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At least 721 records · Page 40Linked to original sources

PubMed2000

Spinal repair in immature animals: a novel approach using the South American opossum Monodelphis domestica.

1. The adult mammalian central nervous system (CNS) is unable to regenerate following injury and repair has only been seen when implants of peripheral nervous tissue, fetal tissue or Schwann cells are used, or antibodies or trophic molecules applied. However, the immature mammalian CNS has revealed a capacity to repair without extrinsic influence. 2. The marsupial mammal provides a unique opportunity to access the immature CNS without invasive in utero surgery. In particular, the South American opossum Monodelphis domestica is an ideal animal for spinal cord injury studies examining the ability of the immature CNS to repair after injury. 3. The Monodelphis spinal cord may be examined for its response to injury either as an in vitro or in vivo system and, therefore, is a flexible model, allowing many different questions to be addressed by the most suitable approach. 4. The immature Monodelphis CNS was able to support fibre growth that reappeared 4 days after a crush at P3-P8 in vitro. Conduction was also restored at this time, accompanied by synaptic connections. 5. A cut lesion performed in vivo on Monodelphis spinal cords at P7 took longer to repair, with fibres reappearing across the injury site 2 weeks after the lesion; greater disruption to structure was noted both during early stages of repair and in adulthood. 6. Neural pathway tracing with dextran amine from the lumbar cord to the brain in adult Monodelphis, which received spinal lesions at P7, revealed a similar distribution of labelled cells in brainstem and mid-brain nuclei to that of control animals. 7. Studies of the locomotor behaviour of adult Monodelphis that had received either a cut or crush lesion at P7-P8 showed remarkably similar abilities to control animals when performing complex tasks. 8. The results of spinal cord injury studies with the immature Monodelphis CNS may help in the development of treatments for spinal injury patients.

Animals↗

PubMed1981

The luteinizing hormone releasing hormone-containing pathways and their co-termination with tanycyte processes in and around the median eminence and in the pituitary stalk of the rat.

The origin, course and termination of two luteinizing hormone releasing hormone (LH-RH)-containing pathways were studied in the brain of rats by immunohistochemistry. In addition, the joint termination of LH-RH-containing nerve terminals and tanycyte processes over a rostro-caudally elongated belt surrounding the median eminence (ME) is described. The preoptico-infundibular tract originates from neurons confined to a pyramid-shaped area between the anterior commissure, the organum vasculosum laminae terminalis (OVLT) and the most caudal level of the suprachiasmatic nucleus (SCH). The axons of these neurons form three fascicles. Fibres of the median fascicle run in caudal direction on the dorsal and ventral surfaces of the optic chiasma. Fibres of the medial fascicle run along the lateral border of the SCH towards the retrochiasmatic area. Fibres of the lateral fascicle course laterally in close contact with the concave dorsomedial surface of the optic tract. These latter fibres gradually turn in medial direction and reach the lateral margin of the ME. The caudal LH-RH fibre tract was characterized only partially because the perikarya giving rise to these fibres were not identified. The fibres run rostrally among the ependymal cells of the mesencephalic aqueduct and form two fascicles. The fibres of the mammillary fascicle enter, and seem to terminate, in the medial mammillary nucleus, while the fibres of the tuberal fascicle course rostrally and join the fibres of the preoptico-infundibular tract. The surface areas of the brain along which LH-RH fibres terminate (retrochiasmatic area, inframammillary region, lateral margin of the ME) were found to display a special surface covering formed by tanycyte processes. The course of LH-RH fibre tracts described here is in good agreement with earlier experimental results on the localization of neural pathways controlling ovulation and the secretion of pituitary gonadotropic hormones. The significance of the joint termination of LH-RH fibres and tanycyte processes, especially in areas where portal capillaries are absent, remains unclear.

Animals↗

PubMed1985

Subcortical functions in language: a working model.

The current paper explains a model of subcortical language functions that focuses on dynamic interactions between the cortex, the thalamus, and the basal ganglia in the production of spoken language. The model was derived from (a) studies of subcortical lesions and language, (b) studies of subcortical stimulation and language, (c) knowledge regarding neural pathways between various cortical and subcortical structures, and (d) indications that preverbal monitoring of language occurs. In the current model, the thalamus plays roles in cortical arousal and activation and in preverbal semantic monitoring. The basal ganglia function to regulate the degree of excitation conveyed from the thalamus to the cortex and to time the release of formulated language for motor programming. Consistency with classical syndromes of aphasia and potential applications to other areas in the neurosciences are discussed. The current theory, unlike previous formulations, is specific enough that testable hypotheses can be derived.

Aphasia↗

PubMed2002

The molecular turn in psychiatry: a philosophical analysis.

Biological psychiatry has been dominated by a psychopharmacologically-driven neurotransmitter dysfunction paradigm. The objective of this paper is to explore a reductionist assumption underlying this paradigm, and to suggest an improvement on it. The methods used are conceptual analysis with a comparative approach, particularly using illustrations from the history of both biological psychiatry and molecular biology. The results are that complete reduction to physicochemical explanations is not fruitful, at least in the initial stages of research in the medical and life sciences, and that an appropriate (non-reducible) integrative principle--addressing a property of the whole system under study--is required for each domain of research. This is illustrated in Pauling's use of a topological integrative principle for the discovery of the functioning of proteins and in Watson and Crick's use of the notion of a genetic code as an integrative principle for the discovery of the structure of genes. The neurotransmitter dysfunction paradigm addresses single molecules and their neural pathways, yet their interactions within the CNS as a whole seem most pertinent to mental disorders such as schizophrenia. The lack within biological psychiatry of an integrative principle addressing a property of the CNS as a whole may be responsible for the empirical failure of orthomolecular psychiatry, as well as for the central role that serendipity has played in the study of mental disorders, which is dominated by the neurotransmitter paradigm. The conclusion is that research in biological psychiatry may benefit from using, at least initially, some integrative principle(s) addressing a property of the CNS as a whole, such as connectionism or a hierarchical notion.

Biological Psychiatry↗

PubMed2006

Toxic effects on gustatory function.

A large number of substances and disease processes may impact the sense of taste. Toxic substances may cause taste dysfunction from their effects on the gustatory system from the salivary gland, to the taste bud, to the central neural pathways. A number of external toxins, including industrial compounds, tobacco, and alcohol, may adversely affect taste, most commonly through local effects in the oral cavity. Blood-borne toxins, such as medications and those present in autoimmune and other systemic disorders (e.g. renal or liver failure), have access to all parts of the gustatory system, and thus may exhibit varied effects on taste function. An understanding of these potential toxins and their impact on gustation will help physicians better recognize, and potentially limit the impact of such taste alterations on their patients.

Diabetes Complications↗

PubMed1987

Some central neural mechanisms governing resting and behaviorally coupled control of blood pressure.

Systems in the brain control blood pressure by maintaining life-sustaining, resting (tonic) levels and adjusting blood pressure in association with changes in regional blood flow appropriately coupled to behavior or environmental stimulation. Tonic levels of blood pressure are mediated by neurons in the medulla oblongata. The critical neurons appear to correspond to the epinephrine-containing cells of the so-called C1 group located in the rostral ventral lateral medulla. These also mediate baroreceptor reflex responses. Behaviorally coupled changes in blood pressure are often highly stereotyped and vary depending on the behavior being performed in both animals and humans. These reactive circulatory adjustments are largely mediated by forebrain regions working in concert with the medullary centers. Some of the largest increases in blood pressure occur in response to aversive emotional arousal. In hypertensive animals and humans, such changes, which are normally buffered by reflex mechanisms in the brainstem, are exaggerated. In the rat, the neural pathway mediating the coupling, through aversive emotional conditioning, of blood pressure responses to acoustic stimuli involves the transmission of sensory signals through the primary auditory projection system to the medial geniculate body, where the input is then relayed subcortically to the amygdala. The amygdala, presumably by way of connections with the hypothalamus, and from there to the brainstem or spinal cord, controls the learned emotional response. These findings, which implicate a largely unrecognized sensory relay to the amygdala in emotional learning, represent the first demonstration of a direct link between primary sensory system and autonomic control regions in the mammalian brain.

Animals↗

PubMed1993

Processing of photic information within the intergeniculate leaflet of the lateral geniculate body: assessed by neuropeptide Y immunoreactivity in the suprachiasmatic nucleus of rats.

Entrainment of the circadian pacemaker in the suprachiasmatic nucleus is accomplished by two neural pathways, the retinohypothalamic and geniculohypothalamic tracts. The geniculohypothalamic tract, which originates from the intergeniculate leaflet and a portion of the ventral lateral geniculate nucleus, is composed of fibers immunoreactive to neuropeptide Y. To assess the processing of photic information by the geniculohypothalamic tract, neuropeptide Y immunoreactivity in the suprachiasmatic nucleus of rats kept under various external lighting conditions was determined by enzyme immunoassay of micropunched tissues. Neuropeptide Y levels in the suprachiasmatic nucleus steadily increased when rats were exposed to continuous light and reached a peak in 2 h before returning to basal level. The amount of increase did not depend on intensity and duration of light exposure. A light pulse as short as 5 min elicited a similar rise in neuropeptide Y, indicating that the response is due to the sudden transition from dark to light. This response, however, was only observed when the dark to light transition occurred at circadian time 0 (subjective dawn) of the pacemaker. A light pulse at circadian time 0, which effectively induces the increase in neuropeptide Y level, does not significantly shift the phase of the circadian rhythm. This observation indicates that the photic pathway utilizing neuropeptide Y may be functional only when the endogenous circadian rhythm is synchronized to external light and dark cycles. Administration of an excitatory amino acid antagonist (MK-801) blocked the increase of neuropeptide Y by light, while an agonist (N-methyl-D-aspartate) induced similar facilitatory effects to that of light on the neuropeptide Y level in the rat suprachiasmatic nucleus. These results suggest that the geniculohypothalamic tract processes photic information so as to facilitate distinction of the transition between light and darkness that occurs either at subjective dawn or dusk.

Animals↗

PubMed2003

Acid challenge delays gastric pressure adaptation, blocks gastric emptying and stimulates gastric fluid secretion in the rat.

Functional dyspepsia can be associated with impaired gastric relaxation in response to food intake and delayed gastric emptying. In this study, we investigated whether luminal hydrochloric acid (HCl) may reproduce these motor alterations in phenobarbital-anaesthetized rats via activation of extrinsic neural pathways. Intragastric pressure (IGP) changes induced by a 2-mL fluid bolus were recorded with an oesophageal catheter, and gastric emptying was determined via the fluid volume recovered from the stomach 30-min post-bolus. Experiments involving acute nerve transections or pharmacological blockade of nitric oxide synthesis revealed that the initial increase of IGP after a 0.35 mol L(-1) HCl bolus is dampened by duodenogastric and gastrogastric relaxation reflexes depending on vagal and splanchnic pathways as well as nitric oxide. Compared with saline, HCl (0.15-0.5 mol L(-1)) delayed the subsequent decrease (adaptation) of IGP, inhibited gastric emptying and stimulated gastric fluid secretion as seen in stomachs with ligated pylorus. The acid-evoked delay in IGP adaptation and inhibition of gastric emptying involved duodenogastric and duodenopyloric extrinsic nerve reflexes, whereas the gastric fluid secretion was independent of the extrinsic innervation. It is proposed that the gastropyloric motor changes induced by luminal acid challenge have a bearing on the motor disturbances underlying functional dyspepsia.

Animals↗

PubMed1999

The Drosophila NSF protein, dNSF1, plays a similar role at neuromuscular and some central synapses.

The N-ethylmaleimide sensitive fusion protein (NSF) was originally identified as a cytosolic factor required for constitutive vesicular transport and later implicated in synaptic vesicle trafficking as well. Our previous work at neuromuscular synapses in the temperature-sensitive NSF mutant, comatose (comt), has shown that the comt gene product, dNSF1, functions after synaptic vesicle docking in the priming of vesicles for fast calcium-triggered fusion. Here we investigate whether dNSF1 performs a similar function at central synapses associated with the well-characterized giant fiber neural pathway. These include a synapse within the giant fiber pathway, made by the peripherally synapsing interneuron (PSI), as well as synapses providing input to the giant fiber pathway. The latency (delay) between stimulation and a resulting muscle action potential was used to assess the function of each class of synapses. Repetitive stimulation of the giant fiber pathway in comt produced wild-type responses at both 20 and 36 degrees C, exhibiting a characteristic and constant latency between stimulation and the muscle response. In contrast, stimulation of presynaptic inputs to the giant fiber (referred to as the "long latency pathway") revealed a striking difference between wild type and comt at 36 degrees C. Repetitive stimulation of the long latency pathway led to a progressive, activity-dependent increase in the response latency in comt, but not in wild type. Thus the giant fiber pathway, including the PSI synapse, appears to function normally in comt, whereas the presynaptic inputs to the giant fiber pathway are disrupted. Several aspects of the progressive latency increase observed in the long latency pathway can be understood in the context of the activity-dependent reduction in neurotransmitter release we observed previously at neuromuscular synapses. These results suggest that repetitive stimulation causes a progressive reduction in neurotransmitter release by presynaptic inputs to the giant fiber neuron, resulting in an increased latency preceding a giant fiber action potential. Thus synapses presynaptic to the giant fiber appear to utilize dNSF1 in a manner similar to the neuromuscular synapse, whereas the PSI chemical synapse may differ with respect to the expression or activity of dNSF1.

Animals↗

PubMed1981

Hormonal control of cell form and number in the zebra finch song system.

Administration of testosterone (T), 17 beta-estradiol (E2), or 5 alpha-dihydrotestosterone (DHT) to female zebra finch chicks (Poephila guttata) at hatching exerts effects on brain sexual differentiation. Within a telencephalic station (the nucleus robustus archistriatalis, RA) of the neural pathway which participates in the efferent control of song, masculinization of several indices of neuronal size is induced by exposure to T or E2. Within RA, a sensitive assay of a single neuron's sexually differentiated state is the diameter of its soma. By this criteria, all of the neurons within RA can be masculinized with a sufficient dose of T. As the dose of T is progressively decreased, the proportion of RA neurons which undergo the transition from female to male falls, while the magnitude of the change in soma size remains basically unaltered. Administration of T or DHT masculinizes the number of neurons in RA.

Animals↗

PubMed1992

Transection of the stria terminalis without damage to the medial amygdala does not alter behavioural sodium regulation in rats.

Damage to the medial region of the amygdala has been shown to impair mineralocorticoid-induced sodium appetite, while leaving intact sodium appetite induced through sodium depletion. This effect may result from the interruption of the flow of information through the stria terminalis (ST), a neural pathway linking the medial amygdala with the ventral forebrain. We determined the effect of transecting the ST of the rat, at a point remote from the medial amygdala, on sodium appetite induced with the administration of mineralocorticoids and with the natriuretic furosemide. Similar to control and amygdala lesioned rats, rats with ST knife-cuts displayed a normal sodium appetite following treatment with furosemide. However, unlike medial amygdala lesions, transection of the ST alone did not block mineralocorticoid-induced sodium appetite. Therefore, the inability of mineralocorticoids to induce a salt appetite in medial amygdala lesioned rats does not result from damage to the stria terminalis.

Amygdala↗

PubMed2006

Noise reduction of coincidence detector output by the inferior colliculus of the barn owl.

A recurring theme in theoretical work is that integration over populations of similarly tuned neurons can reduce neural noise. However, there are relatively few demonstrations of an explicit noise reduction mechanism in a neural network. Here we demonstrate that the brainstem of the barn owl includes a stage of processing apparently devoted to increasing the signal-to-noise ratio in the encoding of the interaural time difference (ITD), one of two primary binaural cues used to compute the position of a sound source in space. In the barn owl, the ITD is processed in a dedicated neural pathway that terminates at the core of the inferior colliculus (ICcc). The actual locus of the computation of the ITD is before ICcc in the nucleus laminaris (NL), and ICcc receives no inputs carrying information that did not originate in NL. Unlike in NL, the rate-ITD functions of ICcc neurons require as little as a single stimulus presentation per ITD to show coherent ITD tuning. ICcc neurons also displayed a greater dynamic range with a maximal difference in ITD response rates approximately double that seen in NL. These results indicate that ICcc neurons perform a computation functionally analogous to averaging across a population of similarly tuned NL neurons.

Acoustic Stimulation↗

PubMedDate not supplied

The relationship of optokinetic nystagmus to pursuit eye movements, vestibular nystagmus and to saccades in humans. A clinical study.

The relationship of mean velocity of optokinetic nystagmus (OKN) to pursuit eye movements (PEM), to vestibular nystagmus and to voluntary saccades was analysed in 10 patients with peripheral vestibular lesions and in 30 patients with central vestibular lesions. PEM and vestibular nystagmus were significantly correlated to OKN, suggesting that a common neural pathway is used in the generation of these eye movements. Weak or no correlation was found between saccadic peak velocity and slow phase velocity of OKN. Using multiple linear regression analysis, it was found that 78.5% of the variation in the slow-phase velocity of OKN could be explained by a synthesis of PEM and vestibular test data. PEM test data were more powerful than those of vestibular nystagmus in deduction of OKN. The possible appearance of slow build-up of OKN could not be deduced from the reduction of PEM. Hence, the relationship between PEM and OKN in man is not a simple linear one, but is more complex.

Adolescent↗

PubMed2005

Rostral ganglia are required for induction but not expression of crayfish escape reflex habituation: role of higher centers in reprogramming low-level circuits.

It is widely assumed that learning results from alterations in the strength of synapses within the neural pathways that mediate a learned behavioral response and that these alterations are directly caused by training-induced activity of neurons connected by the changing synapses. Initial evidence for this view came from studies of habituation of defensive reflexes in several invertebrate species. However, more recent studies of habituation of the escape reflex in one of these species, the crayfish, have shown that habituation is substantially caused by tonic inhibitory input from cephalic ganglia; this descending inhibition suppresses the activity of neurons within the escape circuit, which reside in caudal ganglia. Such control by descending inhibition indicates that animals with encephalized nervous systems do not entirely abdicate to low-level circuitry the important decision of whether to habituate to stimuli that might warn of danger. Higher centers in fact play a major role in controlling the habituation of this potentially life-saving protective response. Another way for higher centers to control lower ones would be to induce alteration of the lower center's intrinsic properties. Here, we show that, whereas descending input from higher ganglia is needed to induce habituation, once established, habituation persists even after rostral ganglia are disconnected. This provides evidence that lower-level neural circuits can be reprogrammed through transient interaction with higher ganglia to decrease their intrinsic tendency to produce escape.

Animals↗

PubMed1983

Evidence that the nigrotegmental GABAergic projection mediates stereotypy induced by apomorphine and intranigral muscimol.

The substantia nigra plays a pivotal role in the relay of output from the striatum. One neural pathway from substantia nigra projects GABAergic fibers to the caudal mesencephalic tegmentum, terminating in the vicinity of the pedunculopontine nucleus (PPN). To evaluate the functional importance of this projection in the mediation of stereotyped behaviors of striatal and nigral origin, we microinjected low doses of the GABA agonist, muscimol, bilaterally into the vicinity of the PPN. This muscimol treatment resulted in a total blockade of all stereotyped behaviors normally elicited by systemic apomorphine or by intranigral muscimol. Blockade was not observed in animals microinjected with muscimol into the dorsal reticular formation, 1 mm above the level of the PPN. Our results indicate that the nigrotegmental projection may play a crucial role in the expression of stereotyped and dyskinetic behaviors of basal ganglia origin.

Animals↗

PubMed2004

Integration of neural responses originating from different regions of the cortical somatosensory map.

The neural pathways responsible for detecting peripheral tactile stimuli are well known; however, the interactions between different somatosensory regions have been less well investigated. This study demonstrates how the contralateral sensory response of rat barrel cortex to whisker stimulation is affected by stimulation of contralateral forepaw and ipsilateral whisker and forepaw. The barrel cortex in the right hemisphere was located using optical imaging. A 16-channel multielectrode was used to measure field potentials evoked by contralateral electrical stimulation of the whisker pad. A standard response in the right barrel cortex to single pulse electrical stimulation of the contralateral whisker pad was modulated by applying conditioning stimulation to one of three other regions of the body (the ipsilateral whisker pad, the ipsilateral or contralateral forepaws). In conditions where the standard contralateral whisker stimulus preceded the conditioning pulse, the size of response was identical to when it was stimulated alone. However, when the ipsilateral whisker and contralateral forepaw conditioning stimuli preceded the contralateral whisker pad stimulation, up to a 35% reduction in the contralateral whisker response was observed. These results confirm and extend previous studies [Proc. Natl. Acad. Sci. U. S. A. 97 (2000) 11026-11031; J. Neurosci. 21 (2001) 5251-5261], which show bilateral integration of neural activity within the rat somatosensory system. Furthermore, the longer latency of the inhibition following stimulation of the contralateral forepaw suggests the possible involvement of extracortical circuitry.

Animals↗

PubMed1996

Network analysis of positron emission tomography regional cerebral blood flow data: ensemble inhibition during episodic memory retrieval.

Two important objectives in the neuroscience of memory are (1) identification of neural pathways involved in memory processes; and (2) characterization of the pattern of interactions between these pathways. Functional neuroimaging can contribute to both of these goals. Using image subtraction analysis of regional cerebral blood flow data measured with positron emission tomography, we identified brain regions that changed activity during episodic memory retrieval (visual work recognition). Relative to a baseline reading task, decreased activity was observed in bilateral prefrontal, bilateral anterior and posterior temporal, and posterior cingulate cortices. Brain regions showing increased activity were the right prefrontal (different from deactivated regions), left anterior cingulate, and left occipital cortices, and vermis of cerebellum. We then performed a network analysis with structural equation modeling to test the hypothesis that regional decreases came about through active inhibition by regions showing increased activity during retrieval. This analysis demonstrated that the influence of activated regions on deactivated regions was more negative during retrieval than during reading, confirming the inhibition hypothesis. Such confirmation could not have been made from the subtraction analysis alone because decreases can come about, at the very least, through reduction of functional influences as well as by active inhibition. The concepts of ensemble excitation and inhibition, as defined through network analysis, are introduced. We argue that is is critical to examine the combined pattern of excitatory and inhibitory influences to fully appreciate the neural basis of episodic memory.

Analysis of Variance↗

PubMed1998

A method of combining biocytin tract-tracing with avidin-biotin-peroxidase complex immunocytochemistry for pre-embedding electron microscopic labeling in neonatal tissue.

A new method that allows the combination of avidin-biotin-peroxidase visualization of antigens and silver-intensified gold labeling of biocytin, a rapid tract-tracer, is described. The method provides a practical tool for in vivo and in vitro studies of chemically specified afferent-target relationships and particularly in developing neural pathways where biocytin is invaluable as a rapidly transporting, sensitive tracer requiring little permeabilizing agents. Transported biocytin was first visualized with silver-intensified colloidal gold conjugated to anti-biotin IgG. This was followed by blocking of all unbound biotin groups of biocytin in the tissue with an Avidin-Biotin blocking kit. Finally, a second antigen, neuronal nitric oxide synthase NOS or GluR2/3 subunit of AMPA receptors, was visualized selectively with avidin-biotin-peroxidase/DAB. This protocol allowed visualization of two chromagens that could be distinguished by electron microscopy. The presence of biocytin was evident by silver particles, while accumulation of peroxidase reaction product marked only the antibody labeling: no cross-reaction between biocytin and the avidin-biotin-peroxidase was observed.

Animals↗