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PubMed2004

Neural pathways controlling central and peripheral oxytocin release during stress.

Oxytocin is released from the pituitary gland in response to a variety of stressful stimuli, including noxious stimuli, conditioned fear and exposure to novel environments. These responses are believed to be mediated, at least in part, by noradrenergic projections from the medulla oblongata, and some of these noradrenergic neurones also contain prolactin-releasing peptide (PrRP). Central administration of either PrRP or noradrenaline stimulates oxytocin secretion into the circulation. Stressful stimuli activate PrRP-containing noradrenergic neurones in the medulla oblongata, and it is thus possible that PrRP/noradrenergic projections to the hypothalamus mediate oxytocin responses to stressful stimuli. Here, the roles of brainstem PrRP/noradrenergic projections to the hypothalamus in oxytocin responses to different kinds of stressful stimuli are reviewed, with a particular emphasis on conditioned fear. Roles of dendritic oxytocin release during stress and metabolic factors affecting stress pathways are also discussed.

Animals↗
PubMed2006

Behavioral motifs and neural pathways coordinating O2 responses and aggregation in C. elegans.

BACKGROUND: Simple stimuli can evoke complex behavioral responses coordinated by multiple neural circuits. O(2) is an important environmental variable for most animals. The nematode C. elegans avoids high O(2), and O(2) levels regulate its foraging and aggregation. RESULTS: Here, we dissect aggregation and responses to O(2) gradients into behavioral motifs and show how O(2) responses can promote aggregation. To remain in a group, C. elegans continually modify their movement. Animals whose heads emerge from a group will reverse or turn, thereby returning to the group. Re-entry inhibits further reversal, aiding retention in the group. If an animal's tail exits a group during a reversal, it switches to forward movement, returning to the group. Aggregating C. elegans locally deplete O(2). The rise in O(2) levels experienced by animals leaving a group induces both reversal and turning. Conversely, the fall in O(2) encountered when entering a clump suppresses reversal, turning, and high locomotory activity. The soluble guanylate cyclases GCY-35 and GCY-36, which are expressed in head and tail neurons, promote reversal and turning when O(2) rises. Avoidance of high O(2) is also promoted by the TRP-related channel subunits OCR-2 and OSM-9, and the transmembrane protein ODR-4, acting in the nociceptive neurons ASH and ADL. Both O(2) responsiveness and aggregation can be modified by starvation, but this is regulated by natural variation in the npr-1 neuropeptide receptor. CONCLUSIONS: Our work provides insights into how a complex behavior emerges from simpler behavioral motifs coordinated by a distributed circuit.

Animals↗
PubMed1981

Neural pathways involved in the hypothalamic integration of autonomic responses.

Recent mapping studies of hypothalamic and autonomic mechanisms have considerably extended our understanding of the anatomy of this system. The pattern of connections emerging from physiological, anatomical, and histochemical experiments suggests several conclusions about the functional organization of the system as well. Recent evidence supports the idea that the hypothalamic (and other limbic) areas involved in the control of ingestion and metabolism form the rostral pole of a longitudinally and hierarchically organized system that elaborates autonomic responses that influence the energy economy of the animal. Substantially the same pathways are apparently responsible for the modulation of ingestive behavior as well. This circuitry, the "visceromotor system" in Nauta's terminology, seems to weld afferent inputs, particularly those of the gustatory and visceral receptors, into a coordinated integrative control strategy influencing autonomic responses. In addition, the system seems to have unique tissue properties, at least at its two periventricularly located sites of integration with special access to both humorally and ventricularly circulated substrates. These nodes, the basomedial hypothalamus and the vagal complex of the medulla, seem to share similar biochemical specializations reflected in susceptibility to goldthioglucose toxicity, specific insulin binding, and susceptibility to alloxan diabetes.

Afferent Pathways↗
PubMed1978

Neural pathways common to vestibular and optokinetic eye movements.

To determine how vestibular and optokinetic eye movement signals share the central oculomotor neural organization, optokinetic afternystagmus was superposed on vestibular nystagmus in the monkey. To a first approximation there was algebraic additivity in the velocity domain. This result suggests that vestibular and optokinetic eye movements are integrated at a level of neural organization above the ocular motoneurons, at a level in which neural signals are coded in terms of eye movement velocity rather than eye position.

Animals↗
PubMed1990

[The neural pathway from nucleus accumbens to amygdala in morphine analgesia of the rabbit].

The purpose of this study was to explore possible neural connections between the nucleus accumbens and amygdala involved in analgesia. The latency of the escape response elicited by radiant heat applied on snout of the rabbit was taken as an index for nociception. It was found that: (1) the analgesic effect elicited by intra-accumbens injection of morphine was attenuated dose-dependently by intra-amygdala administration of opioid antagonist naloxone, or antisera against met-enkephalin (ME) or beta-endorphin (beta-EP), suggesting the involvement of ME and beta-EP in the accumbens-amygdala connection; (2) the analgesia produced by intra-amygdaloid injection of morphine was not affected by naloxone administered to nucleus accumbens, suggesting a one-way connection between the two nuclei; (3) the analgesia of intra-accumbens injection of morphine was significantly attenuated by muscimol, the GABA receptor agonist, and enhanced by bicuculline methochloride, the GABA receptor antagonist injected into the same site where morphine was administered. The results suggest that the analgesic effect of morphine administered to the nucleus accumbens is mediated by the suppression of the GABAergic inhibitory neurons located within the nucleus.

Amygdala↗
PubMed2005

Subthalamic neurons coordinate basal ganglia function through differential neural pathways.

The subthalamic nucleus (STN) is a key component of basal ganglia circuitry that mediates a variety of motor functions. The STN neurons send glutamatergic projections to the output structures of basal ganglia, including the substantia nigra pars reticulata (SNr) and the entopeduncular nucleus, and also innervate the globus pallidus (GP). However, the mechanism by which the STN regulates motor functions in the neural circuitry is not fully understood. Here we performed conditional ablation of the STN neurons by using immunotoxin-mediated cell targeting. We then analyzed dopamine (DA)-mediated motor behavior and firing activity of the SNr and GP neurons. Ablation of the STN neurons increased spontaneous movement and reduced hyperactivity in response to DA stimulation. Ablation of these neurons modulated the pattern and rate of spontaneous firing of the SNr neurons, although it did not substantially affect spontaneous firing of the GP neurons. The ablation attenuated DA-induced suppression of the firing rate of the SNr neurons and inhibited DA-induced elevation of the rate of the GP neurons. In addition, pharmacological blockade of GP activation in response to DA stimulation inhibited the suppression of SNr activity and the resultant motor activation. These results suggest that the STN neurons suppress spontaneous behavior through their direct projection to the output neurons and that, in response to DA, they contribute to expression of behavior by acting on the output neurons mainly through the GP-mediated pathways. We conclude that the STN coordinates motor behavior through differential neural pathways depending on the state of DA transmission.

Action Potentials↗
PubMed1985

Retrograde tracing of neural pathways with a protein gold complex. II. Electron microscopic demonstration of projections and collaterals.

This paper describes a sensitive method for tracing neural connections at the electron microscopic (EM) level using a new compound produced through the coupling of colloidal gold particles to a wheat germ agglutinin horseradish peroxidase conjugate (the WGA*HRP-gold complex). Visualization of retrogradely labeled cells at the EM level was achieved either directly by gold particles scanning or after silver enhancement. By using different sizes of gold particles individually coupled to WGA*HRP and injected in different brain areas EM detection of multiple retrograde labeling was possible. Thus retrogradely labeled cells were first identified at the light microscopic level through HRP histochemistry with tetramethylbenzidine as a chromogen and then examined under the electron microscope after osmication and embedding. Gold particles were readily identified as electron dense, round dots in spherical grey vesicles. Identification of different sizes of gold particles often localized in the same vesicle established that the protein-gold complex can be used to study collateralisation of parental axons.

Animals↗
PubMed2006

Brain Fos expression during 48 h after cisplatin treatment: neural pathways for acute and delayed visceral sickness.

Cancer chemotherapy drugs, such as cisplatin, are extremely potent for producing nausea and vomiting. The acute effects of these treatments are partly controlled using anti-emetic drugs, but the delayed effects (>24 h), especially nausea, are much more difficult to treat. Furthermore, cisplatin induces a long-term (up to 48 h) increase in pica in rats. Pica is manifested as an increase in consumption of kaolin (clay) and is used as a measure of visceral sickness. It is unknown what brain pathways might be responsible for this sickness associated behavior. As a first attempt to define this neural system, rats were injected (i.p.) with 3, 6, or 10 mg/kg cisplatin (doses reported to produce pica) and sacrificed at 6, 24, or 48 h to determine brain Fos expression. The primary results indicate: 1) increasing the dose of cisplatin increased the magnitude and duration of brain Fos expression, 2) most excitatory effects on hindbrain nucleus of the solitary tract (NTS) and area postrema (AP) Fos expression occurred within 24 h after cisplatin injection, 3) 6 and 10 mg/kg cisplatin treatment produced large increases in Fos expression in the central amygdala (CeA) and bed nucleus of the stria terminalis (BNST), including 48 h after injection, and 4) cisplatin treatment produced little effect on Fos expression in the paraventricular and supraoptic nuclei of the hypothalamus. These results indicate that cisplatin activates a neural system that includes the dorsal vagal complex (NTS and AP), CeA, and BNST.

Animals↗
PubMed2001

Is the recovery of stepping following spinal cord injury mediated by modifying existing neural pathways or by generating new pathways? A perspective.

The recovery of stepping ability following a spinal cord injury may be achieved by restoring anatomical connectivity within the spinal cord. However, studies of locomotor recovery in animals with complete spinal cord transection suggest that the adult mammalian spinal cord can acquire the ability to generate stepping after all descending input is eliminated and in the absence of neuronal regeneration. Moreover, rehabilitative gait training has been shown to play a crucial role in teaching existing spinal pathways to generate locomotion and appropriately respond to sensory feedback. This brief review presents evidence that neural networks in the mammalian spinal cord can be modulated pharmacologically and/or with task-specific behavioral training to generate weight-bearing stepping after a spinal injury. Further, the role that spinal learning can play in the management of humans with spinal cord injury is discussed in relation to interventions that are designed primarily to enhance neuronal regeneration.

Animals↗
PubMed2006

Task-guided selection of the dual neural pathways for reading.

The visual perception of words is known to activate the auditory representation of their spoken forms automatically. We examined the neural mechanism for this phonological activation using transcranial magnetic stimulation (TMS) with a masked priming paradigm. The stimulation sites (left superior temporal gyrus [L-STG] and inferior parietal lobe [L-IPL]), modality of targets (visual and auditory), and task (pronunciation and lexical decision) were manipulated independently. For both within- and cross-modal conditions, the repetition priming during pronunciation was eliminated when TMS was applied to the L-IPL, but not when applied to the L-STG, whereas the priming during lexical decision was eliminated when the L-STG, but not the L-IPL, was stimulated. The observed double dissociation suggests that the conscious task instruction modulates the stimulus-driven activation of the lateral temporal cortex for lexico-phonological activation and the inferior parietal cortex for spoken word production, and thereby engages a different neural network for generating the appropriate behavioral response.

Acoustic Stimulation↗