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PubMed2003

Puberty: a period of both organizational and activational effects of steroid hormones on neurobehavioural development.

During perinatal development, steroid hormones act on the central nervous system (CNS) to organize neural circuits. These circuits remain relatively dormant until hormonal stimulation received in adulthood acts on the CNS to activate adult reproductive physiology and behaviour. In this review, the proposal is put forward that, in addition to perinatal development, puberty serves as another period of neural maturation mediated by both steroid-dependent and -independent events that further organize and shape the behavioural potential of the adult organism. In support of this thesis, data are summarized that clearly show the organizational effects of the pubertal rise in gonadal hormones on mating behaviour and other steroid-mediated behaviours exhibited in adulthood, and on the neural pathways that mediate these behaviours. The importance of determining whether this sensitive period of neural development during puberty is a 'critical period' is also discussed, as well as whether perturbations of the nervous system during pubertal development may result in negative behavioural and physiological outcomes in adulthood. It is concluded that puberty is not merely a time when increasing levels of gonadal steroids activate the neural circuits organized during perinatal development, but also a time of further organization of the CNS, which allows for appropriate behaviours to emerge in adulthood.

Animals↗

PubMed1984

Neurochemical psychiatry as a source of hypotheses concerning the role of homeostatic mechanisms in brain function.

Numerous homeostatic mechanisms regulate impulse traffic in the neural pathways of the brain. If, for whatever reason, these mechanisms are unable to maintain neural activity within normal levels, the resulting disruption of the balance of impulse traffic produces brain dysfunction such as mental or neurological disorders. Drug treatment of these disorders involves the use of agents that return impulse traffic to homeostatic levels. Such agents have been found only for certain disorders such as Parkinson's Disease, certain affective disorders and some aspects of schizophrenia. The development of therapeutic interventions for currently untreatable conditions such as Huntington's Chorea or Alzheimer's Disease and the design of drugs for the more efficient treatment of psychiatric disorders, would be greatly facilitated by more detailed knowledge of the specific homeostatic mechanisms controlling brain function.

Brain↗

PubMed1992

Corticotropin-releasing factor: long-lasting facilitation of the acoustic startle reflex.

Intracerebroventricular infusion of corticotropin-releasing factor (CRF) (0.1-1.0 micrograms) produced a pronounced, dose-dependent enhancement of the acoustic startle reflex in rats. This excitatory effect began about 20-30 min after infusion, grew steadily over the 2 hr test period, and lasted at least 6 hr. Higher doses of CRF (10 micrograms) often produced marked facilitation and then inhibition of startle that oscillated repeatedly with a period of 10-20 min. CRF-enhanced startle did not result from an increase in sensitization produced by repetition of the startle stimulus or from a blockade of habituation. Peripheral injections of the autonomic ganglionic blockers hexamethonium (10 mg/kg) or chlorisondamine (3 mg/kg) slightly attenuated the magnitude of CRF-enhanced startle, suggesting a partial role of peripheral sympathetic activation. Intracerebroventricular infusion of the CRF antagonist alpha-helical CRF9-41 (alpha hCRF; 25 or 50 micrograms) blocked CRF-enhanced startle when infused 5 min prior to CRF, indicating a central site of action. CRF-enhanced startle also was reversed when alpha hCRF was given 90 min after infusion of CRF. This suggests that exogenously applied CRF remains in the brain for a very long time after administration or that CRF given exogenously initiates a process that results in a long-lasting activation of endogenous CRF. Because the startle reflex is elevated by both conditioned and unconditioned fear, these data lend further support to the idea that CRF infusion produces a behavioral state that resembles fear or anxiety. Because startle is mediated by a well-defined neural pathway, CRF-enhanced startle may provide a useful behavioral assay to analyze the neural systems upon which exogenous CRF acts to produce its behavioral effects.

Acoustic Stimulation↗

PubMed1975

Sorting of signals from thermosensitive areas.

Of the several models proposed for the neural regulation of temperature in cold-exposed animals, two have been previously restated in dynamic form using CSMP. Subsequently, computer simulations have led to the design and execution of experiments for selection of the more appropriate model for cold-exposed rats. These experiments, as described in the present paper, have been interpreted as being consistent with the model which sorts signals from thermosensitive areas and channels the selected signals over separate neural pathways to independently control each mode of heat production. Since this model requires multiplication of neural signals, possible neuronal mechanisms which may underline such multiplication are discussed. In addition, parameter variation to account for febril responses and rate sensitivity have been evaluated.

Animals↗

PubMed1985

Neural regulation of the cardiovascular system during exercise.

Neural components important in control of the cardiovascular system during exercise can be divided into central nervous system (CNS) components and peripheral components. CNS components would include the cerebral cortex, cerebellum, medullary region of the brain stem, and the spinal cord. Peripheral components would include the efferent limbs of the autonomic nervous system and afferent fibers carrying information to the CNS. The neural pathways involved in the control of cardiovascular system during exercise and the relationship between the various neural components have been actively pursued in the last few years. Several new studies suggest that information arising from the active muscles and the cardiovascular system itself may be important in the control of the cardiovascular system during exercise. The cerebellum may play a modulating role in the cardiovascular response. The information from the peripheral afferent fibers, the cerebellum, and the cerebral cortex is integrated in the brain to result in overall neural control. Exercise training probably modifies the central integration of information and modifies the cardiovascular response to exercise and other stresses.

Afferent Pathways↗

PubMed1989

Nervous regulation of metabolism.

As described previously, the regulatory roles played by the autonomic nervous system on blood glucose homeostasis is well documented in comparison with those on fat and protein metabolism. It can be summarized as follows: It was shown that an increase in blood glucose concentration produced an increase in the activity of the pancreatic branch of the vagus nerve whereas it induced a decrease in the activity of the pancreatic branch of the splanchnic nerve and adrenal nerve. It was also shown that a decrease in blood glucose concentration activated the sympatho-adrenal system and suppressed vago-pancreatic system. It seems rational that these responses are involved in the maintenance of blood glucose level. Studies on the innervation of the liver led us to a conclusion that sympathetic innervation of the liver plays a role in eliciting a prompt hyperglycemic response through liberation of norepinephrine from the nerve terminals, and that the vagal innervation synergically worked with the humoral factor (insulin) for glycogen synthesis in the hyperglycemic condition. The glucose-sensitive afferents from the liver seem to initiate a reflex control of blood glucose level. The gustatory information on early insulin response (EIR), reported by Steffens (1976), is supported by the electrophysiological observations. Mei's reports (1981) also indicated the importance of information from the intestinal glucoreceptors in the reflex control of insulin secretion via the vagus, which has been proved electrophysiologically. The role of integrative function of the hypothalamus and brainstem through neuronal networks on neural control of blood glucose homeostasis is evident. On the neural control of fat metabolism, it is evident that the sympathetic outflows to the brown adipose tissue as well as white adipose tissue predominantly play important roles. However, there is still little information on the central mechanism played by the hypothalamus on the fat metabolism and the neural pathways from the hypothalamus to the sympathetic motoneurons innervating adipose tissues. The reports on the neural control of protein metabolism are very few. Only several studies were reported on the liver function in relation to the protein metabolism. Further extensive studies should be expected.

Adipose Tissue↗

PubMed2004

Neural crest cells: a model for invasive behavior.

Neural crest cells are the embryonic precursors of the neurons and glia of the peripheral nervous system, pigment cells, and connective tissue in the face, neck and heart. They are induced near the junction of the neural plate and embryonic ectoderm and undergo an epithelial to mesenchymal transition (EMT). Neural crest cells then display invasive behavior and migrate into the surrounding tissues along specific pathways. Neural crest cells are amenable to study in tissue culture, and the molecules that regulate their development can be studied in vivo with antisense techniques as well as with the expression of gain and loss-of-function constructs. Mutations in factors that regulate neural crest cell survival or differentiation can lead to cell death or the premature cessation of their migration, resulting in craniofacial abnormalities, pigmentation defects and the absence of enteric neurons. This paper reviews recent advances in our understanding of neural crest cell induction and migration, emphasizing both avian and amphibian models. Cell facts: The embryonic progenitors of pigment cells, the neurons and glia of the peripheral nervous system, as well as connective tissue in the face, neck and heart. Induced to form at the boundary of the neuroepithelium and embryonic ectoderm. Expression of the transcription factors Snail, Slug and FoxD3 leads to delamination from the neural tube. Invasive motility not unlike that of tumor cells can be studied in vitro. Express proteases, distinctive cell surface receptors and glycoproteins to acquire an invasive phenotype. Mutations of transcription factors expressed by the neural crest or in other factors that inhibit their premature differentiation can lead to survival and migration-associated birth defects.

Animals↗

PubMed1989

Pain perception in a man with total corpus callosum transection.

While classical and current theories of pain emphasize the critical role of central neural pathways that represent the contralateral body surface and cross within the spinal cord, the role of neural input representing the ipsilateral body surface is uncertain. In the present experiments with a complete corpus callosum-sectioned patient, both tactile and low intensity noxious stimuli (43-47 degrees C) ipsilateral to the responding cerebral hemisphere were poorly perceived and/or rated low on verbal and visual analogue scales (VAS). Surprisingly, however, high intensity noxious thermal stimuli (49-51 degrees C) were rated on verbal or visual analogue scales as very intense and unpleasant, thereby reflecting both sensory-discriminative and motivational-affective dimensions of pain. Thus, the pathways and mechanisms subserving this ipsilateral input have high thresholds for activation, but once activated are sufficient to evoke all of the critical dimensions of the experience of pain.

Adult↗

PubMed2001

Neural induction takes a transcriptional twist.

Over the past decade, several molecules have been identified that influence neural cell fate in vertebrate embryos during gastrulation. The first neural inducers studied were proteins produced by dorsal mesoderm (the Spemann organizer); most of these proteins act by directly binding to and antagonizing the function of bone morphogenetic proteins (BMPs). Recent experiments have suggested that other secreted signals, such as Wnt and FGF, may neuralize ectoderm before organizer function by a different mechanism. Neural effector genes that mediate the response of ectoderm to secreted neuralizing signals have also been discovered. Interestingly, most of these newly identified neuralizing pathways continue the theme of BMP antagonism, but rather than antagonizing BMP protein function, they may neuralize tissue by suppressing Bmp expression. Down-regulation of Bmp expression in the prospective neural plate during gastrulation seems to be a shared feature of neural induction in vertebrate embryos. However, the signals used to accomplish this task seem to vary among vertebrates. Here, we will discuss the role of the recently identified secreted signals and neural effector genes in vertebrate neurogenesis.

Animals↗

PubMed2000

The obesity epidemic: metabolic imprinting on genetically susceptible neural circuits.

The apparent obesity epidemic in the industrialized world is not explained completely by increased food intake or decreased energy expenditure. Once obesity develops in genetically predisposed individuals, their obese body weight is avidly defended against chronic caloric restriction. In animals genetically predisposed toward obesity, there are multiple abnormalities of neural function that prime them to become obese when dietary caloric density and quantity are raised. Once obesity is fully developed, these abnormalities largely disappear. This suggests that obesity might be the normal state for such individuals. Formation of new neural circuits involved in energy homeostasis might underlie the near permanence of the obese body weight. Such neural plasticity can occur during both nervous system development and in adult life. Maternal diabetes, obesity, and undernutrition have all been associated with obesity in the offspring of such mothers, especially in genetically predisposed individuals. Altered brain neural circuitry and function often accompanies such obesity. This enhanced obesity may then be passed on to subsequent generations in a feed-forward, upward spiral of increasing body weight across generations. Such findings suggest a form of "metabolic imprinting" upon genetically predisposed neural circuits involved in energy homeostasis. Centrally acting drugs used for obesity treatment lower the defended body weight and alter the function of neural pathways involved in energy homeostasis. But they generally have no permanent effect on body weight or neural function. Thus, early identification of obesity-prone mothers, infants, and adults and treatment of early obesity may be the only way to prevent the formation of permanent neural connections that promote and perpetuate obesity in genetically predisposed individuals.

Animals↗

PubMed1997

The legacy of the Wernicke-Lichtheim model.

Wernicke established an integrated model of the relation between higher cognitive functions and neurophysiological structure of the human brain in 1874. The previous Bouillaud/Broca view envisaged a mosiac map of centres for specific functions, each of which had no clear inter-relation with other centres or with input/output pathways, and with no theoretical explanation of how each centre operated in relation to more basic neural elements. Wernicke's model overcame these objections, and, with Lichtheim's systematization in 1885, the "Wernicke-Lichtheim model" became the standard neuropsychological theory. In this model, each normal higher function is explained in terms of an underlying neural pathway that includes the input/output systems, related functions employ portions of the pathways used for other functions, pathological syndromes are explained by reference to where in the pathway damage occurred, and previously unobserved pathological syndromes can be predicted. Development of the model at the hands of Lissauer, Dejerine, Liepmann, Geschwind, Heilman, and Ellis and Young is traced.

History, 19th Century↗

PubMed1976

Integration of the cardiovagal mechanism in the medulla oblongata of the cat.

The central cardiovagal mechanism of the medulla oblongata was explored by stimulation and ablation techniques in the anesthetized cat. Insertion of an electrode into the nucleus solitarius (NS) occassionally evoked slight and transient bradycardia, but similar mechanical irritation to the nucleus ambiguus (NA) usually evoked prolonged and intense bradycardia. Electrical stimulation of the dorsal motor nucleus of the vagus (DNV) produced no or little bradycardia. Stimulation of NS and NA consistently produced cardiac slowing with a latency of less than 2 s and the effect was more prominent in the NA. Contralateral vagotomy did not significantly affect the bradycardia on the NS and NA stimulation but ipsilateral vagotomy caused a complete abolition. Lesions of the NA or DNV largely or completely abolished the bradycardia consequent to NS stimulation. Extensive destruction of the NS and/or DNV did not affect the bradycardia resulting from NA stimulation. Destruction of the ventral midline area partially reduced th bradycardia on NS STIMULATION BY 36-54%. The results suggest that the sequence of the three vagal nuclei for cardiac inhibition runs in the following order: NS, DNV, and NA. Synaptic connections are probably scanty in the DNV. Part of the vagal pathway passes through the ventral midline area before it reaches the NA. A scheme of the neural pathway for reflex bradycardia of vagal origin has been proposed.

Animals↗

PubMed1987

An odor discrimination model with application to kin recognition in social insects.

The problem of discriminating between a number of similar, nonspecific odors is discussed with special reference to the phenomenon of kin and nestmate discrimination in social insects. Guided by the basic physiological and anatomical features of the olfactory sensory receptors and neural pathways in insects, a model is presented for the process of odor discrimination. The model hypothesizes neural processing capabilities that include the logarithmic transformations of electrical potentials to generate a scalar quantity representing the "similarity" of two multivalued signals. The model thereby quantifies the notion of phenotype matching that appears in the kin recognition literature, and makes the concept of a recognition template more precise. The hypotheses underlying the model suggest a number of neurophysiological studies that should be undertaken, while the model itself provides a basis for integrating several areas of research pertaining to kin recognition in particular species of animals.

Algorithms↗

PubMed1993

Enhancement of the acoustic startle response by stimulation of an excitatory pathway from the central amygdala/basal nucleus of Meynert to the pontine reticular formation.

The acoustic startle response (ASR) is a simple motor reaction to intense and sudden acoustic stimuli. The neural pathway underlying the ASR in rats is already fairly well understood. As the ASR is subject to a variety of modulations, this reaction can serve as a model for vertebrate neuroethologists to investigate the neural mechanisms mediating sensorimotor transfer and their extrinsic modulation. We report here on experiments in rats which were undertaken in order to investigate the neural mechanisms underlying the enhancement of the ASR. An increased amplitude of the ASR can be observed during states of conditioned and unconditioned fear. By employing neuroanatomical tract-tracing methods, we describe a pathway from neurons of the medial division of the central amygdaloid nucleus (cA) and the basal nucleus of Meynert (B) to the caudal pontine reticular nucleus (PnC), an important relay station in the acoustic startle pathway. Extracellular recordings from acoustically responsive neurons in the PnC showed that electrical stimulation of the cA/B facilitates the tone-evoked response of these neurons. Behavioural tests following chemical stimulation of the cA/B with NMDA (N-methyl-d-aspartate) in awake rats indicated that activation of this pathway increases the ASR. The lack of sufficient spatial resolution of our stimulation techniques did not allow us to differentiate the relative contributions of the cA and the B to this effect. As the amygdaloid complex has been implicated in emotional behaviour, particularly in the mediation of fear, these findings substantiate the concept that the amygdaloid complex plays a key role for the enhancement of the ASR by conditioned and unconditioned fear.

Amygdala↗

PubMed2003

Musings on the wanderer: what's new in our understanding of vago-vagal reflexes? V. Remodeling of vagus and enteric neural circuitry after vagal injury.

The vago-vagal reflexes mediate a wide range of digestive functions such as motility, secretion, and feeding behavior. Previous articles in this series have discussed the organization and functions of this important neural pathway. The focus of this review will be on some of the events responsible for the adaptive changes of the vagus and the enteric neutral circuitry that occur after vagal injury. The extraordinary plasticity of the neural systems to regain functions when challenged with neural injury will be discussed. In general, neuropeptides and transmitter-related enzymes in the vagal sensory neurons are downregulated after vagal injury to protect against further injury. Conversely, molecules previously absent or present at low levels begin to appear or are upregulated and are available to participate in the survival-regeneration process. Neurotrophins and other related proteins made at the site of the lesion and then retrogradely transported to the soma may play an important role in the regulation of neuropeptide phenotype expression and axonal growth. Vagal injury also triggers adaptive changes within the enteric nervous system to minimize the loss of gastrointestinal functions resulting from the interruption of the vago-vagal pathways. These may include rearrangement of the enteric neural circuitry, changes in the electrophysiological properties of sensory receptors in the intramural neural networks, an increase in receptor numbers, and changes in the affinity states of receptors on enteric neurons.

Animals↗

PubMed2002

Electrophysiological study of vocal-fold mobility disorders using a magnetic stimulator.

In the field of neurolaryngology, there has been a great interest in neurophysiological studies, such as neurography, for the assessment of the integrity of the laryngeal neural pathway. Such tools provide an indication about the site and the nature of the nerve lesion. We have tried to use a magnetically evoked potential to assess the corticolaryngeal pathway in order to provide normative data on laryngeal nerve conductivity and to evaluate the integrity of the laryngeal neural system in patients with vocal-fold mobility disorders. This study was conducted on 26 subjects (10 normal volunteers and 16 patients with vocal-fold immobility) who were primarily selected on the basis of a comprehensive laryngeal evaluation including laryngo-videostroboscopy assessment. Transcranial (cortical) and mastoid (peripheral) magnetic stimulations were performed to evoke muscle action potentials of the thyro-arytenoid (TA) and cricothyroid muscles (CT). In normal volunteers, cortical stimulation leads to contralateral responses (cortical latency) after 10.9 and 11.3 ms and ipsilateral responses after 8.3 and 9.4 ms for right CT and TA muscles, respectively. There was a significant prolongation of cortical latency of the left TA compared with the right TA muscle, whilst no such significant difference was observed in the CT muscles. Peripheral stimulation evoked response (peripheral latency) after 2.8 and 2.7 ms in the right CT and TA, respectively, with the same significant prolongation of the left TA response compared with the right side. Amongst the patient groups, variable patterns of laryngeal muscle response latencies occurred, including normal response latency, lack of response of CT and TA muscles, prolonged peripheral latency with secondary prolonged cortical latency and prolonged cortical latency with normal peripheral latency. The results indicate that the magnetically evoked potential of laryngeal muscles offers an easy, non-invasive technique and could have a role in the assessment of the integrity of corticolaryngeal pathways.

Adult↗

PubMed1998

Nitric oxide modulates cholinergic reflex pathways to the longitudinal and circular muscle in the isolated guinea-pig distal colon.

1. The involvement of nitric oxide (NO) in enteric neural pathways underlying reflex responses of the longitudinal muscle (LM) and circular muscle (CM) layers activated by mucosal stimulation was examined in the isolated guinea-pig distal colon. 2. A segment of colon spanned two partitions (10 mm apart), which divided the organ bath into three chambers: a recording chamber where LM and CM tension was measured; a stimulation chamber where mucosal stimulation was applied; and a middle chamber separating them. 3. Brushing the mucosa anal and oral to the recording site evoked simultaneous oral contraction and anal relaxation of both the LM and CM. 4. N omega-nitro-L-argininel-NA; 100 microM) or N omega-nitro-L-arginine methyl ester (L-NAME; 100 microM) applied to the middle chamber or stimulation chamber decreased the oral contractile response of the LM and CM (by about 30-40 %), but increased the anal relaxation (> 600 %) and exposed an anal contraction (> 1000 % increase) of both muscles. The addition of L-NA to the recording chamber reduced the anal relaxation of the LM and CM and the anal contraction of the LM, but slightly increased the anal contraction of the CM. 5. S-Nitroso-N-acetylpenicillamine (SNAP; 10 microM), an NO donor, reversed the effects of L-NA in the middle or stimulation chambers. 6. 1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ; 10 microM), a soluble guanylate cyclase inhibitor, mimicked the effects of L-NAin the middle chamber or stimulation chamber, but these effects were not reversed by SNAP. 7. The oral contractile responses, and the anal relaxation and contractile responses of the LM and CM produced by L-NA in the stimulation or middle chambers, were blocked by hexamethonium (300 microM) in any chamber. Atropine (1 microM) in the recording chamber reduced the contractile responses of the LM and CM. 8. In conclusion, endogenous NO facilitates and depresses release of acetylcholine from interneurons in ascending and descending nervous pathways, respectively. These NO effects are mediated through soluble guanylate cyclase in cholinergic interneurons

Animals↗

PubMedDate not supplied

Foraging for brain stimulation: toward a neurobiology of computation.

The self-stimulating rat performs foraging tasks mediated by simple computations that use interreward intervals and subjective reward magnitudes to determine stay durations. This is a simplified preparation in which to study the neurobiology of the elementary computational operations that make cognition possible, because the neural signal specifying the value of a computationally relevant variable is produced by direct electrical stimulation of a neural pathway. Newly developed measurement methods yield functions relating the subjective reward magnitude to the parameters of the neural signal. These measurements also show that the decision process that governs foraging behavior divides the subjective reward magnitude by the most recent interreward interval to determine the preferability of an option (a foraging patch). The decision process sets the parameters that determine stay durations (durations of visits to foraging patches) so that the ratios of the stay durations match the ratios of the preferabilities.

Animals↗