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PubMed1985

Intracortical 5,7-dihydroxytryptamine depletes brain serotonin concentrations without affecting spontaneous activity.

Microinjections of either 2 or 4 micrograms of the serotonergic neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) were made into either the right or left frontal cortex of male rats pretreated with desmethylimipramine. Although both the 2 and 4 micrograms doses produced significant depletions of serotonin concentrations in the cortex and median raphe, neither dose produced a significant increase in spontaneous activity. This is in contrast to our findings with the noradrenergic neurotoxins, 6-hydroxydopamine and DSP-4, which produced hyperactivity following right but not left hemisphere injections. These findings do not rule out the involvement of 5-HT in the asymmetrically elicited hyperactivity but they do suggest some transmitter and neural pathway specificity to the lateralized response to cortical injury.

5,7-Dihydroxytryptamine↗

PubMed1986

Selective antagonism by clonidine of the stereotyped and non-stereotyped motor activity elicited by atropine.

The effects of clonidine, an indirectly-acting cholinergic antagonist, on 5 behaviors elicited by atropine (locomotion, rearing, sniffing, grooming and gnawing) were studied in rats. Clonidine did not alter the prevalence or magnitude of atropine-elicited locomotion and rearing. In contrast, clonidine suppressed the occurrence and degree of 3 stereotyped behaviors, namely, sniffing, grooming and gnawing. This selectivity of clonidine suggests differences in the neural pathways subserving the various stereotyped motor activities.

Animals↗

PubMed1988

Locomotor activity and stereotypy in rats following repeated apomorphine treatments at 1-, 3-, or 7-day intervals.

In two experiments, the effects of repeated intermittent administration of a relatively high dose of apomorphine (5 mg/kg) on locomotor activity and/or stereotypic behavior in rats was determined. In Experiment 1, male rats were given ten subcutaneous (SC) injections of apomorphine or vehicle and tested for locomotor activity and stereotypy. The first nine injection test sessions were given at 3-day intervals and the tenth injection test session was given 18 days following the ninth session. In Experiment 2, male rats were tested for locomotor activity following ten SC injections of apomorphine or vehicle with either a one- or seven-day interval between injections. Major findings were as follows: a) apomorphine produced progressively greater increases in locomotor activity with each succeeding injection (i.e., sensitization); b) sensitization to the locomotor activity stimulating effects of apomorphine developed with interinjection intervals of one, three, and seven days; c) the sensitization effect was maintained over the 18-day drug-free break; and d) the effect of apomorphine on stereotypic behavior did not significantly change with repeated injections. These findings indicate that even a single dose of apomorphine induces relatively long-lasting neurobiological changes. Moreover, these findings are consistent with the view that separate neural pathways mediate locomotor activity and stereotypy in rats.

Age Factors↗

PubMed1989

Multimodal effects of acute exposure to toluene evidenced by sensory-evoked potentials from Fischer-344 rats.

Male Fischer-344 rats were exposed by inhalation to 500, 2000, 5000, 8000 and 16000 ppm toluene for 30 min in two experiments. Exposures up to 8000 ppm in Experiment 1 caused concentration-related changes in the click-elicited brainstem auditory-evoked response (CBAER), flash-evoked potential (FEP) and somatosensory-evoked potential (SEP). Latencies of CBAER components were prolonged and amplitudes of late components were increased by toluene. Toluene did not detectably alter the latencies of FEP or SEP components. Early FEP component-amplitudes were increased and late component-amplitudes were decreased; toluene also induced a poststimulus oscillation in the FEP. Most component-amplitudes of the SEP were substantially increased, but N2P2 amplitude appeared to be more sensitive than other components to depressant effects of the solvent. The same effects on the CBAER were observed in Experiment 2, but a more substantial increase in the amplitudes of late components elicited by tone pips suggested that frequency-dependent cochlear irritation might underlie previously observed subchronic ototoxicity. These effects were increased by exposure to 16000 ppm toluene. Effects like those observed in Experiment 1 were noted on the FEP, but the oscillations were less with exposure to 16000 than 8000 ppm. Changes in the SEP were evident within 2 minutes of exposure onset, and amplitudes increased over the course of about 15 min, leveling off or decreasing thereafter. The amplitude of the N2P2 component was again less influenced than other components during exposure to 8000 ppm and was reduced to less than baseline amplitude by 16000 ppm. Effects of concentration and rates of development and recovery were systematically related to SEP component latency. Toluene appears to have both enhancing and inhibiting effects on neural pathways serving sensory systems, depending on the modality and the site of generation of the components within modalities. A particular balance between these properties might relate to the hedonic characteristics of this abused solvent.

Acoustic Stimulation↗

PubMed1989

D-cycloserine, a positive modulator of the N-methyl-D-aspartate receptor, enhances performance of learning tasks in rats.

Glycine has recently been shown to positively modulate the N-methyl-D-aspartate (NMDA) subclass of acidic amino acid receptors which are important in neural pathways involved in learning and memory. We report that d-cycloserine (DCS), an antimycobacterial agent known to cross the blood-brain barrier, binds with high affinity to this glycine modulatory site, functions as a positive modulator, and facilitates performance of learning tasks in rats. In addition, DCS appears to be a potent cognitive enhancer at doses lower than those required for antibacterial activity. Based on these data, we propose that modulation of NMDA receptors via glycinergic mechanisms may be a means of influencing cognitive processes.

Animals↗

PubMed1990

Crossed aphasia in Chinese: a clinical survey.

According to our clinical observations from various aspects of stroke patients, such as the total incidence of aphasia, the incidence of aphasia after left brain damage of the dextrals, the aphasia that occurs in patients without hemiplegia, and the types of aphasia, a much higher incidence of crossed aphasia is seen among the stroke patients of the Han (the largest ethnic group in China) as compared with the Uighur-Kazaks (U-K) in China and the Occidentals documented in the literature. Motor aphasia is most common and pure sensory or posterior aphasia is rarely seen in Han patients. The distinct features of the Chinese language is a possible explanation for this difference. We suspect that language function of the Han is not localized in the left brain but in the right or both hemispheres. There is no definite Wernicke's area in the left brain of the Chinese people and the neural pathway of the language function in the brain of the Chinese people is not similar to people who speak phonetic languages. Consequently the universal applicability of the theories of cerebral laterality of the language function and dominant hemisphere established by Dax and Broca are questioned in this paper.

Adult↗

PubMed1979

Space motion sickness.

Space motion sickness, presumably triggered by sudden entry into a weightless environment, occurred with unexpected frequency and severity among astronauts who flew the Skylab missions. Recovery from symptoms was complete within 3-5 days, and as revealed by the Skylab M131 Human Vestibular Function Experiment, all crewmembers were immune to experimentally induced motion sickness after mission day 8. This syndrome has been recognized as a possible threat to the early mission well-being and operational efficiency of at least some individuals who will fly space missions in the future. The causes of space motion sickness are not clearly understood, nor have satisfactory methods been identified to date for its prediction, prevention and treatment. In order to minimize the potential impact of this syndrome on Space Shuttle crew operations the National Aeronautics and Space Administration has organized a broad program of inter-disciplinary research involving a large number of scientists in the United States. Current research on the etiology of space motion sickness is based to a large extent on the so called sensory conflict theory. Investigations of the behavioral and neurophysiological consequences of intralabyrinthine, as well as intermodality sensory conflict are being performed. The work in this area is being influenced by the presumed alterations that occur in otolith behavior in weightlessness. In addition to sensory conflict, the possible relationship between observed cephalad shifts of body fluids in weightlessness and space motion sickness is being investigated. Research to date has failed to support the fluid shift theory. Research underway to identify reliable test methods for the prediction of susceptibility to space motion sickness on an individual basis includes attempts to (a) correlate susceptibility in different provocative environments; (b) correlate susceptibility with vestibular and non-vestibular response parameters, the latter including behavioral, hemodynamic and biochemical factors and (c) correlate susceptibility with rate of acquisition and length of retention of sensory adaptation. Controlled studies are also being performed during parabolic flight as a means of attempting to validate predictive tests for susceptibility to this syndrome. Research to develop new or improved countermeasures for space motion sickness is underway in two primary areas. One of these involves anti-motion sickness drugs. Significant achievements have been realized with regard to the identification of new highly efficacious drug combinations, dose levels and routes of administration. Although pronounced individual variations must be accounted for in selecting the optimum drug and dose level, combinations of promethazine plus ephedrine or scopolamine plus dexidrine are presently the drugs of choice. Work is also underway to identify side effects associated with anti-motion sickness drug use and to identify new drugs which may selectively modify activity in central neural pathways involved in motion sickness. In addition to research on drugs, efforts are being made to develop practical vestibular training methods. Variables which influence rate of acquisition of adaptation, length of retention of adaptation and transfer of protective adaptation to new environments are being evaluated. Also, included in this area is the use of biofeedback and autogenic therapy to train individuals to regulate autonomic responses associated with motion sickness. While valuable new knowledge is expected to evolve from these combined research programs, it is concluded that the final validation of predictive tests and countermeasures will require a series of controlled space flight experiments.

Adaptation, Physiological↗

PubMed1991

Non-adrenergic, non-cholinergic nervous system and overnight airway calibre in asthmatic and normal subjects.

Increased parasympathetic tone does not fully explain the night-time bronchoconstriction responsible for nocturnal cough and wheezing in asthmatic subjects. The overnight variation in function of the other neural pathway innervating bronchial smooth muscle--the non-adrenergic, non-cholinergic (NANC) system--was thus examined. NANC function was tested after parasympathetic and beta-adrenergic blockade in 12 normal subjects and 12 patients with mild asthma by comparing the bronchodilator effect (measured as oscillatory resistance, Ros) of capsaicin (an NANC stimulant) at 0400 h with that at 1600 h. The order in which capsaicin or diluent was given was randomised, and observers were blind as to which substance had been inhaled. Bronchodilatation was greater at 1600 h than at 0400 h in both the normal subjects (mean decrease in Ros 1-3 min after capsaicin at 1600 h 9% [SEM 1], at 0400 h -2% [1]; p less than 0.001) and the asthmatic group (1% [1], -7% [2]; p = 0.001). The results suggest that inhibition of NANC function in the early morning may contribute to overnight bronchoconstriction.

Adult↗

PubMed1993

Regional content of enteric substance P and vasoactive intestinal peptide during intestinal inflammation in the parasitized ferret.

Our aim was to characterize and quantitate changes in two key neuropeptides, substance P (SP) and vasoactive intestinal peptide (VIP), that are involved in governing neurally-mediated gastrointestinal (GI) reflex activity during enteric inflammation in the ferret. Neuropeptide content was determined by radioimmunoassay of extracts of jejunal, ileal and colonic muscularis externa from uninfected ferrets and ferrets infected with enteric stages of the parasitic nematode, Trichinella spiralis. Increased myeloperoxidase activity (MPO), an enzymatic marker of inflammation, occurred in all three gut regions. Histopathological changes were present only in the small intestine. Significant reductions were detected in both SP (72% decrease) and VIP (62% decrease) in the inflamed jejunum. Ileal concentrations of both SP (77% decrease) and VIP (46% decrease) were also decreased during T. spiralis infection compared to uninfected ferrets. Only SP (58% decrease) concentration showed a significant change in colonic tissues from infected ferrets; colonic VIP was unaltered. Parasite-induced inflammation caused significant changes in peptide-containing enteric neural pathways and might contribute to functional GI motor disturbances that occur during nematode infections in mammalian hosts.

Animals↗

PubMed1995

Altered neuropeptide content and cholinergic enzymatic activity in the inflamed guinea pig jejunum during parasitism.

We investigated the effects of an enteric infection with the parasitic nematode, Trichinella spiralis, on peptidergic and cholinergic neural pathways of the guinea pig jejunum. The content of the enteric neuropeptides, substance P (SP) and vasoactive intestinal peptide (VIP), and the activities of the key cholinergic enzymes, acetylcholinesterase (AChE) and choline acetyltransferase (ChAT), were measured and compared in extracts of jejunal muscularis externa (ME) obtained from uninfected jejunum and T. spiralis-inflamed jejunum. Significant decreases were detected in both SP immunoreactivity and AChE activity on days 6 and 10 postinfection (PI) in nematode-infected guinea pig jejunum compared to uninfected controls. The maximum changes observed for SP and AChE both occurred on day 10 PI and were evident as decreases of 37% and 48%, respectively, from the mean uninfected control values for SP and AChE. In contrast, VIP immunoreactivity and ChAT activity showed no significant changes during the enteric phase of T. spiralis infection. Nematode-evoked histopathological changes in jejunal tissues from infected animals were associated with significant increases in myeloperoxidase (MPO) activity, an index of inflammation intensity, which occurred on day 6 PI (885% of mean control) and day 10 PI (469% of mean control) coinciding temporally with the significant decrease in SP content and AChE activity during infection. Thus, intestinal motor disturbances observed in mammalian hosts during enteric nematode infections involve inflammation-generated changes in the neurohumoral control of smooth muscle function.

Acetylcholinesterase↗

PubMed1982

Circulating opioids: possible physiological roles in central nervous function.

Evidence is reviewed regarding the release of endorphins by such diverse conditions as stress, long distance running, acupuncture, sexual activity, suggestion and ritualistic dancing ceremonies. Additional evidence is cited regarding possible physiological roles of endorphins in antinociception, socialization, euphoria, some mental disorders, drive states and vegetative functions. The concentration of this latter type of evidence is on conditions during which endorphins seem to be exerting effects on a number of different systems together (for example, euphoria is almost always accompanied by analgesia), and the possibility is suggested that the activation of a number of functions together may be due to a global activation of opiate receptors throughout the CNS. A possible basis for this global activation arises from results from this laboratory indicating the presence of a blood-borne opioid hormone, secreted by the pituitary or by an endocrine gland under pituitary control, which is capable of passing from the blood into the CNS. This diffuse endorphinergic system, which is complementary to the well-established endorphinergic neuronal systems in the CNS, thus derives its property of global action on opiate receptors by the diffuse means by which the hormone reaches its target sites, i.e., by passing through the blood brain barrier. Thus, while each specific endorphin-mediated function can be activated by the activation of its respective neural pathway, it is proposed that the hormonal endorphinergic mechanism is activated to produce a global response provoked by conditions to which a more generalized response, including physiological and behavioural changes, is most appropriate.

Animals↗

PubMedDate not supplied

Role of vesical afferent nerve fibres involved in the control of internal anal sphincter motility.

The neural pathways involved in the interactions between urinary bladder and internal anal sphincter (IAS) were studied in anaesthetized spinal cats. Activation of vesical afferents produced in the IAS a reflex increase in the electrical activity and a reflex inhibition of the excitatory responses evoked by stimulation of one hypogastric nerve. Both reflexes are achieved partly in the lumbar spinal cord and partly within the inferior mesenteric ganglion.

Anal Canal↗

PubMed1985

The ventromedial hypothalamic area and the vagus are neural substrates for anticipatory insulin release.

It has been clearly demonstrated in a number of animal species including man, that insulin secretion can occur in response to sensory stimuli associated with meal taking and in advance of any ingestional rise in blood nutrients. The neural basis of this anticipatory insulin rise is poorly delineated and was therefore investigated in two experiments. In the first, rats with electrolytic lesions of the ventromedial hypothalamic area (VMH), or sham lesions were assessed and in the second experiment rats with bilateral subdiaphragmatic vagotomies or sham vagotomies were studied. In both experiments rats with jugular cannulae were conditioned to expect a meal 5 min following the beginning of a complex (light, tone and odor) stimulus. On the test trial the stimulus was given but no meal was forthcoming. Blood was sampled via the jugular catheter before and during the stimulus presentation. In both experiments the control rats showed a significant insulin rise during the stimulus presentation. However, neither the VMH-lesioned nor the vagotomized rats showed any significant change in insulin levels. The results clearly demonstrate an insulin rise to a complex sensory stimulus which has been paired with food and further show the dependence of that response on the integrity of the hypothalamic-vagal-visceral neural pathway. It is suggested that the VMH receives meal-associated sensory input and employs that information to prepare the animal metabolically for incoming nutrients. One aspect of this anticipatory mechanism is a vagally mediated insulin secretion.

Animals↗

PubMed1994

Anal and rectal motility responses to distension of the urinary bladder in the cat.

The neural pathways and possible transmission mechanisms of the integrated autonomic nervous control of the urinary bladder and anorectum, were investigated in chloralose anaesthetized cats. Bladder distension and spontaneous detrusor contractions increased internal anal sphincter-tone, a response which was blocked by an alpha-adrenoceptor antagonist. Moreover, a nicotinic transmission step was present. Both the afferent and efferent limbs of the reflex were conveyed in the postganglionic hypogastric nerves and the preganglionic lumbar splanchnic nerves. Intact connection with the central nervous system was therefore essential. Contrasting to the specific reflex response in the internal anal sphincter, bladder distension also elicited a nociceptive vaso-pressor response. Rectal motility appeared to be unaffected by bladder distension.

Adrenal Glands↗

PubMed1995

Neural control of penile erection in the rat.

The role of autonomic and somatic neural pathways involved in the control of penile erectile tissue was investigated in an in vivo rat model. Intracavernous pressure (ICP) changes were recorded during single or combined electrical stimulation of peripheral nerves in anesthetized rats. Stimulation of the pelvic and cavernous nerves elicited similar ICP increases. Ganglionic blockade abolished the response to pelvic nerve stimulation. Stimulation of the hypogastric nerve, the sensory or motor branches of the pudendal nerve, or the paravertebral sympathetic chain at L4-L5 by themselves did not produce any change in ICP. Stimulation of some of these nerves caused changes in ICP when combined with cavernous nerve stimulation. Stimulation of the paravertebral sympathetic chain reduced the ICP increases elicited by cavernous nerve stimulation. A decrease in ICP in response to cavernous nerve stimulation was also elicited by stimulation of the peripheral cut end of the sensory branch of the pudendal nerve or in paralyzed rats, the motor branch of the pudendal nerve. After sectioning the two branches of the pudendal nerve, stimulation of the sympathetic chain still reduced the ICP increase in response to cavernous nerve stimulation. Stimulation of the motor branch of the pudendal nerve during erection elicited by cavernous nerve stimulation was responsible for an additional ICP increase, which reached suprasystolic values. The present study confirms a proerectile role for parasympathetic pathways. Sympathetic fibers conveyed in both branches of the pudendal nerve exert an antierectile role in the rat. We identified an antierectile sympathetic outflow, originating in the caudal sympathetic chain, the anatomical arrangement of which remains unknown. In this model, penile erection appeared to be dependent on the recruitment of sacral parasympathetic outflow. Additional recruitment of efferent somatic fibers present in the motor branch of the pudendal nerve could participate in more rigid erection. This study provides new information about the organization of the pathways through which the rat penis is innervated, and would be of interest to investigators in the field of male sexual function.

Anesthesia↗

PubMed1987

Early ontogeny of kappa-opioid receptor regulation of prolactin secretion in the rat.

Although both mu- and kappa-opioid components of prolactin (PRL) secretion have been identified in the adult rat, the neural pathways through which these multiple receptor subtypes modulate PRL secretion have not been thoroughly investigated. The present study utilizes the differential ontogeny of opioid systems which alter PRL release to examine the mechanisms by which mu- and kappa-receptors regulate prolactin. The responses of PRL, corticosterone and growth hormone to opioid receptor subtype-specific agonists were studied in neonatal rats. The PRL response to the kappa-agonist, U50488, preceded the response to the mu-agonist, morphiceptin. Like adults, neonates demonstrated a growth hormone, but not a PRL, response to the delta agonist, [D-pen2,pen5]enkephalin. U50488-induced PRL secretion was not attenuated by cyproheptadine in adults or neonates, suggesting that the kappa-opioid mechanism operates independently of serotonin. In contrast, the PRL response to morphine was attenuated in adult rats. In addition, U50488 decreased median eminence dopamine synthesis in both adults and neonates. These findings suggest that the early developing, serotonin-independent opioid regulation of PRL is mediated through kappa-receptors, while the later-developing mechanism which requires intact serotonergic transmission works through mu-receptors. kappa-Receptors appear to regulate PRL secretion by directly inhibiting the activity of tuberoinfundibular dopamine neurons, while mu-receptors might regulate the tonic dopaminergic inhibition of PRL through a serotonergic pathway.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1989

Direct in utero perception of light by the mammalian fetus.

The primary neural pathway for entrainment of circadian rhythms in rodents is the retinohypothalamic tract, which conveys lighting information from the retina to a biological clock in the hypothalamic suprachiasmatic nuclei (SCN). In a precocious rodent species, the spiny mouse, the retinohypothalamic tract is present and functioning within the SCN on the day of birth, as assessed by HRP histochemistry and 14C-labeled 2-deoxyglucose autoradiography, respectively. Furthermore, direct perception of environmental lighting was observed in fetal spiny mice late in gestation. Direct, retina-mediated fetal light perception appears to be a less potent entraining agent than maternal cues communicating time-of-day information to the fetal spiny mouse. Nevertheless, direct fetal light perception may reinforce maternal entraining signals during the prenatal period and therefore be of physiological significance for entrainment of circadian rhythmicity in the fetus.

Animals↗

PubMed1987

Suppression of the immune response by benzodiazepine receptor inverse agonists.

24 h after administration of a single dose of the benzodiazepine receptor inverse agonists N'-methyl-beta-carboline-3-carboxamide (FG 7142) and 3-carbomethoxy-4-ethyl-6,7-dimethoxy-beta-carboline (DMCM), a profound suppression of the immune response was observed in rodents. This immunosuppression was manifest as a decrease in phytohemagglutinin (PHA) and concanavalin-A (Con-A) stimulated T cell proliferation in rats and mice administered FG 7142 and a decrease in allogeneic cytotoxic T lymphocyte activity in mice administered either FG 7142 or DMCM. The effects of FG 7142 were antagonized by the prior administration of Ro 15-1788, a benzodiazepine receptor antagonist. These findings demonstrate that the neural pathways subserved by benzodiazepine receptors can modulate immune function, and suggest that these receptors may be involved in the stress-induced modulation of immune function.

Animals↗