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Importance of the paraventricular nucleus of the hypothalamus as a component of a neural pathway between the brain and the testes that modulates testosterone secretion independently of the pituitary.

We previously reported that in adult male rats, the intracerebroventricular (icv) injection of corticotropin-releasing factor (CRF) or the beta-adrenergic agonist isoproterenol (ISO) significantly inhibited the ability of human chorionic gonadotropin (hCG) to stimulate testosterone (T) secretion. The finding that this phenomenon also took place when LH release had been blocked with an LHRH antagonist suggested that icv CRF and ISO did not alter Leydig cell function by influencing the activity of pituitary gonadotrophs. We therefore proposed the existence of a neural pathway connecting the brain to the testes, whose activation by icv CRF or ISO interfered with T secretion. Based on the intratesticular injection of the transganglionic tracer pseudorabies virus, we recently identified the paraventricular nucleus (PVN) of the hypothalamus as a component of this neural link. The aim of the present work was to investigate the functional role of this brain area in mediating the ability of CRF and ISO to inhibit the ability of hCG to stimulate T secretion. We first demonstrated that local microinfusion of CRF or ISO directly into the PVN mimicked the effect of their icv injection, suggesting that the PVN does indeed represent a site of action of ISO and CRF in altering Leydig cell responsiveness to gonadotropin. In contrast, neither CRF nor ISO microinfusion into the central amygdala or the frontal cortex influenced hCG-stimulated T secretion. To further investigate the role of the PVN in ISO- and CRF-induced blunting of hCG stimulation of T, we determined the effect of icv CRF or ISO on testicular activity of rats with electrolytic lesions of the PVN. These lesions, which did not in themselves influence Leydig cell responsiveness to hCG, blocked the effect of both icv ISO and CRF on hCG-induced T release. Collectively, these results support the hypothesis that CRF- and ISO-induced activation of cells in the area of the PVN decreases the ability of gonadotropin to release T and suggests that this nucleus represents an important site of the proposed neural connection between the brain and the testes.

Adrenergic beta-Agonists↗

Differentiation of the neural pathways mediating cortically induced and dopaminergic activation of the central pattern generator (CPG) for rhythmical jaw movements in the anesthetized guinea pig.

The central pattern generator (CPG) for rhythmical jaw movements (RJMs) was activated, in the anesthetized guinea pig, by systemic injection of a specific dopamine agonist, apomorphine (APO). It was shown that APO induced RJMs required an intact superior colliculus, and were blocked by low doses (0.05-1.0 mg/kg) of haloperidol (HAL), a dopamine antagonist. This is in contrast to the neural pathways mediating RJMs evoked by repetitive electrical stimulation of the masticatory cortex which remained effective following both lesions of the superior colliculus and administration of HAL. These results suggest that there are at least two anatomically separate and pharmacologically distinct command centers for activation of the CPG for RJMs in the guinea pig.

Animals↗

Specification of distinct dopaminergic neural pathways: roles of the Eph family receptor EphB1 and ligand ephrin-B2.

Dopaminergic neurons in the substantia nigra and ventral tegmental area project to the caudate putamen and nucleus accumbens/olfactory tubercle, respectively, constituting mesostriatal and mesolimbic pathways. The molecular signals that confer target specificity of different dopaminergic neurons are not known. We now report that EphB1 and ephrin-B2, a receptor and ligand of the Eph family, are candidate guidance molecules for the development of these distinct pathways. EphB1 and ephrin-B2 are expressed in complementary patterns in the midbrain dopaminergic neurons and their targets, and the ligand specifically inhibits the growth of neurites and induces the cell loss of substantia nigra, but not ventral tegmental, dopaminergic neurons. These studies suggest that the ligand-receptor pair may contribute to the establishment of distinct neural pathways by selectively inhibiting the neurite outgrowth and cell survival of mistargeted neurons. In addition, we show that ephrin-B2 expression is upregulated by cocaine and amphetamine in adult mice, suggesting that ephrin-B2/EphB1 interaction may play a role in drug-induced plasticity in adults as well.

Animals↗

The central neural pathways involved in micturition in the neonatal rat as revealed by the injection of pseudorabies virus into the urinary bladder.

Pseudorabies virus was injected into the wall of the urinary bladder in 2- and 12-day-old rats in order to examine developmental changes in the central neural pathways controlling micturition. Forty-eight hours after virus injection, virus-labeled neurons were identified in the lumbosacral spinal cord but not in the brain. Sixty to seventy-two hours after virus injection in both 2- and 12-day-old rats, infected neurons were detected in Barrington's nucleus, nucleus paragigantocellularis, nucleus reticularis gigantocellularis, A5 area, nucleus raphe obscurus, locus subcoeruleus, periaquaductal gray, red nucleus, paraventricular nucleus and cerebral cortex. These results in neonatal rats are similar to those reported in adult rats. Thus, it is likely that the supraspinal neural circuitry which underlies micturition in the adult animal is already organized in the neonatal rat during the early postnatal period even though the supraspinal micturition reflex pathway does not become functional until the third postnatal week.

Aging↗

Construction of a model demonstrating neural pathways and reflex arcs.

Employment opportunities in the future will require higher skills and an understanding of mathematics and science. As a result of the growing number of careers that require solid science and mathematics training, the methods of science education are undergoing major reform. To adequately equip students for technologically advanced positions, new teaching methods must be developed that prepare tomorrow's workforce for the challenges of the 21st century. One such method is the use of models. By actively building and manipulating concrete models that represent scientific concepts, students are involved in the most basic level of Piaget's learning scheme: the sensorimotor stage. Models are useful in reaching all students at the foundational levels of learning, and further learning experiences are rapidly moved through higher learning levels. This success ensures greater comprehension and understanding compared with the traditional methods of rote memorization. We developed an exercise for the construction of an inexpensive, easy-to-build model demonstrating neural pathways and reflex arcs. Our exercise also includes many supplemental teaching tools. The exercise is designed to fulfill the need of sound physiological teaching materials for high school students.

Animals↗

Intramural neural pathways between the duodenum and sphincter of Oddi in the Australian brush-tailed possum in vivo.

1. Balloon distension of the duodenum 2 cm oral or anal to the sphincter of Oddi-duodenal junction elevated the amplitude of spontaneous sphincter of Oddi phasic contractions by 37.7 +/- 8.5 or 120.1 +/- 79.8%, respectively (mean +/- S.E.M., both n = 6, P < 0.05, Wilcoxon test). To further investigate this response, this study aimed to determine if: (i) electrical field stimulation (EFS) of the duodenum influences sphincter of Oddi activity; (ii) intramural nerves mediate the response; and (iii) nicotinic and/or muscarinic receptors are involved. 2. Electrical field stimulation (70 V, 0.5 ms; 5-60 Hz, 10-20 s) of the duodenal anterior serosal surface 2-4 cm oral or anal to the sphincter of Oddi-duodenal junction, produced excitatory responses in the sphincter of Oddi in anaesthetized Australian brush-tailed possums (n = 45). 3. These responses were frequency dependent, maximal at 30 Hz (n = 4) and abolished by tetrodotoxin (9 micrograms kg-1 I.A.; n = 6), or by crushing the duodenum (n = 3). Hexamethonium bromide (30 mg kg-1 I.V.) did not significantly alter the response to duodenal EFS either oral (n = 6) or anal (n = 8) to the sphincter of Oddi-duodenal junction. Atropine sulphate (30 micrograms kg-1 I.V.) reduced the response to duodenal EFS oral and anal to the sphincter of Oddi-duodenal junction to 11.2 +/- 5.8 (n = 6) and 45.0 +/- 26.8% (n = 8), respectively (both P < 0.05). 4. Bilateral cervical vagotomy and guanethidine infusion (10 mg kg-1 over 15 min I.V.) did not significantly alter the responses to duodenal EFS (n = 7). 5. Excitatory intramural neural pathways between the sphincter of Oddi and the segment of duodenum 4 cm oral and anal to the sphincter of Oddi-duodenal junction have been demonstrated. These postganglionic pathways may involve muscarinic receptors.

Animals↗

Evidence for a glutamatergic neural pathway in the myenteric plexus.

The objective of this study was to determine whether L-glutamate (L-Glu) may serve as a neurotransmitter candidate in the guinea pig myenteric plexus. We observed that [3H]Glu and gamma-[3H]aminobutyric acid were synthesized from [3H]glutamine and released from neurons of the myenteric plexus during K+ and 1,1-dimethyl-4-phenylpiperazinium-evoked depolarization in a concentration-dependent manner. Muscle tension studies performed on ileal longitudinal muscle-myenteric plexus (LM-MP) preparations revealed that L-Glu [mean effective dose (ED50) 2.5 x 10(-5) M] produced concentration-dependent contractions, which were unaffected by hexamethonium but abolished by tetrodotoxin, atropine, and magnesium, suggesting that L-Glu acts via N-methyl-D-aspartate (NMDA)-type receptors that stimulate a cholinergic neural pathway unaffected by ganglionic blockade. In addition, L-Glu (ED50 4 x 10(-5) M) and NMDA (ED50 2 x 10(-4) M) stimulated concentration-dependent release of [3H]acetylcholine (ACh) from LM-MP sections, which was inhibited by tetrodotoxin, magnesium, and the NMDA receptor antagonist D-2-amino-5-phosphonovaleric acid (AP-5). L-Glu-mediated release of [3H]ACh was enhanced by theophylline (10-6 M) and 3-isobutyl-1-methylxanthine (1 mM) and was significantly reduced by the adenylate cyclase inhibitor, 2',5'-dideoxyadenosine (10(-4) M) and somatostatin-14 (10(-6) M), which inhibits adenosine 3',5'-cyclic monophosphate (cAMP)-dependent cholinergic transmission in the myenteric plexus. These studies suggest that L-Glu may serve as an excitatory neurotransmitter in the myenteric plexus via its action on NMDA-type receptors, which are coupled to cAMP-dependent release of ACh.

Acetylcholine↗

Neural pathways involved in food allergy signaling in the mouse brain: role of capsaicin-sensitive afferents.

There is increasing evidence supporting the notion that brain-gut communication is crucial for the manifestation of functional gastrointestinal (GI) disorders. Employing denervation by neonatal capsaicin treatment, we investigated here the role of unmyelinated C-fibers in food allergy signaling in the brain. We found that 90 min after oral ovalbumin (OVA) challenge, allergic mice present increased c-fos expression in emotionality-related brain areas such as the paraventricular nucleus of the hypothalamus (PVN) and the central nucleus of the amygdala (CeA). Food allergy also induced enhanced Fos immunoreactivity in the nucleus of tractus solitarii (NTS) of OVA-immunized animals. We also show that while the degree of Fos staining in the NTS of allergic mice was only diminished by neonatal capsaicin, it was completely blocked in the PVN. However, capsaicin did not modify food allergy-induced c-fos expression in the CeA. In conclusion, this study provides evidence showing that unmyelinated C-fibers are part of the neural pathways involved in food allergy-induced activation of specific brain areas, particularly the PVN and to a lesser extent the NTS.

Analysis of Variance↗

Evidence for involvement of the neural pathway containing the peripheral vagus nerve, medullary visceral zone and central amygdaloid nucleus in neuroimmunomodulation.

It is now evident that a bidirectional communication network exists between the central nervous system (CNS) and immune system (IS). However, the way in which the IS passes inform to the brain is not quite clear.In the present study, one of the neural pathways involved in the cytokine-to-brain communication was investigated in the rat. This pathway starts at the vagal nerve projecting to the medullary visceral zone (MVZ), an arc-shape band from the dorsomedial to ventrolateral area in the middle-caudal segment of the medulla oblongata, and terminates at the central amygdaloid nucleus (Ce) which receives projections from large catecholaminergic neurons in the MVZ. Animals were randomly divided into two experimental groups. Triple-labeling was used in Group I animals to combine wheat germ aggulutinin-conjugated horseradish peroxidase (WGA-HRP) retrograde tracing with anti-Fos and anti-tyrosine hydroxylase (TH) immunostaining. WGA-RP was stereotaxically injected into the unilateral Ce of the animals and, after a survival period of 48 h, intraperitoneal (IP) injection of lipopolysaccharide (LPS) was performed. Seven kinds of labeled neurons were observed in the MVZ, namely, HRP-, Fos- or TH-singly-labeled neurons; Fos/HRP-, Fos/TH- or HRP/TH-doubly-labeled neurons; and Fos/HRP/TH-triply-labeled neurons. As for Group II animals, bilateral subdiaphragmatic vagotomy (SDV) or sham operation was performed, followed 4 weeks later by IP injection of LPS. The number of Fos-positive neurons within the Ce and MVZ was significantly lower (P<0.01) in rats having SDV when compared with those receiving sham operation. Our results suggest that part of the peripheral immune information can be conveyed through the vagus to the catecholaminergic neurons in the MVZ, where it is transported to the Ce. The MVZ is a neural relay station in the immune-to-brain communication and might play a significant role in neuroimmuno-modulation via the vagus-MVZ-Ce pathway.

Amygdala↗

An intrinsic neural pathway for long intestino-intestinal inhibitory reflexes.

We studied the mechanisms of initiation and pathways for the propagation of intestino-intestinal inhibitory reflexes induced by close intraarterial injections of neostigmine in conscious dogs. Two or three T-shaped catheters were surgically implanted in the intestinal branches of the superior mesenteric artery to inject pharmacologic agents locally in 10-15-cm-long segments. Migrating myoelectric complexes were recorded by a set of 10 electrodes and strain-gauge transducers. Close intraarterial injection of neostigmine initiated strong contractions of long duration in the perfused segment that terminated phase III activity in progress 90-150 cm distal or proximal to the cannulated sites and stopped its further migration. Atropine or 4-diphenylmethoxy-N-methylpiperidine methiodide injected just before neostigmine administration through the same catheter blocked both the local contractile effects and the reflex inhibition of phase III activity. Pirenzepine or hexamethonium injected in a similar manner did not affect the local response to neostigmine but blocked the reflex inhibition of phase III activity. A transection and reanastomosis in the mid-small intestine blocked the reflex inhibition by close intraarterial injection of neostigmine beyond the transection site. Pirenzepine, atropine, or hexamethonium injected through a middle catheter also blocked the reflex inhibition of phase III activity beyond the site perfused with these cholinergic antagonists. Close intraarterial administration of 4-diphenylmethoxy-N-methylpiperidine methiodide at a middle site had no effect on reflex inhibition. We concluded that strong spasmodic contractions in the small intestine initiate an intestino-intestinal inhibitory reflex in both directions. This reflex is mediated through an intrinsic neural pathway involving nicotinic and M1 muscarinic receptors.

Animals↗

Internal vs external generation of movements: differential neural pathways involved in bimanual coordination performed in the presence or absence of augmented visual feedback.

It is commonly agreed that a functional dissociation with respect to the internal vs external control of movements exists for several brain regions. This has, however, only been tested in relation to the timing and preparation of motor responses, but not to ongoing movement control. Using functional magnetic resonance imaging (fMRI), the present study addressed the neuroanatomical substrate of the internal-external control hypothesis by comparing regional brain activation for cyclical bimanual movements performed in the presence or absence of augmented visual feedback. Subjects performed a bimanual movement pattern, either with the help of on-line visual feedback of the movements (externally guided coordination) or with the eyes closed on the basis of an internal representation of the movement pattern (internally generated coordination). Visual control and baseline rest conditions were also added. Results showed a clear functional dissociation within the network involved in movement coordination. The hMT/V5+, the superior parietal cortex, the premotor cortex, the thalamus, and cerebellar lobule VI showed higher activation levels when movements were guided by visual feedback. Conversely, the basal ganglia, the supplementary motor area, cingulate motor cortex, the inferior parietal, frontal operculum, and cerebellar lobule IV-V/dentate nucleus showed higher involvement when movements were internally generated. Consequently, the present findings suggest the existence of distinct cortico-cortical and subcortico-cortical neural pathways for externally (augmented feedback) and internally guided cyclical bimanual movements. This provides a neurophysiological account for the beneficial effect of providing augmented visual feedback to optimize movements in normal and motor disordered patients.

Adult↗

Frequency dependence of synchronization of cochlear nerve fibers in the alligator lizard: evidence for a cochlear origin of timing and non-timing neural pathways.

The dependence of synchronization of spike discharges on tone frequency was measured in cochlear nerve fibers of anesthetized alligator lizards at 21 degrees C. Synchronization measures were based on the fundamental component of a Fourier analysis of the instantaneous discharge rate in response to tone bursts. Measurements were obtained from fibers innervating hair cells in both the region of the cochlea that contains a tectorial membrane (tectorial fibers) and the region where hair-cell stereocilia are free-standing in scala media (free-standing fibers). Both rate and synchronization tuning-curves were measured automatically as a function of tone frequency. For tectorial fibers, the shapes of synchronization tuning-curves are roughly similar to the shapes of rate tuning-curves: the characteristic frequencies (CF's) of both curves are approximately equal. For free-standing fibers, the shape of synchronization tuning-curves differ markedly from those of rate tuning-curves. The CF's of synchronization and rate tuning-curves differ - the ranges are 0.2-0.6 kHz and 1-4 kHz, respectively - and the two CF's are uncorrelated. Synchronization filter-functions, which are contours of synchronization index at constant average discharge rate, were measured as a function of tone frequency for both tectorial and free-standing fibers. These synchronization filter-functions have the shapes of lowpass filters. For the populations of tectorial fibers and of free-standing fibers taken separately, these functions are independent of CF. The corner frequency of these functions is 0.50 +/- 0.038 kHz for tectorial fibers and 0.37 +/- 0.037 kHz for free-standing fibers. We conclude that these populations are characterized by different synchronization filters. For free-standing fibers, synchronization filter-functions measured at average driven discharge rates of about 20 and 40 spikes/s do not differ appreciably, and the high-frequency slope is -80 to -115 dB/decade. The results show that tectorial fibers encode timing information for low-level stimuli, whereas free-standing fibers do not. It is proposed that in the alligator lizard, neural pathways that encode timing information originate in the tectorial region and those that encode non-timing information originate in the free-standing region.

Acoustic Stimulation↗

Two neurotropic viruses, herpes simplex virus type 1 and mouse hepatitis virus, spread along different neural pathways from the main olfactory bulb.

Several neurotropic viruses enter the brain after peripheral inoculation and spread transneuronally along pathways known to be connected to the initial site of entry. In this study, the pathways utilized by two such viruses, herpes simplex virus type 1 and mouse hepatitis virus strain JHM, were compared using in situ hybridization following inoculation into either the nasal cavity or the main olfactory bulb of the mouse. The results indicate that both viruses spread to infect a unique and only partially overlapping set of connections of the main olfactory bulb. Both quantitative and qualitative differences were observed in the patterns of infection of known primary and secondary main olfactory bulb connections. Using immunohistochemistry for tyrosine hydroxylase combined with in situ hybridization, it was shown that only herpes simplex virus infected noradrenergic neurons in the locus coeruleus. In contrast, both viruses infected dopaminergic neurons in the ventral tegmental area, although mouse hepatitis virus produced a more widespread infection in the A10 group, as well as infecting A8 and A9. The results suggest that differential virus uptake in specific neurotransmitter systems contributes to the pattern of viral spread, although other factors, such as differences in access to particular synapses on infected cells and differences in the distribution of the cellular receptor for the two viruses, are also likely to be important. The data show that neural tracing with different viruses may define unique neural pathways from a site of inoculation. The data also demonstrate that two viruses can enter the brain via the olfactory system and localize to different structures, suggesting that neurological diseases involving disparate regions of the brain could be caused by different viruses, even if entry occurred at a common site.

Animals↗

Humoral versus neural pathways for fever production in rats after administration of lipopolysaccharide.

BACKGROUND: These studies address the question of the relative roles of humoral and neural pathways in the genesis and control of the fever component of the acute phase response. METHODS: Two experiments were performed to examine the effect of vagotomy (VagX) on the febrile response to intraperitoneal (i.p.) and intra-arterial (i.a.) lipopolysaccharide (LPS), and plasma cytokine and LPS concentrations after intravenous (i.v.) or i.p. injections of LPS. In experiment 1, body temperature (T(B)) was obtained from unperturbed animals by using radio transmitters and telemetry after injection of LPS i.a. or i.p. In the second study, serial blood samples were obtained for cytokine and LPS assay after injection of LPS either i.v. or i.p. Colonic temperatures (T(C)) were obtained from indwelling thermistors. RESULTS: The maximal increments in T(B) for animals receiving LPS i.a. and i.p. with or without VagX were not different from one another: sham vagotomy (Sham-VagX) + LPS i.a., 1.20 +/- 0.26 degrees C; VagX + LPS i.a., 1.23 +/- 0.64 degrees C; Sham-VagX + LPS i.p., 1.45 +/- 0.27 degrees C; VagX + LPS i.p., 1.50 +/- 0.35 degrees C (F = 1.12, p = 0.36). Neither were the four resulting response curves for T(B) different from one another. Plasma levels of LPS, tumor necrosis factor-alpha, and interleukin-6 were significantly elevated at 45 minutes after LPS injection by either the i.v. or i.p. routes, preceding any increments in T(B), and were not effected by VagX. CONCLUSION: Fever development for animals receiving LPS in experiment 1 demonstrates a temporal relationship -- with increments in plasma levels of LPS and pyrogenic cytokines obtained in experiment 2 after administration of LPS either i.p. or i.v. Vagotomy had no discernible effect on the responses regardless of the route of administration of LPS.

Acute-Phase Reaction↗

Capsaicin-sensitive neural pathway mediates atrial natriuretic factor (ANF) release in response to physiological stimuli.

Increases in intravascular volume are detected by mechanoreceptors situated at the junctions of the great veins with the atria. We had previously shown that localized distension of the superior vena caval/right atrial junction, simulating increased cardiac preload, elicits release of ANF remotely from the atrial appendage. We proposed that ANF secretion is stimulated via intrinsic neural pathways running from the venoatrial junctions to the appendage. We developed a technique whereby non-adrenergic, non-cholinergic sensory nerves could be selectively destroyed in the heart of adult rats by instilling capsaicin into the pericardial space. Four days later, the animals were killed, and isolated perfused atria were prepared with small balloons positioned so that the superior vena caval/right atrial junction could be discretely stretched. Immunoreactive ANF secretion into the perfusate was measured. Although distension of the venoatrial junction increased ANF secretion from the control atria, there was no such response in the denervated atria. We conclude (A) that local application of capsaicin to the heart of adult rats induces selective functional neural deficits and (B) that information regarding distension of the junction of the great veins and the atria is normally transmitted across the atrium via these nerves to stimulate ANF secretion from peptide stores located in the atrial appendage. We propose that these pathways are crucial to ensure appropriate ANF secretion in response to an increase in circulating blood volume.

Animals↗

Neural pathways in tactile object recognition.

OBJECTIVE: To define further the brain regions involved in tactile object recognition using functional MRI (fMRI) techniques. BACKGROUND: The neural substrates involved in tactile object recognition (TOR) have not been elucidated. Studies of nonhuman primates and humans suggest that basic motor and somatosensory mechanisms are involved at a peripheral level; however, the mechanisms of higher order object recognition have not been determined. METHODS: The authors investigated 11 normal volunteers utilizing fMRI techniques in an attempt to determine the neural pathways involved in TOR. Each individual performed a behavioral paradigm with the activated condition involving identification of objects by touch, with identification of rough/smooth as the control. RESULTS: Data suggest that in a majority of individuals, TOR involves the calcarine and extrastriatal cortex, inferior parietal lobule, inferior frontal gyrus, and superior frontal gyrus-polar region. CONCLUSIONS: TOR may utilize visual systems to access an internal object representation. The parietal cortices and inferior frontal regions may be involved in a concomitant lexical strategy of naming the object being examined. Frontal polar activation likely serves a role in visuospatial working memory or in recognizing unusual representations of objects. Overall, these findings suggest that TOR could involve a network of cortical regions subserving somatosensory, motor, visual, and, at times, lexical processing. The primary finding suggests that in this normal study population, the visual cortices may be involved in the topographic spatial processing of TOR.

Adult↗

Ascending neural pathways in the rat ileum in vitro--effect of capsaicin and involvement of nitric oxide.

The aim of the present study was to develop and characterize an in vitro model of the rat ileum in which activation of the orally projecting neural excitatory pathway of the myenteric reflex is produced by electrical field stimulation anally to the recording site. The motility of a 10-cm segment of rat ileum was recorded using a perfused manometric assembly with side holes 2 and 4 cm orally to the stimulation site. Electrical field stimulation caused a contractile response in the oral but not in the aboral direction of the stimulation site. The contractile response, which was maximal using low stimulus frequencies (3 or 5 pulses per second (pps)) and decreased with higher frequencies (10 or 20 pps), was blocked by atropine (10(-6) M) at all frequencies tested after acute and after prolonged (greater than 30 min) treatment. The maximal contractile response at 3 pps was abolished by hexamethonium (10(-4) M), tetrodotoxin (5 x 10(-7) M) and by complete transection of the muscular wall between the stimulation and the recording site. Acute administration of capsaicin (8 x 10(-7) M) to the bath reduced the lag between the start of the electrical stimulation and the onset of the contractile response. Higher concentrations of capsaicin (10(-5) M) reduced the contractile response, but this was partly due to an unspecific effect of capsaicin. Blockade of nitric oxide (NO) synthesis by L-NG-nitro-arginine-methyl ester (L-NAME) (3 x 10(-4) M) augmented the contractile response to anal stimulation by 222.4% and reduced the lag period by 54.5%, whereas the stereoisomer D-NAME had no significant effect. The potentiating effects of L-NAME were reversed in the presence of L-arginine (3 x 10(-3) M) but not in the presence of the stereoisomer D-arginine (3 x 10(-3) M). This model can be used to study ascending neural pathways in the rat small intestine. The ascending excitatory response is abolished by atropine and hexamethonium and is modulated by capsicin-sensitive fibers. The ascending pathway is under tonic inhibition of metabolites of the L-arginine-NO pathway.

Analysis of Variance↗

Input and output changes of an identified neural pathway are correlated with associative learning in Hermissenda.

The effect of associative training on an identified putative motoneuron (MN1) in an identified visual input-output neural pathway was studied in Hermissenda crassicornis. The increased impulse frequency of the MN1 cell in response to a light step (MN1-LR) was found to be smaller up to 54 hr after associative training with paired light and rotation stimuli. No change was found in animals which received these training stimuli randomly. The MN1 activity in darkness, namely, baseline impulse frequency, spike amplitude, input resistance, and resting potential, did not change after training. The MN1-LR was positively correlated on retention days with the behavioral latency of the animal to enter the illuminated area of a light intensity gradient. However, the input resistance of the type B photoreceptor was inversely correlated with this behavioral latency as well as with MN1-LR. These findings suggest that the reduction of MN1-LR may be caused by the biophysical changes which have been found in the type B photoreceptor membrane. Furthermore, these findings support several other studies which indicate that specific biophysical changes in the type B photoreceptor membrane play a causal role in the observed behavioral modifications after associative training in Hermissenda.

Animals↗