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PubMed2006

Dissociation of food and opiate preference by a genetic mutation in zebrafish.

Both natural rewards and addictive substances have the ability to reinforce behaviors. It has been unclear whether identical neural pathways mediate the actions of both. In addition, little is known about these behaviors and the underlying neural mechanisms in a genetically tractable vertebrate, the zebrafish Danio rerio. Using a conditioned place preference paradigm, we demonstrate that wildtype zebrafish exhibit a robust preference for food as well as the opiate drug morphine that can be blocked by the opioid receptor antagonist naloxone. Moreover, we show that the too few mutant, which disrupts a conserved zinc finger-containing gene and exhibits a reduction of selective groups of dopaminergic and serotonergic neurons in the basal diencephalon, displays normal food preference but shows no preference for morphine. Pretreatment with dopamine receptor antagonists abolishes morphine preference in the wildtype. These studies demonstrate that zebrafish display measurable preference behavior for reward and show that the preference for natural reward and addictive drug is dissociable by a single-gene mutation that alters subregions of brain monoamine neurotransmitter systems. Future genetic analysis in zebrafish shall uncover further molecular and cellular mechanisms underlying the formation and function of neural circuitry that regulate opiate and food preference behavior.

Analysis of Variance↗

PubMed1987

The aetiology of mirror writing: a new hypothesis.

Twenty-eight cases of mirror writing were seen during a period of three and a half years. These consisted of 12 patients with essential tremor, nine with Parkinson's disease, three with spino-cerebellar degeneration and four other cases. There were no cases of hemiparesis, aphasia, apraxia, agnosia or confusion. Fragmentary reversals were excluded from this study. Since essential tremor, Parkinsonian tremor and cerebellar tremor can be abolished by a stereotaxic produce applied to the thalamus, a common neural pathway via the thalamic nuclei may exist in these disorders. The existence is therefore proposed of some neural mechanism that controls the higher cerebral function of writing via the thalamus.

Dominance, Cerebral↗

PubMed1994

Anatomical identification of a postsynaptic dorsal column system in a reptile, Caiman crocodilus.

The presence of a postsynaptic dorsal column system was investigated in reptiles, Caiman crocodilus. Several experiments were undertaken. First, a cytoarchitectonic analysis of the spinal cord was performed to identify its laminar organization. Second, the termination of dorsal root fibers in the dorsal horn of the upper cervical cord, brachial enlargement, and lumbar intumescence was studied utilizing anterograde tracing techniques. Third, placement of retrograde tracers into the dorsal column nucleus identified spinal cord neurons that projected to the dorsal column nucleus. These experiments document that, in addition to direct primary dorsal root input, a second pathway exists whereby nonfacial somatosensory information can reach the dorsal column nucleus in this reptilian group. This neural path arises primarily from neurons in the ipsilateral lamina V and, to a much lesser extent, from lamina IV in the cervical area and, to a far smaller degree, from the thoracic and lumbar dorsal horn. Each of these laminae whose neurons project to the dorsal column nucleus receive direct dorsal root input. This neural circuit in Caiman is similar to a neural pathway described in pigeons and several mammalian groups. These observations suggest that a postsynaptic dorsal column system is phylogenetically ancient and may well be a feature common to all amniotes.

Afferent Pathways↗

PubMed2003

Brain surgery in motor areas: the invaluable assistance of intraoperative neurophysiological monitoring.

AIM: Surgery for tumors in the central and precentral region, as much as for insular tumors, places at risk the functional integrity of the motor cortex and the subcortical motor pathways. These procedures may therefore benefit from the assistance of intraoperative neurophysiological monitoring (INM). INM consists of "mapping" and true "monitoring" (the continuous "on-line" assessment of the functional integrity of neural pathways) techniques. In spite of the large interest in mapping techniques, monitoring techniques have received less attention. We describe our experience with intraoperative neurophysiological mapping and monitoring of motor tracts during surgery for brain gliomas in or near motor areas, in order to support the feasibility and reliability of monitoring as an essential adjunct to mapping during surgery in these areas. METHODS: Between September 2000 and January 2002, 51 patients were surgically treated for brain gliomas located in the precentral gyrus (45.1%), the postcentral gyrus (23.5%), anterior to the precentral gyrus (15.6%), or in the insula (15.6%). INM of the motor system consisted of monitoring muscle motor evoked potentials (mMEPs) recorded via needle electrodes inserted into the controlateral upper and lower extremity muscles and elicited by transcranial multipulse electrical stimulation (TES). Once the dura was open and the central sulcus was identified using the phase reversal technique, mMEPs were elicited by direct stimulation of the motor cortex (DCS). Motor mapping was performed with a monopolar electrode using the same stimulation parameters as used for monitoring except for much lower intensity (up to 20 mA). RESULTS: Ninety-eight percent of the patients exhibited recordable baseline mMEPs. The success rate of the phase reversal technique was 95.8%. Eight patients presented disappearance of mMEPs during tumor removal. Using corrective measures, all intraoperative changes in mMEPs were reversed in time to prevent an irreversible complete injury to the motor system and no patient lost mMEPs at the end of the operation. At discharge, 66% of the patients remained at their preoperative status, 4% improved, and 24% had a mild worsening as compared to the preoperative status assessed using the Medical Research Council scale; 6% of the patients presented a moderate to severe supplementary motor area syndrome. CONCLUSION: Monitoring techniques significantly implement the reliability and effectiveness of INM since these provide: 1) continuous "on-line" assessment of the functional integrity of motor pathways with higher chance to early detect a progressive mechanical or vascular injury to the neural tissue, as compared to mapping techniques; 2) lower risk to induce intraoperative seizures and strong muscular twitches as compared to the single pulse mapping technique; 3) possibility to monitor motor pathways using TES also when there is no direct access to the motor cortex.

Adult↗

PubMed1994

Effects of cocaine on sensory inhibition in rats: preliminary data.

The purpose of this study was to determine the effect of cocaine on inhibitory sensory processing mechanisms in the brain. To accomplish this aim, recording electrodes were surgically placed into the vertex region of 12 rats. After recovery from surgery, rats were injected once daily for 5 days with either cocaine (20 mg/kg, IP) or saline. Immediately and 23 hr after each injection, the rats were tested for sensory gating mechanisms. They were presented with a series of two clicking sounds, a conditioning and testing click, delivered 0.5 sec apart, and the amplitude of the N40 responses to each of these clicks was recorded. The ratios of the amplitude of the N40 response to the testing click over that of the conditioning click (T/C ratio) were calculated for each animal for each testing period. The T/C ratios of the control (Saline-injected) animals were less than one, indicating that the conditioning stimulus was able to activate inhibitory neural pathways, producing a decrease in the response to the testing stimulus. The T/C ratios of the cocaine-treated animals were significantly greater than those of controls when the tests were conducted either immediately after injection or 23 hr later. These observations suggest that cocaine can impair mechanisms involved in the gating of responses to auditory stimuli. The higher T/C ratio found at 23 hr after cocaine injection suggests that an impairment in the gating mechanism may be produced by an arousal response that is associated with the environment in which the animals had been injected with cocaine.

Acoustic Stimulation↗

PubMed1996

Glycinergic inhibition in the turtle spinal cord regulates the intensity and pattern of fictive flexion reflex motor output.

Application of strychnine sulfate (10-50 mu M) to the anterior hindlimb enlargement of the turtle spinal cord increased the amplitude of the ipsilateral fictive flexion reflex and revealed a contralateral (crossed) fictive flexion reflex response to cutaneous stimulation of the foot. Strychnine abolished the crossed inhibition of fictive flexion reflex that was normally evoked by contralateral foot stimulation, unmasking the crossed excitation. Our observations are consistent with the hypothesis that intraspinal inhibition mediated by strychnine-sensitive glycine receptors regulates the amplitude of fictive flexion reflex motor output and confines the response to the appropriate neural pathways.

Animals↗

PubMed1989

Correlations between various measures of head size and auditory brainstem response latencies.

The literature is mixed concerning the degree to which between-subject variance in the latencies of the auditory brainstem response (ABR) relates to differences in the length of the auditory pathway. Most investigations have used one of several measures of head size to indirectly index brain size and neural pathway length. While some studies have found a positive correlation between head size and the latencies of the ABR, others have reported little or no relationship. We hypothesized that the differences between studies result from differences in the head dimensions measured, the precision of measurement technique, and issues of sampling. We therefore decided to use the International 10-20 system of electrode placement to provide reproducible skull benchmarks on which to base head size measures, to obtain measures of head size via two procedures, and to control external variables that might influence the ABR. The results show that head size has a moderate positive influence on the latencies of the ABR given precise head size measures.

Adult↗

PubMed1999

Macronutrient-specific dietary selection in rodents and its neural bases.

The only evidence for nutrient selection comes from baseline or treatment effects on nutrient intakes that are qualitatively similar when sensorily contrasting forms of each macronutrient are investigated and/or dietary compositions and strains of rat or mouse are different within or between laboratories. By that criterion the only potential case of a treatment reliably altering macronutrient selection identified in the present review of the literature is d-norfenfluramine, fluoxetine and paraventricular serotonin (5-HT) reducing the intake of dextrin-containing diets at early dark. The only clear example of reverse effects of an agonist and an antagonist on dietary intake was found with serotonergic agents. Claims for catecholaminergic or opioid involvement in protein intake and peptidergic involvement in carbohydrate intake were not substantiated. There remain the issues of which learnt macronutrient-specific postgastric actions and sensory cues from the affected diet rely on the neural pathway(s) on which the drug is acting to alter dietary selection. Until experiments address these questions, the neural bases of nutrient-specific appetites will remain unknown. Drug effects must be consistent across differently textured and flavoured versions of each macronutrient tested.

Animals↗

PubMedDate not supplied

Color shifts induced by S-cone patterns are mediated by a neural representation driven by multiple cone types.

This study investigated chromatic induction from inhomogeneous background patterns. Previous work showed that a background pattern detected by only S cones induced strong color shifts in a nearby test area (Monnier & Shevell, 2003). In that work, the S-cone patterns were composed with constant L- and M-cone stimulation over the entire background; in terms of L and M cones, therefore, the background was uniform. S-cone stimulation was varied over space to produce S-cone-isolated background patterns. These S-cone patterns, however, established spatial structure (the pattern) at both the receptoral level (S-cone stimulation) and the postreceptoral level (S/(L+M)). Here, these two levels of pattern representation were unconfounded to determine whether color shifts induced by S-cone patterns were due to spatial structure within an S-cone-specific neural pathway versus a pathway that combines responses from S cones and other cone types (e.g. S/(L+M)). The results showed that the induced color shifts were mediated by signals within a pathway that combines responses from multiple cone types. These results are consistent with a +s/-s spatially antagonistic neural receptive field, which is found in some neurons in V1 and V2.

Color↗

PubMed2006

Metabolic sensing neurons and the control of energy homeostasis.

The brain and periphery carry on a constant conversation; the periphery informs the brain about its metabolic needs and the brain provides for these needs through its control of somatomotor, autonomic and neurohumoral pathways involved in energy intake, expenditure and storage. Metabolic sensing neurons are the integrators of a variety of metabolic, humoral and neural inputs from the periphery. Such neurons, originally called "glucosensing", also respond to fatty acids, hormones and metabolites from the periphery. They are integrated within neural pathways involved in the regulation of energy homeostasis. Unlike most neurons, they utilize glucose and other metabolites as signaling molecules to regulate their membrane potential and firing rate. For glucosensing neurons, glucokinase acts as the rate-limiting step in glucosensing while the pathways that mediate responses to metabolites like lactate, ketone bodies and fatty acids are less well characterized. Many metabolic sensing neurons also respond to insulin and leptin and other peripheral hormones and receive neural inputs from peripheral organs. Each set of afferent signals arrives with different temporal profiles and by different routes and these inputs are summated at the level of the membrane potential to produce a given neural firing pattern. In some obese individuals, the relative sensitivity of metabolic sensing neurons to various peripheral inputs is genetically reduced. This may provide one mechanism underlying their propensity to become obese when exposed to diets high in fat and caloric density. Thus, metabolic sensing neurons may provide a potential therapeutic target for the treatment of obesity.

Animals↗

PubMed2001

Enhancement of short-term synaptic plasticity by prior environmental stress.

All chemical synapses can rapidly up- or downregulate the strength of their connections to reshape the postsynaptic signal, thereby stressing the informational importance of specific neural pathways. It is also true that an organism's environment can exert a powerful influence on all aspects of neural circuitry. We investigated the effect of a prior high-temperature stress on the short-term plasticity of a neuromuscular synapse in the hindleg tibial extensor muscle of Locusta migratoria. We found that the prior stress acted to precondition the synapse by increasing the upper temperature limit for synaptic transmission during a subsequent stressful exposure. As well, preexposure to a stressful high-temperature environment increased short-term facilitation of excitatory junction potentials concurrent with a decrease in excitatory junction potential amplitude and a reduction in its temporal parameters. We conclude that a stressful environment can modify synaptic physiological properties resulting in an enhancement of short-term plasticity of the synapse.

Analysis of Variance↗

PubMed2004

Long-latency reflexes in patients with Behçet's disease.

OBJECTIVE: Recent studies demonstrate that the subclinical involvement of motor pathways is frequently observed in patients with Behçet's disease (BD). Long-latency reflexes (LLR) provide information about the continuity of both ascending and descending neural pathways. Our aim was to evaluate the utility of LLR and somatosensory-evoked potentials (SEP) in demonstrating subclinical neural involvement in patients with BD. METHODS: Twenty-nine patients with BD were studied by means of SEP and LLR. Bilateral median nerve SEPs and LLRs evoked by electrical stimulation of both median nerves were recorded. The latency of second component of LLR (LLR2), the duration of LLR2-HR (Hoffmann reflex, spinal reflex component of LLR) interval, peak to peak amplitude of LLR2 and the amplitude ratio of LLR2/HR were analyzed. The data obtained from patients were compared with those of 20 control subjects. RESULTS: LLR2 latencies and the durations of LLR2-HR interval were significantly prolonged in patients with BD (p=0.001 for both parameters). Increased duration of LLR2-HR interval was the most frequent abnormality observed in the study (37.9%). CONCLUSION: Our findings suggest that LLR is a useful technique to demonstrate subclinical neural involvement in patients with BD.

Adult↗

PubMed1990

Disorders of gastrointestinal motility in neurologic diseases.

Neurologic diseases can affect the bowel at several levels of innervation--by altering the electrical activity that controls smooth muscle, the enteric nervous system, or the extrinsic neural pathways to the gut. This review concentrates on disorders of motility that occur in conjunction with diseases of the extrinsic neural supply (from the level of the brain to the postganglionic fibers) and those generalized disorders that affect gut smooth muscle. Modern technology, such as gastrointestinal scintigraphy and manometric techniques that measure esophageal, gastroduodenal, and anorectal motility (intraluminal pressures), has provided better methods to study the pathophysiologic aspects of gut motility in diseases of the nervous system. Distinguishing the neuropathies of the extrinsic nervous system from those of the intrinsic (enteric) nervous system is not always possible because the available techniques evaluate only the end-organ--that is, the motor function of the gut. Degenerative or infiltrative (myopathic) disorders of gut smooth muscle, however, can be distinguished from such neuropathies, and careful and systematic evaluation of autonomic function can often identify the level of disordered function in the neural-gut axis.

Autonomic Nervous System Diseases↗

PubMed1998

Human Wnt-13 is developmentally regulated during the differentiation of NTERA-2 pluripotent human embryonal carcinoma cells.

The Wnt gene family encodes a series of conserved glycoproteins that regulate pattern formation during embryogenesis, in a variety of tissues including the nervous system. As with other genes that control embryonic cell differentiation, members of the Wnt family have also been implicated in tumourigenesis. To search for Wnt genes involved in human teratocarcinomas, with a possible role in human embryogenesis, we used RT-PCR primed with degenerate oligonucleotides to analyse mRNA from differentiating cultures of the pluripotent human embryonal carcinoma (EC) cell line NTERA-2. NTERA-2 EC cells differentiate into neurons and other cell types when induced with retinoic acid. Wnt gene expression was not detected in the undifferentiated EC cells, but Wnt-related PCR fragments were amplified from differentiating cultures, 4-14 days after induction with retinoic acid. The RT-PCR products were composed primarily of DNA fragments corresponding to the recently identified human Wnt-13 gene. No other Wnt-related genes were identified. Northern analysis confirmed induction of Wnt-13 as a 2.4 kb mRNA during the early phases of retinoic acid-induced differentiation, and during differentiation along a non-neural pathway induced by hexamethylene bisacetamide (HMBA), but not in the terminally differentiated neurons. Wnt-13 remained expressed in non-neural differentiated NTERA-2 cells, even several weeks after the induction of differentiation. The time course of induction, its induction by HMBA, and its persistence in differentiated cells indicate that Wnt-13 expression is not dependent upon direct activation by retinoic acid. Wnt-13 was not detected, or only detected at low levels, in other human EC cells. However, it was found to be expressed at a high level in one malignant teratoma cell line, 577MF, that does not exhibit an EC phenotype although it was derived from a testicular teratocarcinoma. At least two members of the human frizzled gene family, thought to encode receptors for Wnt proteins, were also expressed in the NTERA-2 cells, suggesting the presence of a mechanism by which endogenously expressed Wnt-13 could modulate the histogenesis of teratocarcinomas by mediating interactions between sub-populations of differentiating EC cells. We note that Wnt-13 maps to chromosome 1p13, a region reported to be subject to relatively frequent loss of heterozygosity in germ cell tumours. Further analysis indicated that 465 bp of the published Wnt-13 sequence, within the predicted 5' UTR, is incorrect and is possibly derived from a human mitochondrial DNA sequence.

Acetamides↗

PubMed1990

Acute cerebral hemorrhage changes the nocturnal surge of plasma melatonin in humans.

The diurnal rhythm of plasma melatonin was studied in 46 Chinese patients with acute cerebral hemorrhage. The state of consciousness of each patient was assessed clinically. The individual sites of lesion were determined by computerized tomography scanning. One to five days after stroke, blood samples were collected by venipuncture at 1000 and 1400 h in the daytime and 0200 and 0400 h at night. Plasma melatonin was extracted by dichloromethane and determined by radioimmunoassay. It was found that patients with lesions in the brain stem or in the third and lateral ventricles had melatonin levels significantly different from the other subjects in that these values were lower and lacking a nocturnal rise. These results are consistent with the presumptive retina-pineal pathway proposed in humans. Dramatic blunting or obliteration of the nocturnal melatonin surge in the blood was also observed in some patients with lesions in the frontal lobe, fronto-parietal lobe, parieto-temporal lobe, and basal ganglia. These brain regions are not involved in the retina-pineal pathway described in rodents or humans. Thus, our results suggest that brain regions other than the presumptive retina-pineal neural pathway may play an important role in the generation and/or regulation of the diurnal production and/or secretion of pineal melatonin in humans. However, a global functional disturbance caused by cerebral hemorrhage cannot be ruled out in some cases. It should be noted that many of the lesions leading to a change in the nocturnal rise of plasma melatonin were unilateral lesions. The significance of this finding is presently unknown. In addition, patients without a nocturnal rise of plasma melatonin were mostly comatose. They had lesions in the basal ganglion, fronto-parietal lobe, brain stem, and lateral and third ventricles. The latter findings suggest that in the brain, certain regions responsible for the state of consciousness of the individual may also be important to the dirunal rhythm of pineal melatonin secretion.

Acute Disease↗

PubMed1999

Molecular mechanisms of neural crest formation.

The neural crest is a transient population of multipotent precursor cells named for its site of origin at the crest of the closing neural folds in vertebrate embryos. Following neural tube closure, these cells become migratory and populate diverse regions throughout the embryo where they give rise to most of the neurons and support cells of the peripheral nervous system (PNS), pigment cells, smooth muscle, craniofacial cartilage, and bone. Because of its remarkable ability to generate such diverse derivatives, the neural crest has fascinated developmental biologists for over one hundred years. A great deal has been learned about the migratory pathways neural crest cells follow and the signals that may trigger their differentiation, but until recently comparatively little was known about earlier steps in neural crest development. In the past few years progress has been made in understanding these earlier events, including how the precursors of these multipotent cells are specified in the early embryo and the mechanisms by which they become migratory. In this review, we first examine the mechanisms underlying neural crest induction, paying particular attention to a number of growth factor and transcription factor families that have been implicated in this process. We also discuss when and how the fate of neural crest precursors may diverge from those of nearby neural and epidermal populations. Finally, we review recent advances in our understanding of how neural crest cells become migratory and address the process of neural crest diversification.

Animals↗

PubMed2003

The hypothalamic paraventricular nucleus and carotid receptors modulate hyperglycemia induced by hemorrhage.

The aim of this study was to assess the role of cholinergic transmission in the paraventricular nucleus of the hypothalamus (PVN) and carotid body receptors in mediating a rise in plasma glucose levels in response to hemorrhagic hypotension in rats. Methylatropine (1x10(-9) mol) or 0.15 M NaCl (0.2 microl) was injected into the PVN of Wistar rats weighing 250-300 g bearing a chronic jugular catheter for blood sampling and hemorrhage (1.2 ml/100 g/2 min). Polyethylene cannulae (PE-10) were inserted into the left femoral artery for cardiovascular monitoring. In the other experimental protocol, hemorrhage was performed on rats submitted to bilateral carotid receptor denervation (H-CD). The results show that the hyperglycemic response to hemorrhage was decreased by either methylatropine (H-MA) treatment or bilateral carotid receptor denervation (10.3+/-0.4 mM, control, n=15 vs. 7.7+/-0.2 mM, H-MA, n=12, and 7.6+/-0.3 mM, H-CD, n=5, p<0.01). Furthermore, methylatropine did not affect the recovery of blood pressure after hemorrhage-induced hypotension, suggesting that the metabolic and pressor adjustments have different efferent pathways. Our data demonstrate that cholinergic input from the PVN and carotid receptors (chemo- and/or baroreceptors) might participate in the same neural pathway activated by hemorrhage-induced hypotension that produces hyperglycemia.

Animals↗

PubMed1995

Effects of sodium metabisulphite on guinea pig contractile airway smooth muscle responses in vitro.

BACKGROUND: Sodium metabisulphite (MBS) is known to induce bronchoconstriction in asthmatic patients. The effects of MBS on guinea pig airway smooth muscle and on neurally mediated contraction in vitro have been examined. METHODS: Tracheal and bronchial airway segments were placed in oxygenated buffer solution and electrical field stimulation was performed in the presence of indomethacin (10(-5) M) and propranolol (10(-6) M) for the measurement of isometric tension. Atropine (10(-6) M) was added to bronchial tissues. RESULTS: Concentrations of MBS up to 10(-3) M had no direct effect on airway smooth muscle contraction and did not alter either tracheal smooth muscle contraction induced by electrical field stimulation at all frequencies or acetylcholine-induced tracheal smooth muscle contraction. There was a similar response in the absence of epithelium, except for potentiation of the response induced by electrical field stimulation at 0.5 Hz (24 (10)% increase). However, MBS (10(-5), 10(-6) and 10(-7) M) augmented neurally-mediated non-adrenergic non-cholinergic contractile responses in the bronchi (13.3 (3.2)%, 23.8 (9.6)%, and 6.4 (1.6)%, respectively). MBS had no effect on the contractile response induced by substance P, but at higher concentrations (10(-3) M and 10(-4) M) it caused a time-dependent attenuation of responses induced by either electrical field stimulation or exogenously applied acetylcholine or substance P. CONCLUSIONS: MBS had no direct contractile responses but enhanced bronchoconstriction induced by activation of non-cholinergic neural pathways in the bronchus, probably through increased release of neuropeptides. At high concentrations MBS inhibited contractile responses initiated by receptor or neural stimulation.

Acetylcholine↗