The effect of naloxone on trigemino-hypoglossal reflex inhibited by periaqueductal central gray stimulation in rats.
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The aim of the study was to determine whether opioid receptor antagonist naloxone abolishes the influence of periaqueductal central gray (PAG) on nociceptive evoked tongue jerks (ETJ) - a trigemino-hypoglossal reflex induced by tooth pulp stimulation. In rats under chloralose anesthesia three subsequent series of perfusions of lateral ventricles - cerebellomedullary cistern with Mc Ilwain-Rodnight's solution, Met-enkaphalin (Enk-Met) and naloxone were carried out. The amplitudes of tongue jerks induced by tooth pulp stimulation were recorded during subsequent 10 min perfusions. Mean amplitude of tongue movements induced by tooth pulp stimulation was regarded as the indicator of the magnitude of trigemino-hypoglossal reflex. We observed that perfusion of the cerebral ventricles with Enk-Met (100 nmol/mL) inhibited the trigemino-hypoglossal reflex by 46%, whereas naloxone (100 nmol/mL), added to the solution perfusing the cerebral ventricles system, increased the reflex by 42%. The amplitude of ETJ was significantly reduced during PAG stimulation with a train of electrical impulses. After obtaining a significant 93% - inhibition of ETJ, naloxone (100 nmol/mL) was added to the perfusion fluid. This led to a significant increase of the reflex by 68%. The above results suggest that the inhibition of ETJ due to PAG stimulation is partially reversed by naloxone and mediated via interactions with endogenous opioid systems involved in modulation of nociception. (+info)
Reduction of pentylenetetrazole-induced seizure activity in awake rats by seizure-triggered trigeminal nerve stimulation.
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Stimulation of the vagus nerve has become an effective method for desynchronizing the highly coherent neural activity typically associated with epileptic seizures. This technique has been used in several animal models of seizures as well as in humans suffering from epilepsy. However, application of this technique has been limited to unilateral stimulation of the vagus nerve, typically delivered according to a fixed duty cycle, independently of whether ongoing seizure activity is present. Here, we report that stimulation of another cranial nerve, the trigeminal nerve, can also cause cortical and thalamic desynchronization, resulting in a reduction of seizure activity in awake rats. Furthermore, we demonstrate that providing this stimulation only when seizure activity begins results in more effective and safer seizure reduction per second of stimulation than with previous methods. Seizure activity induced by intraperitoneal injection of pentylenetetrazole was recorded from microwire electrodes in the thalamus and cortex of awake rats while the infraorbital branch of the trigeminal nerve was stimulated via a chronically implanted nerve cuff electrode. Continuous unilateral stimulation of the trigeminal nerve reduced electrographic seizure activity by up to 78%, and bilateral trigeminal stimulation was even more effective. Using a device that automatically detects seizure activity in real time on the basis of multichannel field potential signals, we demonstrated that seizure-triggered stimulation was more effective than the stimulation protocol involving a fixed duty cycle, in terms of the percent seizure reduction per second of stimulation. In contrast to vagus nerve stimulation studies, no substantial cardiovascular side effects were observed by unilateral or bilateral stimulation of the trigeminal nerve. These findings suggest that trigeminal nerve stimulation is safe in awake rats and should be evaluated as a therapy for human seizures. Furthermore, the results demonstrate that seizure-triggered trigeminal nerve stimulation is technically feasible and could be further developed, in conjunction with real-time seizure-predicting paradigms, to prevent seizures and reduce exposure to nerve stimulation. (+info)
Pathways for the response of the eye to injury.
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The role of a neural pathway in the disruption of the blood-aqueous barrier of the rabbit after two irritating stimuli, topical nitrogen mustard, and paracentesis, was studied. Retrobulbar anesthesia or section of the ophthalmic division of the trigeminal nerve decreased the breakdown of the blood-aqueous barrier, as measured by protein in the aqueous humor, after topical nitrogen mustard. Sensory denervation, accomplished with retrobulbar alcohol, virtually prevented the protein rise in the aqueous humor. Disruption of the blood-aqueous barrier after paracentesis, however, was not affected by retrobulbar anesthesia or alcohol denervation. Therefore, the increased protein in the aqueous humor after an irritative stimulus appears to be mediated by at least two pathways. The response to a stimulus such as nitrogen mustard depends on sensory innervation and is not mediated by prostaglandins to any important degree. The response to paracentesis does not require sensory innervation and appears to be mediated, at least in part, by prostaglandins. (+info)
Fos expression in the midbrain periaqueductal grey after trigeminovascular stimulation.
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There is an accumulating body of evidence suggesting that the periaqueductal grey (PAG) is involved in the pathophysiology of migraine. Positron emission tomography (PET) studies in humans have shown that the caudal ventrolateral midbrain, encompassing the ventrolateral PAG, has activations during migraine attacks. The PAG may well be involved not only through the descending modulation of nociceptive afferent information, but also by its ascending projections to the pain processing centres of the thalamus. In this study the intranuclear oncogene protein Fos was used to mark cell activation in the PAG following stimulation of the trigeminally-innervated superior sagittal sinus (SSS) in both cats and in nonhuman primates (Macaca nemestrina). Fos expression in the PAG increased following stimulation to a median of 242 cells (interquartile range 236-272) in the cat and 155 cells (range 104-203) in the monkey, compared with control levels of 35 cells (21-50) and 26 cells (18-33), respectively. Activation was predominantly in the ventrolateral area of the caudal PAG suggesting that the PAG is involved following trigeminally-evoked craniovascular pain. (+info)
Excitability of the human trigeminal motoneuronal pool and interactions with other brainstem reflex pathways.
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We studied the properties of motoneurones and Ia-motoneuronal connections in the human trigeminal system, and their functional interactions with other brainstem reflex pathways mediated by non-muscular (Abeta) afferents. With surface EMG recordings we tested the recovery cycles of the heteronymous H-reflex in the temporalis muscle and the homonymous silent period in the masseter muscle both elicited by stimulation of the masseteric nerve at the infratemporal fossa in nine healthy subjects. In four subjects single motor-unit responses were recorded from the temporalis muscle. In six subjects we also tested the effect of the stimulus to the mental nerve on the temporalis H-reflex and, conversely, the effect of Ia input (stimulus to the masseteric nerve) on the R1 component of the blink reflex in the orbicularis oculi muscle. The recovery cycle of the H-reflex showed a suppression peaking at the 5-20 ms interval; conversely the time course of the masseteric silent period was facilitated at comparable intervals. The inhibition of the test H-reflex was inversely related to the level of background voluntary contraction. Single motor units were unable to fire consistently in response to the test stimulus at intervals shorter than 50 ms. Mental nerve stimulation strongly depressed the H-reflex. The time course of this inhibition coincided with the EMG inhibition elicited by mental nerve stimulation during voluntary contraction. The trigeminal Ia input facilitated the R1 component of the blink reflex when the supraorbital test stimulation preceded the masseteric conditioning stimulation by 2 ms. We conclude that the time course of the recovery cycle of the heteronymous H-reflex in the temporalis muscle reflects the after-hyperpolarization potential (AHP) of trigeminal motoneurones, and that the Ia trigeminal input is integrated with other brainstem reflexes. (+info)
Malignant schwannoma of the trigeminal nerve.
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SUMMARY: We present the MR imaging, CT, and clinical findings of a patient with malignant schwannoma of the trigeminal nerve. Local tumor recurrence is frequent and may be mistaken for lymphatic spread. In this report, we emphasize the natural history of this rare tumor and discuss the importance of imaging in diagnosis and surveillance. (+info)
Neonatal deafferentation does not alter membrane properties of trigeminal nucleus principalis neurons.
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In the brain stem trigeminal complex of rats and mice, presynaptic afferent arbors and postsynaptic target cells form discrete modules ("barrelettes"), the arrangement of which duplicates the patterned distribution of whiskers and sinus hairs on the ipsilateral snout. Within the barrelette region of the nucleus principalis of the trigeminal nerve (PrV), neurons participating in barrelettes and those with dendritic spans covering multiple barrelettes (interbarrelette neurons) can be identified by their morphological and electrophysiological characteristics as early as postnatal day 1. Barrelette cells have focal dendritic processes, are characterized by a transient K(+) conductance (I(A)), whereas interbarrelette cells with larger soma and extensive dendritic fields characteristically exhibit low-threshold T-type Ca(2+) spikes (LTS). In this study, we surveyed membrane properties of barrelette and interbarrelette neurons during and after consolidation of barrelettes in the PrV and effects of peripheral deafferentation on these properties. During postnatal development (PND1-13), there were no changes in the resting potential, composition of active conductances and Na(+) spikes of both barrelette and interbarrelette cells. The only notable changes were a decline in input resistance and a slight increase in the amplitude of LTS. The infraorbital (IO) branch of the trigeminal nerve provides the sole afferent input source to the whisker pad. IO nerve transection at birth abolishes barrelette formation as well as whisker-related neuronal patterns all the way to the neocortex. Surprisingly this procedure had no effect on membrane properties of PrV neurons. The results of the present study demonstrate that distinct membrane properties of barrelette and interbarrelette cells are maintained even in the absence of input from the whiskers during the critical period of pattern formation. (+info)
Tonabersat (SB-220453) a novel benzopyran with anticonvulsant properties attenuates trigeminal nerve-induced neurovascular reflexes.
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1. The effects of tonabersat (SB-220453) were evaluated on trigeminal nerve ganglion stimulation-induced sensory-autonomic neurovascular reflexes in the anaesthetized cat. Comparisons were made to intravenous administration of carabersat (SB-204269), and to valproate, gabapentin and lamotrigine following intraduodenal administration. 2. There were no effects on resting blood pressure, heart rate, carotid blood flow or carotid vascular resistance for any compound evaluated. 3. Trigeminal nerve ganglion stimulation increased carotid blood flow by 65% and reduced vascular resistance by 41% with minimal effect on blood pressure (< 10%) and no effect on heart rate. Intravenous infusion of tonabersat or carabersat (both 3.4 micromol h(-1)) produced time related reductions in stimulation-induced responses with a maximal inhibition (relative to control) of 30 +/- 7% (n=4), at 240 min for tonabersat and 33+/-4% (n=3) at 180 min for carabersat. Tonabersat (11.5 micromol h(-1)) produced a similar inhibitory effect (32 +/- 9%, n=4) after 120 min of infusion. 4. Following intraduodenal administration of tonabersat, the maximal inhibition of nerve stimulation-induced responses was 55 +/- 4% at 120 min (n=4) for tonabersat 10 mg kg(-1), and 24+/-2% after 180 min for 1 mg kg(-1) (n=4). 5. Intraduodenal administration of sodium valproate (10 or 100 mg kg(-1) n=4/group) had no effect on neurovascular reflexes. Maximal inhibition of nerve ganglion-stimulated reductions in carotid vascular resistance were observed at 150 min for lamotrigine (50 mg kg(-1), 52+/-12%, n=4) and gabapentin (100 mg kg(-1), 17+/-13%, n=3). Lamotrigine 10 mg kg(-1) produced 22+/-11% (n=3) inhibition after 180 min. 6. These data demonstrate blockade of trigeminal parasympathetic reflexes with tonabersat, carabersat and other anticonvulsants. These agents may therefore have therapeutic benefit in conditions where this type of reflex is evident. (+info)