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At least 181 records · Page 10Linked to original sources

PubMed1974

Neural pathways from thalamus associated with regulation of aggressive behavior.

Small electrolytic lesions were made through electrodes in the thalamus of cats at sites where electrical stimulation elicited attack on a rat. Staining by modified Nauta reduced silver methods revealed that significant degeneration passed caudally from the lesions and entered the midbrain dorsal central gray region. Electrical stimulation of this dorsal midbrain region elicited attack on a rat, and destruction of this region suppressed the attack elicited by thalamic stimulation.

Aggression↗

PubMed1975

Mapping of functional neural pathways by autoradiographic survey of local metabolic rate with (14C)deoxyglucose.

An enzymatic preparation from human brain converts tryptamine to tryptoline (9H-1,2,3,4-tetrahydropyrido(3,4-b)indole) in the presence of 5-methyltetrahydrofolic acid. Similarly, N-methyltryptamine and 5-hydroxytryptamine yield 1-methyltryptoline and 5-hydroxytryptoline, respectively. Neither in vitro nor in vivo formation of these compounds by human tissues has been described.

Animals↗

PubMed2004

Activation of neural pathways associated with sexual arousal in non-human primates.

PURPOSE: To evaluate brain activity associated with sexual arousal, fully conscious male marmoset monkeys were imaged during presentation of odors that naturally elicit high levels of sexual activity and sexual motivation. MATERIAL AND METHODS: Male monkeys were lightly anesthetized, secured in a head and body restrainer with a built-in birdcage resonator and positioned in a 9.4-Tesla spectrometer. When fully conscious, monkeys were presented with the odors of a novel receptive female or an ovariectomized monkey. Both odors were presented during an imaging trial and the presentation of odors was counterbalanced. Significant changes in both positive and negative BOLD signal were mapped and averaged. RESULTS: Periovulatory odors significantly increased positive BOLD signal in several cortical areas: the striatum, hippocampus, septum, periaqueductal gray, and cerebellum, in comparison with odors from ovariectomized monkeys. Conversely, negative BOLD signal was significantly increased in the temporal cortex, cingulate cortex, putamen, hippocampus, substantia nigra, medial preoptic area, and cerebellum with presentation of odors from ovariectomized marmosets as compared to periovulatory odors. A common neural circuit comprising the temporal and cingulate cortices, putamen, hippocampus, medial preoptic area, and cerebellum shared both the positive BOLD response to periovulatory odors and the negative BOLD response to odors of ovariectomized females. CONCLUSION: These data suggest the odor-driven enhancement and suppression of sexual arousal affect neuronal activity in many of the same general brain areas. These areas included not only those associated with sexual activity, but also areas involved in emotional processing and reward.

Animals↗

PubMed1985

Neural pathways mediating the corneal blink reflex and Bell's phenomenon in the cat.

Two central projections from the corneal representation of the sensory trigeminal complex in the cat were demonstrated with horseradish peroxidase, autoradiographic and Golgi methods: (1) to the dorsal subdivision of the ipsilateral facial nucleus that innervates the orbicularis oculi muscle; and (2) to the bordering area between the contralateral central gray matter and the oculomotor nucleus, which receives dendrites of the oculomotor cells innervating the contralateral superior rectus muscle. These two routes probably mediate early responses of the corneal blink reflex and Bell's phenomenon, respectively.

Animals↗

PubMed1997

PKA isoforms, neural pathways, and behaviour: making the connection.

In mammals, the cAMP-dependent protein kinase (PKA) family of enzymes is assembled from the products of four regulatory and two catalytic subunit genes, all of which are expressed in neurons. Specific isoforms of PKA display differences in biochemical properties and subcellular localization, but it has been difficult to ascribe specific physiological functions to any given isoform. The recent development of gene knockout and transgenic mouse models has allowed for a more integrated examination of the in vivo roles of specific PKA isoforms in gene expression, synaptic plasticity, and behaviour.

Animals↗

PubMed2000

Three novel neural pathways to the lacrimal glands of the cat: an investigation with cholera toxin B subunit as a retrograde tracer.

The distribution of ganglion neurons innervating the lacrimal gland (LG) was investigated following injection of cholera toxin B subunit into the LG of the cat. We report the first evidence that the otic ganglion (OG), and superior vagal and glossopharyngeal ganglia are also the sources of innervation of the LG. LG-innervating neurons in the pterygopalatine ganglion and the OG could be divided into two subpopulations: small and large neurons. They may mediate the vasodilatation and secretion, respectively.

Animals↗

PubMed2002

Neural pathways underlying vocal control.

Vocalization is a complex behaviour pattern, consisting of essentially three components: laryngeal activity, respiratory movements and supralaryngeal (articulatory) activity. The motoneurones controlling this behaviour are located in various nuclei in the pons (trigeminal motor nucleus), medulla (facial nucleus, nucl. ambiguus, hypoglossal nucleus) and ventral horn of the spinal cord (cervical, thoracic and lumbar region). Coordination of the different motoneurone pools is carried out by an extensive network comprising the ventrolateral parabrachial area, lateral pontine reticular formation, anterolateral and caudal medullary reticular formation, and the nucl. retroambiguus. This network has a direct access to the phonatory motoneurone pools and receives proprioceptive input from laryngeal, pulmonary and oral mechanoreceptors via the solitary tract nucleus and principal as well as spinal trigeminal nuclei. The motor-coordinating network needs a facilitatory input from the periaqueductal grey of the midbrain and laterally bordering tegmentum in order to be able to produce vocalizations. Voluntary control of vocalization, in contrast to completely innate vocal reactions, such as pain shrieking, needs the intactness of the forebrain. Voluntary control over the initiation and suppression of vocal utterances is carried out by the mediofrontal cortex (including anterior cingulate gyrus and supplementary as well as pre-supplementary motor area). Voluntary control over the acoustic structure of vocalizations is carried out by the motor cortex via pyramidal/corticobulbar as well as extrapyramidal pathways. The most important extrapyramidal pathway seems to be the connection motor cortex-putamen-substantia nigra-parvocellular reticular formation-phonatory motoneurones. The motor cortex depends upon a number of inputs for fulfilling its task. It needs a cerebellar input via the ventrolateral thalamus for allowing a smooth transition between consecutive vocal elements. It needs a proprioceptive input from the phonatory organs via nucl. ventralis posterior medialis thalami, somatosensory cortex and inferior parietal cortex. It needs an input from the ventral premotor and prefrontal cortex, including Broca's area, for motor planning of longer purposeful utterances. And it needs an input from the supplementary and pre-supplementary motor area which give rise to the motor commands executed by the motor cortex.

Animals↗

PubMed1982

Neural pathway involved in the excitation of motoneurones to jaw-opening muscles by stimulation of the orbital cerebral cortex in the cat.

The pathway and synaptic basis for the efferent discharge in the digastric nerve evoked by stimulation of the orbital cortex were studied in cats anesthetized with alpha-chloralose. Transection of the brain stem at the boundary between the pons and the medulla oblongata abolished discharge. Intracellular recording from anterior digastric motoneurones revealed that the orbital cortical stimulation evoked excitatory post-synaptic potentials with a latency that was longer by one synaptic delay than that of spike potentials evoked in medial bulbar reticular neurones making a direct excitatory projection to anterior digastric motoneurones. It was concluded that the excitatory effects was mediated by the medial bulbar reticular formation.

Animals↗

PubMed1984

Neural pathways mediating hypothalamically elicited flight behavior in the cat.

This study has sought to identify hypothalamic pathways mediating flight behavior in the cat. Flight behavior, characterized by an initial pupillary dilatation and followed by vigorous attempts to leap out of the observation chamber, was elicited primarily by electrical stimulation of the medial preoptic region and dorsomedial hypothalamus, and to a lesser extent from the perifornical region. A [14C]-2-deoxyglucose analysis was utilized to examine brain regions functionally activated by stimulation of hypothalamic sites which elicited flight behavior. In a second series of experiments, [3H]leucine injected into regions surrounding electrode tips from which flight had previously been elicited, permitted identification of pathways arising from such functionally characterized sites. We describe for the first time pathways arising from the hypothalamus which mediate flight behavior. In spite of individual variation in placement of electrodes eliciting flight, a consistent pattern of labeling was observed following injection of either [14C]-2-deoxyglucose systemically or [3H]amino acids into the hypothalamus. The primary rostral target structures receiving inputs from flight electrode sites included the nuclei of the diagonal band, bed nucleus of the stria terminalis, medial amygdaloid nucleus, lateral septal nucleus, and anterior medial preoptico-hypothalamus. Caudal to the level of stimulation, the principal target nuclei involved the centrum medianum-parafascicular complex and the midbrain central gray substance. Possible roles of these nuclear regions in organization and regulation of flight behavior is discussed.

Amygdala↗

PubMed2003

Endomorphin-1 causes synovial hypoaemia in rat knee joints via a capsaicin-sensitive neural pathway.

In joints, synthetic mu-opioids reduce inflammatory changes such as protein extravasation and associated oedema formation. However, the effect of endogenous opioid peptides on other inflammatory processes such as altered tissue blood flow has not been investigated. The present study examined the peripheral effects of the endogenous mu-opioid ligand endomorphin-1 (EM-1) on rat knee joint blood flow using laser Doppler perfusion imaging. Topical application of EM-1 (10(-16)-10(-9) mol) to exposed rat knee joints resulted in a dose-dependent increase in synovial vascular resistance with a maximum rise of 56% occurring with the 10(-9) mol dose. Destruction of unmyelinated articular afferents by capsaicin treatment completely abolished the hypoaemic effects of EM-1. These findings suggest that EM-1 acts peripherally in knee joints to decrease synovial blood flow, and this hypoaemic response is dependent on the presence of capsaicin-sensitive nerves.

Analgesics, Opioid↗

PubMed1994

Sexually dimorphic cell groups in the medial preoptic area that are essential for male sex behavior and the neural pathways needed for their effects.

The research summarized here shows that the two major cell groups of the sexually dimorphic area (SDA) of the gerbil hypothalamus are essential for male sex behavior. Bilateral cell-body lesions of either the medial or lateral SDA virtually eliminate mating in sexually experienced male gerbils given exogenous testosterone. Similar deficits occur when the SDA is bilaterally disconnected from the retrorubral field (RRF) as a result of unilateral cell-body lesions in the SDA and contralateral RRF. The A8 cells of the RRF do not account for this effect. Bilaterally disconnecting the SDA from the caudomedial part of the bed nucleus of the stria terminalis (caudal BSTm) also eliminates sexual activity. Disconnecting the SDA from the medial amygdala does not mimic this effect. Neither does disconnecting the medial amygdala from the caudal BSTm. Thus, caudal BSTm neurons that are essential for mating via connections with the SDA do not simply relay information from the medial amygdala.

Amygdala↗

PubMed1996

Involvement of NO-ergic neural pathway in reflex tracheal dilatation during bronchoconstriction in guinea pigs.

The involvement of NOergic nerve in vagal reflex-mediated tracheal dilatation during bronchoconstriction was investigated using the guinea pig in vivo tracheo-bronchi separated preparation. Inhalation of 0.01% histamine to the bronchial site induced a biphasic, vagal reflex tracheal response, i.e., constriction followed by dilatation slightly after bronchial constriction. The reflex tracheal dilatation was inhibited by 49% by local treatment of the tracheal site with 1% propranolol. The residual dilatation in the presence of atropine and propranolol was significantly inhibited by 1% oxyhemoglobin or 1% carboxy-PTIO, NO scavengers. Cyclic GMP content in the tissue of the tracheal site during the reflex tracheal dilatation significantly increased. The increase in cyclic GMP was reduced by treatment of the tracheal site with 1% N omega-nitro-L-arginine methyl ester. These results support a hypothesis that reflex tracheal dilatation during bronchoconstriction may be mediated by not only adrenergic but also NOergic nerves in guinea pigs.

Administration, Inhalation↗

PubMedDate not supplied

Molecular mechanisms and neural pathways mediating the influence of interleukin-1 on the activity of neuroendocrine CRF motoneurons in the rat.

The action of immune-system-derived cytokines to stimulate the release of corticotropin-releasing factor (CRF) from the hypothalamus and the consequent elaboration of ACTH and release of corticosteroids has provided an especially useful model to investigate the nature of the intercommunication of neuroendocrine and immunological pathways. Substantial evidence exists to support the production of cytokines, such as interleukin-1 (IL-1) alpha and beta, within the mammalian central nervous system. The mechanisms and neuronal circuitries involved in the effects of these cytokines of peripheral and central origin on the activity of neuroendocrine CRF motoneurons and the hypothalamic-pituitary-adrenal axis are described. Also included is a discussion of the influence of IL-1 on transduction signals controlling the release and the biosynthesis of CRF in the parvocellular division of the paraventricular nucleus of the hypothalamus and the relationship between these two distinct intracellular processes. The relevance of using immediate early genes as indices of neuronal activity in immune-challenged rats and the possible roles of c-fos and NGFI-B within neuroendocrine CRF motoneurons are outlined. Finally, the effects of acute immune response on neuroendocrine functions and brain neuronal activation are presented.

Animals↗

PubMed1986

Identification of the neural pathway for reinforcement of feeding when Aplysia learn that food is inedible.

Bilateral sectioning of the esophageal nerves that innervate the gut of Aplysia was found to have profound effect on response decrement to inedible food: Time to criterion for cessation of feeding was elevated, no memory of the decrement was present 24 hr after training, and motor patterning during training was altered. The parametric features of response decrement to sustained lip stimulation were examined to determine their resemblance to parameters of response decrement to inedible food after esophageal nerve sectioning. Parameters of response decrement were similar, indicating that after esophageal nerve sectioning response decrement is likely to be the result of sustained lip stimulation. Bilateral nerve sectioning had no effect on decrement due to sustained lip stimulation. Unilateral lesions and lesions of either of the two major divisions of the esophageal nerves had no effect on learning that food was inedible. The data indicate that bilateral nerve sectioning eliminates all stimuli causing negative reinforcement of feeding due to failure to consume food. Based on the data in this and the previous paper, a model is presented suggesting sites of action and mechanisms for learning that foods are edible or inedible in Aplysia.

Animals↗

PubMed1991

Splanchnic osmosensation and vasopressin: mechanisms and neural pathways.

Hypertonic (2 ml, 598 mosmol/kgH2O) solutions were infused over 4 min via a stomach tube in 12 groups (n = 5-10) of conscious rats with indwelling arterial catheters. Mean changes over 4-21 min of plasma arginine vasopressin (AVP) were 6.1 +/- 0.9 for NaCl (P less than 0.01), 9.3 +/- 3.0 for LiCl (P less than 0.01), 4.5 +/- 1.3 for sodium isethionate (P less than 0.01), 2.8 +/- 0.9 for sucrose (P less than 0.025), 3.9 +/- 2.8 for mannitol (P less than 0.01), and -0.1 +/- 0.1 (SE) pg/ml for urea. The AVP responses to NaCl and sucrose were proportional to the rate of gastrointestinal absorption of radiolabeled NaCl and sucrose, respectively. The AVP response to 598 mosmol/kgH2O NaCl was attenuated by 60.6% (P less than 0.001) in rats with lesion of the side branches of the major splanchnic nerves innervating the mesentery of the upper small intestine and the portal vein area, by 34-37% (P less than 0.05) in rats with right or left splanchnic nerve lesions, and was not affected by subdiaphragmatic vagotomy. Changes in systemic plasma osmolality were small and could not explain the AVP responses. Thus splanchnic receptors are osmosensitive, are situated in the mesentery of the upper small intestine and possibly the portal vein area, and project to the spinal cord via the right and left major splanchnic nerves.

Animals↗

PubMed2000

Inhibitory neural pathway regulating gastric emptying in rats.

The relaxation of the pylorus is one of the most important factors for promoting gastric emptying. However, the role of inhibitory neurotransmitters in the regulation of pyloric relaxation and gastric emptying remains unclear. In this study, we investigated the effects of NO biosynthesis inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME), and calcium dependent potassium channel blocker, apamin, on vagal stimulation-induced pyloric relaxation and gastric emptying in rats. Sodium nitroprusside (SNP), adenosine 5'-triphosphate (ATP), vasoactive intestinal polypeptide (VIP) and pituitary adenylate cyclase-activating peptide (PACAP) caused pyloric relaxations in a dose dependent manner in vivo. Apamin (120 microg/kg) significantly reduced ATP and PACAP-induced pyloric relaxations without affecting SNP- or VIP-induced relaxations. Vagal stimulation (10 V, 1 ms, 1-20 Hz)-induced pyloric relaxation was significantly inhibited by L-NAME (10 mg/kg). The combined administration of L-NAME and apamin almost completely abolished vagal stimulation-induced pyloric relaxation. L-NAME and apamin significantly increased spontaneous contractions in the antrum, pylorus and duodenum. Increased motility index by L-NAME and apamin was significantly higher in the pylorus and duodenum, compared to that of antrum. L-NAME and apamin significantly delayed liquid gastric emptying. These results suggest that besides NO, probably ATP and PACAP, act as inhibitory neurotransmitters in the rat pylorus and regulate gastric emptying.

Adenosine Triphosphate↗

PubMed1997

The circumventricular organs form a potential neural pathway for lactate sensitivity: implications for panic disorder.

Patients with panic disorder experience panic attacks after intravenous sodium lactate infusions by an as yet unexplained mechanism. Lactate elicits a panic-like response in rats with chronic dysfunction of GABA neurotransmission in the dorsomedial hypothalamus (DMH). The circumventricular organs, organum vasculosum lamina terminalis (OVLT) and subfornical organ (SFO), are potential sites that could detect increases in plasma lactate levels and activate the DMH. To test this, we obtained baseline heart rate (HR) and blood pressure (BP) responses to lactate infusions in rats fit with femoral arterial and venous catheters. Next, unilateral chronic injection cannulae connected to an Alzet infusion pump filled with the GABA synthesis inhibitor L-allylglycine (L-AG) were implanted into the DMH. Another chronic injection cannula was implanted into the region of the OVLT, SFO, or an adjacent control site, the median preoptic area (MePOA). These rats were tested once again with lactate infusions after injection of either artificial cerebrospinal fluid (ACSF) or tetrodotoxin (TTX) into the CVO sites. Injecting TTX into the OVLT completely blocked the lactate-induced response, whereas TTX injections into the SFO or MePOA did not. Also, direct injections of lactate (100 or 500 nl) into the OVLT elicited robust anxiety-like responses in these rats. These results suggest that the OVLT may be the primary site that detects lactate infusions, activating an anxiety-like response in a compromised DMH, and provide the first neuroanatomical basis for lactate response in panic disorder.

Allylglycine↗

PubMed1981

Neural pathways mediating basal and stress-induced secretion of luteinizing hormone, follicle-stimulating hormone, and testosterone in the rat.

Adult male rats, intact or bearing complete, anterior, or posterior hypothalamic deafferentations (CHD, AHD, or PHD, respectively) or bilateral medial forebrain bundle (MFB) lesions, were acutely exposed to visual, audiogenic, or thermal stress. Two to 30 min after stress onset, the rats were decapitated, and trunk blood was collected from serum LH, FSH, and testosterone (T) determinations. While basal serum LH levels were found to be normal in all experimental groups, FSH levels were reduced in CHD and AHD rats, and serum T concentrations were found to be 3-fold greater than control values in the AHD group. In intact animals, exposure to all modalities caused significant elevations in serum levels of both LH and T, with no effect on FSH secretion. In the CHD and AHD groups, the LH and T responses were eliminated, with the exception of the T response to heat exposure, which persisted in CHD animals. In the PHD group, the LH and T responses persisted and were, in fact, potentiated. Bilateral medial forebrain bundle lesions inhibited the LH and T responses to audiogenic and thermal, but not to visual, stimulation. These data demonstrate that 1) basal FHS, but not LH, secretion is dependent upon extrahypothalamic afferents to the medial basal hypothalamus; 2) acute neurogenic stress stimulates LH and T, but not FSH, secretion; and 3) central nervous system sites, rostral to the medial basal hypothalamus, mediate the stress-induced elevations in LH release.

Acoustic Stimulation↗