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PubMed2004

Hypothalamic neuronal histamine regulates sympathetic nerve activity and expression of uncoupling protein 1 mRNA in brown adipose tissue in rats.

To clarify how hypothalamic neuronal histamine regulates peripheral energy expenditure, we investigated the effect of infusion of histamine into the third cerebral ventricle or discrete hypothalamic regions on sympathetic nerve activity and expression of uncoupling protein 1 (UCP1) mRNA in brown adipose tissue (BAT). Infusion of histamine (200 nmol) into the third cerebral ventricle of anesthetized rats significantly increased the electrophysiological activity of sympathetic nerves (P<0.01) and UCP1 mRNA expression in the BAT (P<0.05). Microinjection of histamine (10 nmol) into the paraventricular nucleus (PVN) and preoptic area (POA) produced similar significant increases in BAT sympathetic nerve activity (P<0.01 for each). By contrast, injection of histamine into the ventromedial hypothalamic nucleus or lateral hypothalamic area had no effect. We conclude that hypothalamic neuronal histamine may regulate energy expenditure in BAT through the activation of sympathetic nerves. The PVN and/or POA appear to be the principal hypothalamic sites that mediate the stimulatory effect of histamine on this efferent pathway.

Action Potentials↗
PubMed2004

A comparison of true and premodulated interferential currents.

OBJECTIVE: To compare true and premodulated interferential currents (IFCs) in terms of sensory, motor, and pain thresholds; maximum electrically induced torque (MEIT); and comfort. DESIGN: Repeated-measures design. SETTING: Laboratory setting. PARTICIPANTS: University student and staff volunteers. INTERVENTIONS: Participants were exposed to 4 different conditions, chosen to evaluate 2 fundamental differences between true and premodulated IFCs. The conditions were different combinations of (1) premodulated or constant-amplitude currents applied at the skin and (2) crossed or parallel current paths. MAIN OUTCOME MEASURES: Sensory, motor, and pain thresholds; MEIT; and subjective reports of relative discomfort were recorded for each of the 4 conditions. Motor to sensory threshold ratios were subsequently calculated to assess depth efficiency of stimulation. RESULTS: The major findings were that crossed currents (true IFC) had no advantage over parallel currents (premodulated IFC) in terms of motor to sensory threshold ratio, MEIT, or comfort, and that premodulated currents produced higher torque values and less discomfort than constant-amplitude currents (true IFC). These results contradict the claimed superiority of true IFC. CONCLUSIONS: The findings indicate that premodulated IFC, delivered via 2 large electrodes, may be clinically more effective than the traditional true IFC arrangement in terms of depth efficiency, torque production, and patient comfort.

Adult↗
PubMed2000

Lesions of the dorsal vagal complex abolish increases in meal size induced by NMDA receptor blockade.

Rats increase meal size and duration after intraperitoneal injection of MK-801, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist. This effect depends upon intact vagal fibers, since the antagonist does not increase intake when visceral afferent and efferent pathways have been interrupted by bilateral subdiaphragmatic vagotomy. NMDA receptors have been demonstrated on vagal afferent fibers and on second-order neurons in the medial subnucleus of the solitary tract (NTS), the area postrema (AP), and the dorsal motor nucleus of the vagus. To determine whether neurons in these structures are crucial for NMDA receptor effects on feeding, we examined the effect of MK-801 on intake of 15% sucrose in rats with aspiration lesions of the AP and adjacent NTS. MK-801 (100 microg/kg, i.p.) significantly increased sucrose intake in these lesioned rats compared to sham-lesioned rats (32.3+/-0.1 ml versus 23.3+/-0.1 ml, P<0.001). However, when the AP/NTS aspiration lesions were combined with bilateral electrolytic destruction of the medial NTS and the DMV, lesioned rats consumed nearly the same amount of sucrose after either saline or MK-801 (25.9+/-2.4 ml versus 24.3+/-3. 0 ml; P=0.687). By contrast, sham-lesioned controls ingested significantly more sucrose following MK-801 compared to saline (19. 8+/-1.0 ml versus 13.1+/-0.8 ml, P<0.001). These results suggest that an intact caudomedial NTS and/or DMV are necessary for increases in intake induced by NMDA receptor blockade. While the AP might participate in MK-801-induced enhancement of intake, it is not essential for this effect.

Animals↗
PubMed2001

Cellular mRNA expression of the transcription factor NGFI-B suggests a gene regulatory role in striatal opiate-peptide neurons.

Previous studies have shown that NGFI-B mRNA is highly expressed in the adult striatum. In the present study we analyzed the anatomical distribution of NGFI-B mRNA within this brain region as well as the degree of co-existence of NGFI-B with different striatal markers in the adult brain. NGFI-B mRNA levels were found to be significantly higher within the dorsomedial portion of the striatum as compared to the ventrolateral striatum. This distribution pattern was maintained throughout the rostro--caudal axis of the striatum. Double in situ hybridization studies showed that striatal NGFI-B mRNA colocalized with a subset of preproenkephalin and prodynorphin positive spiny neurons within the dorsomedial striatum; 22--28% of all opiate-peptide positive cells co-expressed NGFI-B mRNA. NGFI-B did not colocalize with striatal aspiny interneurons expressing choline acetyl transferase mRNA or those containing the calcium-binding protein parvalbumin. The pattern of NGFI-B mRNA expression within different striatal spiny projecting neurons suggests that this transcription factor may have a direct effect on the function of different striatal efferent pathways.

Animals↗
PubMed1999

Prenatal cocaine produces signs of neurodegeneration in the lateral habenula.

The lateral habenula is a nucleus in the dorsal thalamus that innervates midbrain dopaminergic and serotonergic nuclei via projections through its major efferent pathway, the fasciculus retroflexus (FR). It was previously demonstrated that cocaine administered continuously to adult rats over several days produces neurodegeneration in the lateral habenula and FR. Because exposure to cocaine during pregnancy reportedly can cause neurobehavioral deficits, we examined whether rat fetuses exposed to continuous cocaine during the last week of gestation would similarly demonstrate selective neurodegeneration in the lateral habenula. On day 17 of gestation, dams were implanted with two silicone pellets, each containing either vehicle or one of 2 doses of cocaine (80 mg or 55 mg per pellet). Degenerating neurons containing silver deposits were counted in lateral habenula and in the striatum. Cocaine-exposed pups had significantly more silver-stained cells in the lateral habenula than vehicle-treated pups, but similar numbers of silver-stained cells were present in the striatum of all three groups. When similarly treated vehicle- and cocaine-exposed animals were tested behaviorally at 60 days of age, they did not differ on measures of open field activity, open arm avoidance on the elevated plus-maze or conditioned place preference for cocaine, although a linear trend analysis indicated some hyperactivity of the cocaine-pretreated pups during the place preference test. These results indicate that continuous cocaine exposure has selective neurotoxic effects on the habenula of the developing fetus similar to cocaine's effects in the adult.

Animals↗
PubMed1988

Memory dysfunction following unilateral transection of the fornix: a hippocampal disconnection syndrome.

This study presents a case with a discrete nondischarging lesion of the left fornix that resulted in a marked anterograde memory deficit that was defined by the same material, modality and methodologically specific features characteristic of unilateral lesions of the hippocampus. Since the fornix is the major efferent pathway of the hippocampus to the mamillary bodies, septal nuclei and anterior thalamic nuclei, this patient could be considered to have a hippocampal disconnection syndrome.

Adult↗
PubMed1998

Primary motor cortex isolation: complete paralysis with preserved primary motor cortex.

We present a left-sided hemiplegic patient with a cerebrovascular lesion involving the medial part of the right frontal and parietal lobes and the corpus callosum, but sparing the hand area of right primary motor cortex (M1). Several studies using transcranial magnetic stimulation demonstrated functional integrity of the efferent pathways from the right M1, intact sensory afferents to M1, an impairment of transcallosal connection between the bilateral motor cortices, and reduced ipsilateral cortico-cortical inhibition within the right M1. Based on these results, we conclude that the paralysis of this patient was caused by disconnection of the intact M1 from any structures requisite for initiation of movements. The present patient also suggests the importance of various afferents to M1 in voluntary movement. We propose a term of 'primary motor cortex isolation' to designate the paralysis reported here.

Electromyography↗
PubMed1998

Effect of olivocochlear bundle lesion on locomotor activity in rats.

This study was conducted to investigate the effect of olivocochlear bundle (OCB) lesion on spontaneous locomotor activity in Wistar rats. The OCB is an auditory efferent pathway which originates from the superior olivary complex in the brainstem and terminates within the cochlea. It has an inhibitory effect on the auditory end organs. In the present study, the OCB was damaged at the floor of the fourth ventricle using radiofrequency current. The rats' locomotor activities were then monitored weekly for 2 months using an automated Digiscan activity monitor system. Six behavioral variables were collected and analyzed: horizontal activity (HA), total distance (TD), movement time (MT), vertical activity (VA), stereotypy count (SC), and margin time (MGT). Significant time-dependent increases were noted for HA, TD, VA, and SC following OCB lesion. These results of increasing exploratory and stereotyped behaviors may be caused by the rat experiencing more auditory stimulation than before due to OCB dysfunction and may cause the rat to become more curious to explore its surroundings.

Animals↗
PubMed2000

Pain modulation: expectation, opioid analgesia and virtual pain.

To summarize, although there are multiple potential target nuclei for modulating pain transmission and several candidate efferent pathways that exert modulatory control, the most completely described pain modulating circuit includes the amygdala, PAG, DLPT and RVM in the brainstem. Through descending projections, this circuit controls both spinal and trigeminal dorsal horn pain transmission neurons and mediates both opioid and stimulation produced analgesia. Several different neurotransmitters are involved in the modulatory actions of this circuit, which exerts bi-directional control of pain through On cells that facilitate and Off cells that inhibit dorsal horn nociceptive neurons. There is evidence that this circuit contributes to analgesia in humans and may be activated by acute stress or the expectation of relief. Conversely, through the facilitating effect of On cells, this circuit is theoretically capable of generating or enhancing perceived pain intensity. Such an effect could provide a physiological mechanism for the pain enhancing actions of mood, attention and expectation.

Analgesics, Opioid↗
PubMed1984

Circling behaviour induced by electrical stimulation of the medial forebrain bundle, importance of stimulus parameters and dopaminergic processes.

Unilateral electrical stimulation of the substantia nigra or the ventral tegmental area produced postural asymmetry and increased locomotor activity respectively. Concurrent stimulation of the efferent pathways of these two areas (medial forebrain bundle) resulted in contraversive circling behaviour that was dependent upon the current intensity and frequency of the stimuli. The application of biphasic electrical pulses minimised the damage to the brain site stimulated; no decrease in circling intensity over time, nor spontaneous circling after administration of amphetamine or apomorphine without stimulation was observed. The contraversive circling behaviour was induced by activation of the ascending dopaminergic pathways as revealed by the close correlation between the site of stimulation and the localisation of this pathway, its antagonism by haloperidol and its abolishment by pretreatment with reserpine and alpha-methyl-p-tyrosine. Apomorphine likewise inhibited the electrical stimulation-induced circling behaviour. These results are discussed with regard to the influence of the stimulation parameters and the dopaminergic processes involved.

Animals↗
PubMed2000

Behavioral assessments of auditory sensitivity in transgenic mice.

This report summarizes positive reinforcement conditioning procedures for assessing sensory function in transgenic mice. To illustrate these behavioral methods auditory sensitivity was measured in mice lacking alpha9 acetylcholine receptor subunits (alpha9 knock-out mice). These receptors are known to play an important role in the efferent pathways that modify cochlear responses to sound stimuli. The strategies of parameter manipulation that led these subjects through their preliminary training stages to stable threshold performances are described in detail. Techniques for estimating and interpreting sensory thresholds are discussed from the perspective of signal detection analyses. This study found no significant differences between alpha9 knock-out mice and control subjects when hearing thresholds were measured under quiet conditions, as predicted by previous behavioral and electrophysiological evidence.

Acoustic Stimulation↗
PubMed1997

Blood flow increases in common carotid artery, lower lip and palate elicited by lingual nerve stimulation in anesthetized cats.

The purpose of the present study was to examine whether changes in blood flow in the common carotid artery (CCA) reflect those in individual extracranial tissues (lower lip and palate). Changes were evoked at the three sites simultaneously using a somato-parasympathetic reflex activation method in urethane-alpha-chloralose anesthetized, vago-sympathectomized cats. Somato-parasympathetic reflex activation was induced by electrical stimulation of the central cut end of the ipsilateral lingual nerve. The blood flow changes evoked in CCA, lower lip and palate changed in parallel when the stimulus to the blood vessels was changed (by changing the stimulus applied to the afferents or by blocking the efferent pathway). However, when drugs were given intravenously which would act directly on receptors in the blood vessels (including the endothelium) or alter the systemic blood pressure level, the evoked responses in CCA reacted in a quantitatively different manner from those evoked in lower lip and palate. These results suggest that evoked changes in CCA blood flow cannot be regarded as an accurate reflection of changes occurring simultaneously in individual extracranial tissues, at least when examining the effect of such drugs on parasympathetic mediated vasodilation.

Animals↗
PubMed1998

Central histaminergic neurons regulate rabbit tracheal tension through the cervical sympathetic nerve.

We previously showed that stimulation of the posterior hypothalamus decreases tracheal tension and involves central histaminergic neurons. In the present study, we reveal that central histaminergic neurons project to the rostral ventrolateral medulla and affect cervical sympathetic nervous activity in rabbits. Administration of histamine into the fourth ventricle increased cervical sympathetic nervous activity and decreased tracheal tension. These effects were inhibited by administration of a histamine H receptor antagonist, pyrilamine, into the fourth ventricle. Unilateral injection of DL-homocysteic acid into the tuberomammillary nucleus increased cervical sympathetic nervous activity, an effect was antagonized by bilateral injection of pyrilamine into the rostral ventrolateral medulla. The pulse correlogram between the stimulation pulse applied to the tuberomammillary nucleus and the cervical sympathetic nerve activity showed a mode at 150 to 200 ms, which was reduced by pyrilamine administration into the fourth ventricle. Fibers anterogradely labeled by Phaseolus vulgaris leucoagglutinin (PHA-L) injected into the tuberomammillary nucleus were distributed in the A1, A2, C1, and C2 areas which are determined by tyrosine hydroxylase-immunohistochemistry. PHA-L positive neurons were in close contact with tyrosine hydroxylase-immunoreactive neurons in these four areas. Cell bodies in the tuberomammillary nucleus retrogradely labeled with fluorogold from the rostral ventrolateral medulla were immunoreactive with histamine. These results suggest that an excitatory efferent pathway projects from the tuberomammillary nucleus to the cervical sympathetic nerve and that the histaminergic neurons of this pathway influence tracheal tension through the rostral ventrolateral medulla.

Animals↗
PubMed1997

Expression of alpha 7 neuronal nicotinic receptors during postnatal development of the rate cerebellum.

Several lines of evidence suggest that alpha-bungarotoxin-sensitive neuronal nicotinic acetylcholine receptors may play a developmental role by modulating plasticity in neuronal circuits. The alpha 7 subunit, a main component of these receptors, is expressed in most regions of the brain, including the cerebellum, where it is present almost exclusively in Purkinje cells and deep cerebellar nuclei. Purkinje cells constitute the only efferent pathway of the cerebellum and their development involves complex interactions, which have been extensively studied. They therefore provide a potentially useful model for analysis of development plasticity which could be influenced by alpha 7 neuronal nicotinic receptors. In the present study a previously characterized monoclonal antibody (mAb 307) has been used to determine the temporal pattern of expression of the alpha 7 subunit in the developing rat cerebellum. No detectable alpha 7 immunoreactivity is found between P0 and P2. Between P3 and P5, however, the Purkinje cell layer shows moderate immunolabeling. alpha 7 expression in this layer increases rapidly between P8 and P15. This increase in alpha 7 staining, which overlaps in time with important developmental and synaptogenic events, is not uniform throughout the cerebellar cortex. Thus, between P3 and P5 all Purkinje cells are weakly labeled, while at later stages (P8-P15) immunolabeling becomes more intense, but at the same time, disappears from Purkinje cells in rostral lobules. In addition, a very well defined pattern for discontinuous or columnar labeling is detected in regions of the Purkinje cell layer where alpha 7 subunits were being expressed. Finally, at P20, alpha 7 subunit labeling is found again in all Purkinje cells, although with lower intensity. These results suggest that alpha 7 receptor expression is developmentally regulated, with a time course that parallels the final differentiation of Purkinje cells. In addition, the heterogeneous spatial distribution of alpha 7-containing nicotinic receptors indicates that, during cerebellar maturation, these cells may receive different signals that modulate receptor gene expression in a very specific way.

Animals↗
PubMed2002

Propranolol blocks the tachycardia induced by galanin (1-15) but not by galanin (1-29).

The efferent pathways involved in the tachycardia induced by intracisternal injections of the N-terminal galanin fragment (1-15) (GAL (1-15)) and galanin (GAL (1-29)) has been evaluated in rats pretreated with the cholinergic antagonist atropine or the beta-antagonist propranolol. The pretreatment with propranolol significantly blocked the tachycardic and vasopressor effect produced by intracisternal injection of GAL (1-15) (p<0.05), but the pretreatment with atropine did not modify these cardiovascular effects. However, the cardiovascular response elicited by GAL (1-29) is modified by the pretreatment with atropine (p<0.05) but not by propranolol. These findings demonstrate that the central cardiovascular action of GAL (1-15), but not GAL (1-29), is mediated by beta-receptor stimulation and this suggests the existence of a different pathway involved in the cardiovascular response produced by the N-terminal galanin fragment as compared with the parent molecule GAL (1-29).

Animals↗
PubMed2001

Behavioral arrest: in search of the neural control system.

Scientists have spent hundreds of years trying to understand how the brain controls movement. Why has there been so little interest in knowing how the brain STOPS movement? This review calls attention to behavioral phenomena in which an animal or human undergoes temporary total-body arrest of movement, that is, behavioral arrest (BA). These states can be actively induced by visual stimuli, by body and limb manipulations, and by drugs. Historically, these states have been considered as unrelated, and their literature does not cross-connect. What is known about the causal mechanisms is scant, limited mostly to implication of the brainstem in manipulation-induced BA and dopaminergic blockade in the striatum in the case of drug-induced BA. The possibility has not been experimentally tested that all of these states share with each other not only an active global immobility in which awkward postures are maintained, but also underlying neural mechanisms. This review identifies key brainstem, diencephalic, and basal forebrain areas that seem to be involved in causing BA. We review the evidence that suggest a possible role in BA for the following brain structures: entopeduncular nucleus, medullary and pontine reticular zones, parabrachial region, pedunculopontine nucleus and nearby areas, substantia nigra, subthalamic nucleus, ventromedial thalamic nucleus, and zona incerta. Such areas may operate as a BA control system. Confirmation of which brain areas operate collectively in BA would require testing of several kinds of BA in the same animals with the same kinds of experimental tests. Areas and mechanisms might be elucidated through a strategic combination of the following research approaches: imaging (fMRI, c-fos), lesions (of areas, of afferent and efferent pathways), chemical microstimulation, and electrical recording (of multiple units and field potentials, with an emphasis on testing coherence among areas). We suggest the working hypothesis that BA is created and sustained by coherent, perhaps oscillatory, activity among a group of basal forebrain and brainstem areas that collectively disrupt the normal spinal and supraspinal sequencing controls of reciprocal actions on the extensors and flexors that otherwise produce movement.

Animals↗
PubMed1997

Comparable dose-dependent inhibition of AP-7 sensitive strychnine-induced allodynia and paw pinch-induced nociception by mexiletine in the rat.

The blockade of spinal glycine receptors with intrathecal (i.t.) strychnine produces segmentally-localized allodynia in the rat; a reversible and highly reproducible effect that is attained without peripheral or central nerve injury. We investigated the effect of i.v. mexiletine, an orally active congener of lidocaine, on strychnine allodynia and compared the dose-response relationship of mexiletine in normal (noxious paw pinch) versus abnormal (i.t. strychnine) nociceptive conditions. In addition, we determined the dose-response effect of i.t. AP-7 (an NMDA antagonist) on strychnine allodynia. Male, Sprague-Dawley rats, fitted with chronic i.t. catheters, were lightly anesthetized with urethane. Stimulus evoked changes in blood pressure and heart rate were recorded from the left carotid artery and cortical electroence-phalographic (EEG) activity was continuously monitored using subdermal needle electrodes. After i.t. strychnine (40 micrograms), repetitive brushing of the hair (hair deflection) evoked a progressive increase in mean arterial pressure and heart rate, an abrupt motor withdrawal response, and desynchronization of the EEG, equivalent to those elicited by the chemical nociceptive agent, mustard oil (without strychnine). Pretreatment with mexiletine (5-30 mg/kg i.v. 5 min before i.t. strychnine) dose-dependently inhibited the responses evoked by noxious hind paw pinch (no strychnine) and hair deflection (after i.t. strychnine) with equal potency (ED50's = 9.1-17 mg/kg). Below 30 mg/kg, this effect was achieved without a change in EEG synchrony (cortical activity reflecting the level of anesthesia) and without affecting motor efferent pathways. Strychnine allodynia was also significantly blocked by i.t. AP-7. The ED50's and 95% confidence intervals were 1.1 micrograms (0.7-1.8) for mean arterial pressure, 1.7 micrograms (0.5-6.0) for heart rate, and 0.4 microgram (0.07-2.0) for withdrawal duration. Cortical EEG synchrony was unchanged after i.t. AP-7 consistent with a spinal site of action. The data indicate that: (i) robust allodynia can be selectively induced with i.t. strychnine in animals whose somatosensory systems are otherwise normal; (ii) sub-anesthetic doses of i.v. mexiletine inhibit the abnormal responses to low-threshold (A-fiber) afferent input in the strychnine model of allodynia (i.e., in the absence of peripheral or central nerve injury) at doses which affect normal nociception; and (iii) in the presence of i.t. strychnine, low-threshold afferent input activates a spinal NMDA-receptor mediated process normally restricted to noxious afferent input. Systemic mexiletine may have an important spinal site of action in abnormal pain states.

2-Amino-5-phosphonovalerate↗