consistent with its known effects on membrane K currents in other cell types. In alert rats, i.c.v. injection of nociceptin caused a significant decrease in the gain of the hVOR and resulted in a prolongation of post-rotatory nystagmus in darkness. The decrease in VOR gain and the increase in the VOR time-constant was significant even at low doses of nociceptin which did not cause other observable behavioural effects. These findings demonstrate that endogenously released nociceptin may have a hitherto unexplored role in the functional modulation of the neural pathways that mediate vestibular reflexes in vivo.

Action Potentials↗

PubMed1999

Effects of bilateral electrical stimulation of the ventral pallidum on acoustic startle.

The ventral pallidum (VP) is believed to occupy a critical position between the limbic and the motor systems, for transferring motive information into motor commands. To estimate the time course of signaling from the VP to motor outputs, in the present study we examined the effects of bilateral electrical stimulation of the VP on the acoustic startle reflex in awake rats. When the interstimulus interval (ISI) between VP stimulation and acoustic stimulation was shorter than 5 ms, VP stimulation potentiated acoustic startle. When the ISI was longer than 5 ms, VP stimulation inhibited acoustic startle over a large range of ISIs with the maximum inhibition at ISIs between 15 and 25 ms. In contrast, bilateral electrical stimulation of the amygdala did not have a significant inhibitory effect on acoustic startle, but strongly augmented acoustic startle at shorter ISIs (0-10 ms). Compared to unilateral electrical stimulation of the inferior colliculus (IC), bilateral stimulation of the VP gave rise to a rightward shift of the ISI curve, indicating that the neural pathways conveying the inhibitory influence from the VP to the acoustic startle circuit are longer than those from the IC.

Acoustic Stimulation↗