Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Efferent Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 613 records · Page 34Linked to original sources
PubMed1996

Apomorphine and dopamine D(1) receptor agonists increase the firing rates of subthalamic nucleus neurons.

The present study investigated the regulation of spontaneous neuronal activity in the subthalamic nucleus by dopamine receptors using in vivo extracellular single unit recording techniques. Subthalamic nucleus neuronal firing rates were doubled by systemic administration of the nonselective dopamine receptor agonist apomorphine. The response to apomorphine was attenuated in animals anesthetized with chloral hydrate or ketamine. The dopamine D(2)/D(3) receptor agonist quinpirole did not alter subthalamic nucleus neuronal firing rates. Firing rates were increased by the D(1) receptor agonists SKF 38393 and SKF 82958 two- to three-fold; these increases were reversed by the D(1) receptor antagonist, SCH 23390. Autoradiographic studies using [(125)I]SCH 23982 indicated that D(1) family receptors were located along the ventral edge of the subthalamic nucleus and the dorsal aspect of the cerebral peduncle. Local administration of SKF 82958 into the subthalamic nucleus doubled neuronal firing rates; these increases were reversed by systemic administration of SCH 23390. Infusion of SCH 23390 into the subthalamic nucleus prevented systemic SKF 38393 from increasing the firing rates of subthalamic nucleus neurons. These results indicate that apomorphine and D(1) receptor agonists exert an excitatory influence on subthalamic nucleus neuronal activity. In addition, the excitation induced by D(1) receptor agonists appears to be mediated, at least in part, by D(1) receptors located in the vicinity of the subthalamic nucleus. The data suggest that basal ganglia output under conditions of increased dopamine receptor stimulation is influenced by the activation of excitatory subthalamic efferent pathways, as opposed to suppression of these pathways as predicted by current models of basal ganglia function.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1983

Connections of the mesencephalic locomotor region (MLR) III. Intracellular recordings.

The responses of neurons in the area of the cat mesencephalic locomotor region (MLR) following stimulation of the entopeduncular nucleus (EN) were recorded intracellularly. At the end of each experiment a precollicular-postmamillary brainstem transection was performed and stimulation of the recording site(s) was employed to induce locomotion on a treadmill. This procedure was assumed to establish that intracellularly studied cells in the vicinity of a locomotion-inducing site were MLR neurons. About 10% of MLR neurons were found to respond to stimulation of the EN at short latencies. Stimulation of MLR efferent pathways was used to identify output neurons by antidromic activation. Very few MLR output neurons were found to receive EN projections (i.e. to respond at short latency following EN stimulation). These experiments support previous results describing a sparse projection from the EN to the MLR. This projection appears to be functionally varied (EPSP, IPSP and EPSP-IPSP responses were observed in MLR neurons following EN stimulation) and to exert its major influence on interneurons, not on output neurons, of the MLR.

Animals↗
PubMed1984

The distribution of neurons containing delta sleep-inducing peptide in the hippocampal formation.

The distribution of neurons containing immunoreactive delta sleep-inducing peptide (IDSIP) in the hippocampal formation was investigated by immunocytochemistry. For this study, thirteen antisera to the peptide were used. Three antisera were found suitable for immunocytochemistry; the remainder gave only non-specific background staining. Neurons containing IDSIP were demonstrable in the subicular cortex immediately adjacent to CA1. No specific staining was found in other parts of the hippocampal formation including the pyramidal layer of Ammon's Horn and the dentate gyrus. These three antisera also stained cells in the cerebral cortex-primarily temporal, parietal and frontal regions--as well as in the ventral forebrain, although the number of cells in each area varied somewhat with the different antisera. The presence of IDSIP in neurons which constitute the major efferent pathway of the hippocampus, as well as in areas known to be functionally related to the hippocampus, i.e., the adjacent isocortices and ventral forebrain, suggests a possible role for the peptide in the regulation of behavior.

Animals↗
PubMed1986

Oscillatory behavior in inferior olive neurons: mechanism, modulation, cell aggregates.

Inferior olive neurons, in brain slices maintained in vitro, display spontaneous, continuous oscillations of their membrane potential which are consonant with olivary rhythmic activity seen in vivo. This oscillatory behavior was studied with intracellular electrophysiological techniques. The 3-10 Hz rhythmicity of these cells from guinea pigs is tetrodotoxin resistant and dependent on a somatic calcium conductance. The oscillatory behavior can exhibit intrinsic frequency modulation and can be altered by synaptic processes. Synaptic alteration of the oscillatory behavior by afferent sources and extensive electrotonic coupling between cells in local aggregates (shown by Lucifer yellow dye-coupling) provide the substrate for a potent central pattern generator with a well established efferent pathway for control of motor functions.

Animals↗
PubMed1995

Electrophysiological analysis of midbrain periaqueductal gray influence on cardiovascular neurons in the ventrolateral medulla oblongata.

Stimulation of sites in the rostral or caudoventral periaqueductal gray (PAG) results in substantial increases in mean blood pressure (MBP) and heart rate (HR). The efferent pathways from these PAG subregions possibly include a relay in the ventrolateral medulla oblongata (VLM), where neurons involved in maintaining vasomotor tone are located. Extracellular recordings were made from 21 cardiovascular neurons in the rostral VLM (RVLM) and from 6 cardiovascular neurons in the caudal VLM (CVLM) of the rat. These neurons showed barosensitivity and cardiac rhythmicity. In addition, the activity of 54 non- cardiovascular and nonrespiratory units was recorded. Responses to electrical stimulation of sites in the (rostral or caudal) PAG were studied in 16 of the 21 cardiovascular RVLM neurons, the 6 CVLM neurons, and 46 of the 54 noncardiovascular neurons. Eight of the RVLM neurons were excited by rostral PAG stimulation; the poststimulus time histograms showed a constant latency in live units (32 +/- 3 ms). This suggests the presence of relatively direct (although not monosynaptic) excitatory pathways from the rostral PAG to cardiovascular neurons in the RVLM, consisting of slowly conducting fibers (0.2-0.3 m/s). Five RVLM neurons did not respond to rostral PAG stimulation. Three units were tested with caudal PAG stimulation: one was excited, one inhibited, and one was unresponsive. The six cardiovascular CVLM neurons did not respond to PAG stimulation. Of the 46 noncardiovascular neurons, 14 cells were excited, 7 inhibited, and 2 cells antidromically activated. These results confirm earlier findings, extending them to the rostral PAG. They supply further evidence for the influence of the PAG on the cardiovascular function-related neuronal circuitry in the VLM.

Animals↗
PubMed1987

Structural effects of short term and chronic extracochlear electrical stimulation on the guinea pig spiral organ.

To assess the effects of extracochlear electrical stimulation on cochlear structure, guinea pigs were implanted and stimulated with single middle ear electrodes either at round window or promontory sites, and their cochleae examined by transmission electron microscopy. Implanted but unstimulated, or unimplanted control animals were examined in the same way. Alternating current stimulation at the promontory for 2 h at 150 Hz, 500 microA, caused outer hair cell efferent endings to become dense and vacuolated, but no hair cells were damaged. With direct current stimulation at 500 microA for 2 h the basal regions of the stimulated cochlea were badly damaged and many outer hair cells lysed. Long term (up to 1200 h) round window stimulation at 100 or 141 Hz, 15-91 microA rms, did not cause cell death or inner hair cell damage, but basal outer hair cells and their efferent endings were badly affected in both ipsilateral and contralateral cochleae. The compound action potential of the auditory evoked response to broad band click stimuli was not altered by chronic electrical stimulation. It is concluded that chronic stimulation with the parameters used does not threaten cochlear survival, and it is proposed that the bilateral structural changes induced by chronic stimulation are caused by excessive activation of the cochlear efferent pathways.

Animals↗
PubMed1990

Absence of tonic activity of the crossed olivocochlear bundle in determining compound action potential thresholds, amplitudes and masking phenomena in anaesthetised guinea pigs with normal hearing sensitivities.

In Nembutal- or Urethane-anaesthetised guinea pigs N1 audiograms and N1 input-output functions were measured as were compound action potential (CAP) tuning curves under forward masking and simultaneous masking conditions. Then the crossed olivocochlear bundle was lesioned at the floor of the fourth ventricle and the cochlear responses were re-measured. There were never any changes in the N1 audiograms, input-output functions, or the CAP tuning curves. Thus, the crossed efferent pathways do not appear to play any tonic role in determining cochlear threshold sensitivities, selectivities or masking phenomena in anaesthetised guinea pigs with normal hearing sensitivities.

Action Potentials↗
PubMed1991

Effects of the crossed acoustic reflex on distortion-product otoacoustic emissions in awake rabbits.

Recent studies in anesthetized cats suggest that contralateral-sound stimulation acts to suppress ipsilateral neural responses via the medial olivocochlear-efferent system. Activation of this descending efferent pathway presumably influences ipsilateral outer hair cell motility and, thus, cochlear micromechanics, resulting in reduced input to auditory-nerve fibers. The principal aim of the present study was to determine if contralateral-sound stimuli influence the generation of ipsilateral distortion-product otoacoustic emissions, in the ears of awake rabbits. The results showed no effects of contralateral stimuli on these emissions that could not be attributed to the crossed acoustic middle-ear reflex. The findings further indicate that distortion-product otoacoustic emission amplitudes over a wide range of frequencies can be dramatically reduced when the middle-ear reflex is activated.

Acoustic Stimulation↗
PubMedDate not supplied

Cardiorespiratory reflex due to pulmonary J receptors stimulation by acetaldehyde in rats.

Acetaldehyde (AcH) administered intravenously or into the right ventricle induces reflex bradycardia, hypotension, and apnea in the rat. The efferent pathway for this reflex is vagal and probably secondary to pulmonary J receptors stimulation. Located between the alveoli and the pulmonary capillary, J receptors are accessible through the pulmonary circulation and the airways. For this reason, a method for indirect nebulization (IN) of AcH into the airways, that provides a continuous record of respiration without changes in intrapulmonary pressure, was developed. IN of AcH (n = 14) induced bradycardia (64 +/- 3.1%), hypotension (34 +/- 4.2%), and apnea (79%), which were blocked by vagotomy (n = 9). The latencies (s) for bradycardia (0.34 +/- 0.06), hypotension (0.68 +/- 0.11), and apnea (0.25 +/- 0.11) were significantly shorter than those obtained by the intravenous route. Three rats that did not develop apnea had an equivalent response, where both tidal volume and minute ventilation decreased about 40% and these effects were also blocked by vagotomy. Indirect nebulization of AcH allowed us to demonstrate that pulmonary J receptors are responsible for this reflex response.

Acetaldehyde↗
PubMed1995

Seizure susceptibility in immature rats with micrencephaly induced by prenatal exposure to methylazoxymethanol acetate.

The administration of the alkylating neurotoxin methylazoxymethanol acetate (MAM) to pregnant rats on day 15 of gestation induces, in the offspring, a marked micrencephaly, characterized by an impaired formation of interneurons at cortical, hippocampal and striatal levels. Since in man developmental CNS malformations are often associated with severe epileptogenic encephalopathies with seizures appearing in the first months or years of life, we have studied the development of kainic-acid- and bicuculline-induced seizures in 15- and 30-day-old rats, prenatally exposed to MAM. Compared to controls, a higher susceptibility to seizures has been found in micrencephalic rats aged 15 days, while no significant differences have been observed in those aged 30 days. It is hypothesized that the cerebral global anatomical dysgenesis caused by MAM underlies the higher seizure susceptibility shown by animals during the first periods of life. Successively, the processes of adjustment occurring between the cerebral regions affected by the neurotoxic action of MAM and the afferent and efferent pathways spared by the substance may re-establish adequate interneuronal relationships and, therefore, a normal convulsive susceptibility.

Age Factors↗
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↗
PubMed2004

Vestibulosympathetic reflex mediates the pressor response to hypergravity in conscious rats: contribution of the diencephalon.

To investigate the mechanism of arterial pressure (AP) regulation during hypergravity, the AP response to gravitational force was examined in conscious rats and the AP was found to increase, depending on the degree of gravity load induced by centrifugation. At 20 s after application of 2, 3, or 5 G, the AP increased by 9+/-2, 20+/-3, or 24+/-3 mm Hg, respectively. The AP increase during first 60 s was suppressed by vestibular lesion or pretreatment with hexamethonium, suggesting that the vestibular system and sympathetic nerve system be involved, respectively, in the afferent and efferent pathways. To further examine the central pathway of this response, Fos expression in the brain was examined after exposure to 5 G for 90 min. Intense Fos expression was seen in the medial vestibular nucleus, paraventricular hypothalamic nucleus, autonomic nuclei in the brain stem in intact rats, but not in rats with vestibular lesion. To examine the involvement of the diencephalic nuclei in this pressor response, AP was measured under hypergravity in rats with midcollicular transection. In these rats, the AP change was minimal at 2, 3, and 5 G, indicating that nuclei rostral to the transection level were involved in the pressor response. These results indicate that output from the vestibular system project to the diencephalon, and activation of diencephalic nuclei is indispensable to the pressor response via the sympathetic nerve system.

Analysis of Variance↗
PubMed2005

Effect of the acute crowding stress on the rat brown adipose tissue metabolic function.

Our previous results have shown that metabolic and thermal stressors influence interscapular brown adipose tissue (IBAT) metabolic activity by increasing oxygen consumption and, consequently, altering the toxic reactive oxygen species (ROS) production and the antioxidative system activity. Since there is not enough evidence about the effect of psychosocial stressors on these processes, we studied the effect of acute crowding stress on the IBAT and hypothalamic monoamine oxidase (MAO) activity as well as IBAT antioxidative enzymes, manganese (MnSOD), copper-zinc superoxide dismutase (CuZnSOD) and catalase (CAT), as the relevant indicators of IBAT metabolic alternations under the stress exposure and the returning of animals to control conditions. The results indicated that acute crowding stress did not change the hypothalamic and IBAT MAO activities, the generation of ROS and, consequently, the IBAT CuZnSOD and CAT activities. However, all three antioxidative enzymes were affected only after the recovery period. It seems that peripheral overheating of rats during acute crowding changes the stress nature, by becoming more thermal than psychosocial and by suppression the hypothalamic efferent pathways involved in the IBAT thermogenesis regulation. However, it seems that returning of the animals to the control conditions after the stress termination causes the reactivation of IBAT thermogenesis with tendency to normalise the body temperature.

Adipose Tissue, Brown↗
PubMed2003

Differential effects of antipsychotics on haloperidol-induced vacuous chewing movements and subcortical gene expression in the rat.

The behavioral and neurochemical effects of switching from typical to atypical medications have not been evaluated in the rodent models of tardive dyskinesia. Thus, we treated rats with haloperidol-decanoate for 12 weeks, and assessed the effects of additional treatment with olanzapine, haloperidol, clozapine, or vehicle on vacuous chewing movements and expression of transcripts for dopamine receptors, tyrosine hydroxylase, delta-opioid receptor, prodynorphin, preproenkephalin, glutamic acid decarboxylase-65 (glutamic acid decarboxylase (GAD)-65) and GAD-67 and N-methyl-D-aspartate (NMDA) receptor subunits in the striatum and its efferent pathways. Haloperidol-decanoate induced vacuous chewing movements extinguished following an additional 4 weeks of treatment with vehicle, olanzapine or haloperidol, but not clozapine. Post-treatment, vacuous chewing movements in the clozapine group were significantly higher than the vehicle, olanzapine and haloperidol groups. GAD-67 mRNA expression in the globus pallidus was decreased following additional treatment with olanzapine or haloperidol, but not clozapine. Changes in expression of other transcripts were not detected. These findings demonstrate important differences in the effects of typical and atypical antipsychotics on chronic vacuous chewing movements.

Animals↗
PubMed2004

Frequency-dependent changes in the paired-pulse index in the hippocampus of the freely moving adult male rat.

The paired-pulse index (PPI) has been widely used as a measure of modulation of cellular excitability in the hippocampal trisynaptic circuit. This paper presents a quantification of the changes in this measure of neuronal modulation as a result of the application of pulse trains having six different train frequencies (0.1, 1, 5, 8, 15, and 30 Hz) to one of the major efferent pathways to the dentate gyrus, the medial perforant path (MPP). Our findings indicate that the modulation of the first leg of the hippocampal trisynaptic circuit is dependent on the frequency of the "burst train" applied to the perforant pathway. This methodological finding is of importance to all investigators studying hippocampal plasticity via LTP or LTD approaches. The different synaptic mechanisms implicated in being responsible for the changes in the PPI are also discussed.

Afferent Pathways↗
PubMed2006

The inflammatory consequences of psychologic stress: relationship to insulin resistance, obesity, atherosclerosis and diabetes mellitus, type II.

Inflammation is frequently present in the visceral fat and vasculature in certain patients with cardiovascular disease (CVD) and/or adult onset Diabetes Mellitus Type II (NIDDM). An hypothesis is presented which argues that repeated acute or chronic psychologically stressful states may cause this inflammatory process. The mediators are the major stress hormones norepinephrine (NE) and epinephrine (E) and cortisol together with components of the renin-angiotensin system (RAS), the proinflammatory cytokines (PIC), as well as free fatty acids (ffa), the latter as a result of lipolysis of neutral fat. NE/E commence this process by activation of NF(kappa)B in macrophages, visceral fat, and endothelial cells which induces the production of toll-like receptors which, when engaged, produce a cascade of inflammatory reactions comprising the acute phase response (APR) of the innate immune system (IIS). The inflammatory process is most marked in the visceral fat depot as well as the vasculature, and is involved in the metabolic events which culminate in the insulin resistance/metabolic syndromes (IRS/MS), the components of which precede and comprise the major risk factors for CVD and NIDDM. The visceral fat has both the proclivity and capacity to undergo inflammation. It contains a rich blood and nerve supply as well as proinflammatory molecules such as interleukin 6 (IL-6), tumor necrosis factor alpha (TNFalpha), leptin, and resistin, the adipocytokines, and acute phase proteins (APP) which are activated from adipocytes and/or macrophages by sympathetic signaling. The inflammation is linked to fat accumulation. Cortisol, IL-6, angiotensin II (angio II), the enzyme 11(beta) hydroxysteroid dehydrogenase-1 and positive energy balance, the latter due to increased appetite induced by the major stress hormones, are factors which promote fat accumulation and are linked to obesity. There is also the capacity of the host to limit fat expansion. Sympathetic signaling induces TNF which stimulates the production of IL-6 and leptin from adipocytes; these molecules promote lipolysis and ffa fluxes from adipocytes. Moreover, catecholamines and certain PIC inhibit lipoprotein lipase, a fat synthesizing enzyme. The brain also participates in the regulation of fat cell mass; it is informed of fat depot mass by molecules such as leptin and ffa. Leptin stimulates corticotrophin releasing hormone in the brain which stimulates the SNS and HPA axes, i.e. the stress response. Also, ffa through portal signaling from the liver evoke a similar stress response which, like the response to psychologic stress, evokes an innate immune response (IIR), tending to limit fat expansion, which culminates in inflammatory cascades, the IRS-MS, obesity and disease if prolonged. Thus, the brain also has the capacity to limit fat expansion. A competition apparently exists between fat expansion and fat loss. In "western" cultures, with excessive food ingestion, obesity frequently results. The linkage of inflammation to fat metabolism is apparent since weight loss diminishes the concentration of inflammatory mediators. The linkage of stress to inflammation is all the more apparent since the efferent pathways from the brain in response to fat signals, which results in inflammation to decrease and limit fat cell mass, is the same as the response to psychologic stress, which strengthens the hypothesis presented herein.

Atherosclerosis↗
PubMed2006

Referred muscle pain is primarily peripheral in origin: the "barrier-dam" theory.

The mechanisms leading to the frequent occurrence of referred muscle pain (RP) are largely unknown. It is possible that RP is caused by the increased sensitivity of local muscle nociceptors and/or by a central sensitisation. When deep pressure by palpation is used on a subject with smooth fibrotic lesions (myofibrosis) in a muscle, RP can originate as a hyperalgesic cutaneous area, adjacent to, or totally apart from the pressure pain locus. It is currently postulated that a chain reaction is activated implicating triggering of an ever-increasing number of afferent neurons and facilitation of the synaptic connection at the level of the spinal cord, causing more distally a distributed RP via convergent efferent pathways. The human interpretation of this phenomenon can be misleading when the tested person positions, after a few seconds, his RP distally from the site of pressure to the distally located RP area. As a result of what we have found in our experimentally induced RP probes, we hypothesize that deep pressure on a myofibrosis will, in the first place, within a few seconds, increase the nociceptive excitability of the afferent sensitive nerves from the RP area to the local spot of pressure on the muscle, which in return will, in the second place, excite the whole dependent RP area. The mechanism for referred muscle pain proposed in this article is linked to the "pre-local hyper-excitability theory" or "barrier-dam theory". The afferent sensitive peripheral nerves might be entrapped in local muscle hardenings (barrier-dam) with the consequence of the hyper-excitation of pre-local nerves between the distally referred pain area and the local muscular zone of tenderness. The primary pathogenesis of referred muscle pain is likely to be a peripheral sensitization with additionally a central modulation and not vice versa. Clinical and fundamental studies with experimentally induced RP are nevertheless needed to examine the hypothesis.

Animals↗
PubMed2006

Anterograde and retrograde amnesia in a person with bilateral fornix lesions following removal of a colloid cyst.

AD, a 45-year-old man, presented with a severe and global anterograde amnesia following surgery for removal of a colloid cyst. Structural neuroimaging confirmed bilateral lesions to the fornix and a small lesion in the basal forebrain. Testing for remote episodic memory of autobiographical events, and for remote semantic memory of personal and public events, and of famous people, revealed that AD had a severe retrograde amnesia for autobiographical episodes that covered his entire lifetime, and a time-limited retrograde amnesia for semantic memory. Because the fornix and basal forebrain lesions disrupted major afferent and efferent pathways of the hippocampus, it was concluded that the integrity of the hippocampus and its projections are needed to retain and/or recover autobiographical memories no matter how old they are. By contrast, hippocampal contribution to semantic memory is time-limited. These findings were interpreted as consistent with Multiple Trace Theory, which holds that the hippocampal system is essential for recovering contextually rich memories no matter how old they are, but is not needed for recovering semantic memories.

Amnesia, Anterograde↗