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PubMed1990

Neural pathway for aggressive display in Betta splendens: midbrain and hindbrain control of gill-cover erection behavior.

Horseradish peroxidase (HRP) was used to identify parts of the presumptive neural pathway for gill cover erection, a behavioral display pattern performed by Siamese fighting fish (Betta splendens) during aggressive interactions. Motor, motor integration and sensory areas were identified in the medulla and mesencephalon. Motor neurons of the dilator operculi muscle, the effector muscle for gill cover erection, are located in the lateral and medial parts of the caudal trigeminal motor nucleus. Iontophoretic injections of HRP into the lateral trigeminal motor nucleus resulted in labeled cell bodies in two motor areas (medial part of the trigeminal motor nucleus, anterior part of the motor nucleus of cranial nerve IX-X), two parts of the reticular formation (medial and inferior reticular areas), and two nuclei of the octavolateralis system (nucleus medialis, magnocellular octaval nucleus). The HRP injections in the medial part of the caudal trigeminal motor nucleus resulted in labeled cells in the lateral part of the nucleus and in the medial reticular nucleus. Discrete injections of HRP into nucleus medialis revealed a strong axonal projection that terminated in the torus semicircularis. The medial reticular area and both of the octavolateralis nuclei received projections from their contralateral counterparts. Connections between motor areas, and between parts of the reticular formation, may coordinate the performance of gill cover erection with other behavioral patterns used during aggressive display. Connections with the octavolateralis system may provide information on the strength of an opponent's tail beats via the lateral-line system, as well as vestibular information about the fish's own orientation during aggressive display. The organization of inputs to the trigeminal motor nucleus in Betta, a perciform fish, was found to differ from that reported in the common carp, a cypriniform fish. These differences may underlie the different behavioral capabilities of the two groups of fish.

Afferent Pathways↗
PubMed2003

Effect of spinal cord injury on urinary bladder spinal neural pathway: a retrograde transneuronal tracing study with pseudorabies virus.

OBJECTIVES: To determinate the effect of acute and chronic spinal cord injury (SCI) resulting from thoracic cord transection on the urinary bladder spinal neural pathway. METHODS: Seventy-six adult Sprague-Dawley rats were randomly divided into four groups, non-SCI (normal rats undergoing no surgical procedure except pseudorabies virus [PRV] injection), SCI(b) (SCI and PRV injected immediately after SCI), SCI(c) (SCI and PRV injected at 3 weeks after SCI), and SCI(d) (SCI and PRV injected at 3 months after SCI). Transcardiac perfusion fixation was done at appropriate survival periods after PRV injection into the bladder wall tissue. Sections of the dorsal root ganglion, spinal cord, and brain were processed for visualization of the virus by the streptavidin-peroxidase immunohistochemical procedure. RESULTS: The bladder weight of the non-SCI, SCI(b), SCI(c), SCI(d) rats was 144 +/- 9 mg, 142 +/- 8 mg, 486 +/- 51 mg, and 656 +/- 69 mg, respectively. The time-ordered flow charts of PRV tracing were similar in the non-SCI and SCI rats. The cross-sectional area of the labeled dorsal root ganglion cell profiles increased significantly after SCI (P <0.001): 593 +/- 40 microm2, 588 +/- 39 microm2, 815 +/- 53 microm2, and 902 +/- 57 microm2 in the non-SCI, SCI(b), SCI(c), SCI(d) rats, respectively. The number of labeled cells in the dorsal horn in the L6 and S1 segments 3 days after PRV injection markedly increased in chronic SCI rats, as did the number of labeled motor neurons 4 days after injection. CONCLUSIONS: Acute and chronic SCI have no effect on the process of virus transneuronal transport below the level of the lesion. Subsequent to chronic SCI, reorganization of the micturition reflex pathways may occur.

Acute Disease↗
PubMed1978

Neural pathways of a cardiogenic hypertensive chemoreflex.

Excitation of a cardiac chemoreceptor with 5-hydroxytryptamine (serotonin) produces a complex autonomic reflex which includes hypertension, changes in heart rate and contractile force, and disturbances of AV conduction. This study examines the afferent and efferent neural pathways of this autonomic reflex in 60 anesthetized dogs. We used cooling and sectioning techniques in 40 of these, and in 20 others recorded afferent neurograms. The most common afferent pathways for the reflex were found in the left and right recurrent cardiac nerves. No preferential efferent routes to the heart were found, although the nature of the reflex cardiac response could be altered by specific nerve interruption. Cyproheptadine (1 mg/kg iv) regularly abolished both the reflex and the chemoreceptor afferent neural traffic, but injection of a 10 times higher concentration of serotonin (1 mg/ml) readily surmounted the blockade and restored the chemoreceptor neural traffic. Thus cyproheptadine interdicts the reflex at the site of its initiation.

Afferent Pathways↗
PubMed2002

Neuroanatomical and psychopharmacological evidence for interaction between opioid and GABAergic neural pathways in the modulation of fear and defense elicited by electrical and chemical stimulation of the deep layers of the superior colliculus and dorsal periaqueductal gray matter.

The effects of central administration of opioid antagonists on the aversive responses elicited by electrical (at the freezing and escape thresholds) or chemical stimulation (crossings, rearings, turnings and jumps, induced by microinjections of bicuculline) of the midbrain tectum were determined. Central microinjections of naloxone and naltrexone in the mesencephalic tectum caused a significant increase in the freezing and escape thresholds elicited by electrical midbrain tectum stimulation. Furthermore, both opioid antagonists caused a significant decrease in the mean incidence of aversive behavioral responses induced by microinjections of bicuculline in the deep layers of the superior colliculus (DLSC) and in dorsal aspects of the periaqueductal gray matter (DPAG), as compared with controls. These findings suggest an opioid modulation of the GABAergic inhibitory inputs controlling the aversive behavior elicited by midbrain tectum stimulation. In fact, immunohistochemical evidence suggests that the dorsal mesencephalon is rich in beta-endorphin-containing neurons and fibers with varicosities. Iontophoretical microinjections of the neurotracer biodextran in the substantia nigra, pars reticulata (SNpr), show nigro-tectal pathways connecting SNpr with the same neural substrate of the DPAG rich in neuronal cells immunoreactive for opioid peptides. Labeled neurons of the DLSC and periaqueductal gray matter send inputs with varsicosities to ipsi- and contralateral DPAG and ipsilateral SNpr. These findings, in addition to the psychopharmacological evidence for the interaction between opioid and GABAergic mechanisms, offer a neuroanatomical basis of a possible presynaptic opioid inhibition of GABAergic nigro-tectal neurons modulating the fear in aversive structures of the cranial mesencephalon, in a short link, and maybe through a major neural circuit, also in GABA-containing perikarya of nigro-tectal neurons.

Aggression↗
PubMed1994

Differential distribution of nitric oxide synthase in neural pathways to the urogenital organs (urethra, penis, urinary bladder) of the rat.

Axonal tracing techniques were used in combination with histochemical methods (NADPH-diaphorase activity and nitric oxide synthase immunoreactivity) to examine the distribution of nitric oxide synthase (NOS) in the neural pathways to the urogenital organs of the male rat. The major goal of this study was to compare the histochemical properties of the efferent and afferent neurons innervating the urethra with the properties of neurons innervating the penis and bladder. In the major pelvic ganglion (MPG) large percentages of postganglionic neurons innervating the urethra (44%) and the penis (97%) exhibited NADPH-diaphorase (NADPH-d) staining whereas only a small percentage (3.5%) of neurons innervating the bladder were N-d positive. Urethral neurons stained for N-d were on average smaller (33.3 microns diameter) than unstained neurons (54.5 microns diameter). The histochemical difference between the three types of neurons was also reflected in NOS-immunoreactivity (IR); however, the absolute percentage of neurons exhibiting NOS-IR was low: penis (21%), urethra (11%) and bladder (0%). Axonal varicosities staining for N-d or NOS-IR were noted in the MPG in close proximity to unidentified neurons and neurons innervating the urogenital organs. A considerable number of afferent neurons in the lumbosacral dorsal root ganglia (DRG) stained for N-d (64 cells/L6, 35 cells/S1 section); however, only small numbers of neurons (average 1 cell/section) exhibited NOS-IR. N-d activity was detected in a large percentage of urethral (55%) and bladder (80%) afferent neurons in the L6-S1 dorsal root ganglia (DRG) but in relatively few (12%) penile afferent neurons in the L6 ganglia. These results suggest that the contribution of nitric oxide (NO) to neurotransmission varies considerably in different urogenital organs. NO could have a significant role in postganglionic efferent pathways to the urethra and penis but very likely has no role in the efferent pathways to the bladder. Similarly, the prominence of N-d staining in some DRG neurons (e.g. urethra and bladder) but not others (penile) also raises the possibility of a varying role of NO in afferent pathways. However, in these neurons N-d staining was not paralleled by NOS-IR, which was present in only a small percentage of neurons. Thus, N-d staining may not reflect the presence of NO in afferent pathways to the pelvic viscera.

Afferent Pathways↗
PubMed2003

A study on the central neural pathway of the heart, Nei-Kuan (EH-6) and Shen-Men (He-7) with neural tracer in rats.

The purpose of this morphological study was to investigate the relations between meridians, acupoints and viscera using neuroanatomical tracers. The labeled areas of the spinal ganglia, sympathetic chain ganglia, spinal cord and the brain projecting to the heart, Nei-Kuan (EH-6) and Shen-Men (He-7) were observed following injection of WGA-HRP and pseudorabies virus (PRV). The results were as follows. Overlapping bilaterally labeled ganglion areas after heart, Nei-Kuan (EH-6) or Shen-Men (He-7) injection of WGA-HRP were found in middle cervical, stellate and T4 sympathetic and T2-T6 spinal ganglia. In brain, labeled neurons from all three sites were found in the A1 noradrenalin cell group/C1 adrenalin cell group/caudoventrolateral reticular n., n. tractus solitarius, n. ambiguus, rostroventrolateral n., C3 adrenaline cell group, raphe obscurus n., raphe pallidus n., raphe magnus n., lateral paragigantocellular reticular n., locus coeruleus, subcoeruleus n., Kolliker-Fuse n., A5 cell group, central gray matter, paraventricular hypothalamic n. and arcuate hypothalamic n.. In conclusion, these morphological results suggest that the interrelationship of acupoints (Nei-Kuan and Shen-Men) and viscera (heart) may be related to the central autonomic centers of the spinal cord and brain.

Acupuncture Points↗
PubMed1997

Functional anatomy of neural pathways contributing to the control of song production in birds.

In birds, as in humans, vocal control involves the intricate coordination of three major groups of muscles, namely, those of the vocal organ, the respiratory apparatus, and the vocal tract, including the jaw and tongue. The neural pathways involved in the control of each of these groups of muscles are described for songbirds and compared with those in non-oscine birds and mammals. The pathway in songbirds that controls the syrinx, the bird's vocal organ, originates in the telencephalon and projects via the occipito-mesencephalic tract directly upon vocal motoneurons in the medulla. Activity in this pathway configures the syrinx into phonatory positions for the production of species typical vocalizations. Another component of this pathway mediates control of respiration during vocalization, since it projects upon both expiratory and inspiratory groups of premotor neurons in the ventrolateral medulla, as well as upon several other nuclei en route. This pathway appears to be primarily involved with the control of the temporal pattern of song, but is also importantly involved in the control of vocal intensity, mediated via air sac pressure. There are extensive interconnections between the vocal and respiratory pathways, especially at brainstem levels, and it may be these that ensure the necessary temporal coordination of syringeal and respiratory activity. The pathway mediating control of the jaw appears to be different from those mediating control of the syrinx and respiratory muscles. It originates in a different part of the telencephalon and projects upon premotor neurons in the medulla that, on preliminary analysis, appear to be separate from those projecting upon the syringeal motor nucleus. The separateness of this pathway may reflect the imperfect correlation of jaw movements with the dynamic and acoustic features of song. The brainstem pathways mediating control of vocalization and respiration in songbirds have distinct similarities to those in non-oscine birds and in mammals such as cats and monkeys. However, songbirds and parrots, like humans, but unlike other non-songbirds, have developed a special telencephalic vocal control system for the production of learned vocalizations.

Animals↗
PubMed2006

Respiratory responses to cold water immersion: neural pathways, interactions, and clinical consequences awake and asleep.

The ventilatory responses to immersion and changes in temperature are reviewed. A fall in skin temperature elicits a powerful cardiorespiratory response, termed "cold shock," comprising an initial gasp, hypertension, and hyperventilation despite a profound hypocapnia. The physiology and neural pathways of this are examined with data from original studies. The respiratory responses to skin cooling override both conscious and other autonomic respiratory controls and may act as a precursor to drowning. There is emerging evidence that the combination of the reestablishment of respiratory rhythm following apnea, hypoxemia, and coincident sympathetic nervous and cyclic vagal stimulation appears to be an arrhythmogenic trigger. The potential clinical implications of this during wakefulness and sleep are discussed in relation to sudden death during immersion, underwater birth, and sleep apnea. A drop in deep body temperature leads to a slowing of respiration, which is more profound than the reduced metabolic demand seen with hypothermia, leading to hypercapnia and hypoxia. The control of respiration is abnormal during hypothermia, and correction of the hypoxia by inhalation of oxygen may lead to a further depression of ventilation and even respiratory arrest. The immediate care of patients with hypothermia needs to take these factors into account to maximize the chances of a favorable outcome for the rescued casualty.

Animals↗
PubMed2006

Neural pathways involved in the endocrine response of anestrous ewes to the male or its odor.

During the non-breeding season, anestrous ewes do not experience ovarian cycles but exposure to a ram or its odor results in the activation of the luteinizing hormone secretion leading to ovulation. The aim of our work was to identify the neural pathways involved in this phenomenon. Using Fos immunocytochemistry, we examined the brain areas activated by the male or its fleece, in comparison with ewes exposed to the female fleece or the testing room (control group). In comparison with the control group, the male or its odor significantly increases Fos neuronal expression in the main and accessory olfactory bulbs, anterior olfactory nucleus, cortical and basal amygdala, dentate gyrus, ventromedial nucleus of the hypothalamus, piriform and orbitofrontal cortices. The main olfactory bulb, the cortical amygdala and the dentate gyrus are specifically more activated by the male odor than the female odor. Using a procedure of double labeling for Fos and gonadotropin-releasing hormone, we also compared the number of gonadotropin-releasing hormone neurons activated in the four groups of females. The male or its odor significantly increases the number and the proportion of gonadotropin-releasing hormone cells expressing Fos-immunoreactivity in the preoptic area and the organum vasculosum of the lamina terminalis, whereas no such induction of Fos-immunoreactivity was found in gonadotropin-releasing hormone neurons of ewes exposed to the female odor or the testing room. These findings emphasize the role of the main olfactory system in the detection and the integration of the ram odor, and also suggest the participation of the accessory olfactory system. Numerous structures widely distributed seem involved in the processing of the male olfactory cue to reach the gonadotropin-releasing hormone neurons.

Amygdala↗
PubMed2000

[Studies on behavioral and electrographic seizures and structural abnormalities using magnetic resonance image in chronic epilepsy model in rats--hippocampal-entorhinal-tempral neocortex neural pathway].

AIM AND METHODS: Repeated tetanus (60 Hz, 0.4-0.6 mA, 2 s) were delivered into the right and the left dorsal hippocampus (HPC), or into the right and the left medial temporal neocortex (MTNC) respectively to establish chronic temporal lobe epilepsy model in rats. The possible role of the HPC-Entorhinal cortex (EC)-MTNC-Neocortex neural pathway in epileptogenesis was discussed based on observing the abnormalities in behavior and in EEG or depth electrographes and in T2-weighted magnetic resonance images (T2-MRI). RESULTS: 1. Occurrence of primary, secondary WEDS and kindling effects were higher in the right dorsal HPC experimental group than those in other three experimental groups (P < 0.005, P < 0.001). T2-MRI signal hyperintensity was remarkable in lateral ventricles close to the HPC (P < 0.05), but not in the EC or in the MTNC. 2. These T2-MRI intensity increases were related to behavioral abnormalities in some MTNC-stimulated rats. 3. Asymmetric behavioral abnormalities and T2-MRI changes were observed in the left and the right DHPC-stimulated groups. CONCLUSION: HPC may be an "origin" for epileptogenesis and EC may play a "gating" role in it.

Animals↗
PubMed1999

Neuronal nitric oxide synthase in the neural pathways of the urinary bladder.

Nitric oxide (NO) is a unique biological messenger molecule. It serves, in part, as a neurotransmitter in the central and peripheral nervous systems. Neurons containing NO have been identified histochemically by the presence of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) reactivity or immunohistochemically by the antibody for neuronal NO synthase (n-NOS). Previous histochemical or pharmacological studies have raised the possibility that NO may play an important role in the neural pathways of the lower urinary tract. There is also considerable evidence to suggest that n-NOS is plastic and could be upregulated following certain lesions in the lower urinary tract. The present review summarises the distribution of n-NOS containing neurons innervating the urinary bladder and the changes of the enzyme expression in some experimentally induced pathological conditions.

Animals↗
PubMed1989

Stimulation of the rostral ventrolateral medullary neurons increases cortical cerebral blood flow via activation of the intracerebral neural pathway.

In urethane-anesthetized, artificially ventilated rats, electrical or chemical (by L-glutamate) focal stimulations of the rostral ventrolateral medulla (RVLM) produced an increase in cortical cerebral blood flow (CBF). The RVLM-induced cortical vasodilative response was present in animals with spinal cords sectioned at levels of Th3-4 and with bilateral extracerebral cervical sympathetic trunks (CSTs) severed. The RVLM-induced cortical vasodilative response was totally eliminated by an alpha 2 adrenergic blocker, but not by blockers for muscarinic, nicotinic, alpha 1 and beta receptors. It was concluded that there is an intracerebral vasodilative neural pathway including an alpha 2 adrenergic receptor originating in the RVLM for regulation of cortical blood vessels.

Adrenergic Fibers↗
PubMed1995

Contributions of neural pathways to age-related losses in chromatic discrimination.

Chromatic-discrimination thresholds were measured for light mixtures lying along individually determined tritan axes and an axis of constant short-wavelength-sensitive- (S-) cone stimulation for 30 color-normal observers (age range 22-77 years). The stimulus was a foveally viewed 2 degrees, circular bipartite field consisting of a standard and a test light. Heterochromatic flicker photometry was used to equate the retinal illuminance of the stimuli at 120 Td for all observers. All stimuli were presented in Maxwellian view. Age-related losses in chromatic discrimination depended on the level of cone stimulation. At relatively lower levels of S- and long-wavelength-sensitive (L-) cone stimulation, discrimination thresholds were elevated for older relative to younger observers. As the level of simulation increased for these two cone types, thresholds converged, on average, for all observers. Application of a model of chromatic discrimination mediated by an S-cone pathway suggests that there is no significant age-related change in Weber fractions and that age-related losses in chromatic discrimination are due, at least in part, to spontaneous neural noise arising in the pathway and/or neural changes that multiplicatively scale all incident light.

Adult↗
PubMed1988

Neural pathways and pharmacological modulation of defecation reflex in rats.

1. A new method was developed for quantitative studies on defecation reflex in urethane-anesthetized rats which involves the continuous infusion of saline (0.1 ml/min) to distend a balloon placed in the rectum. At threshold values, the balloon was expelled during an active rectal contraction. 2. Balloon expulsion was greatly delayed or even abolished by i.v. hexamethonium. Cord transection at the upper cervical level increased defecation threshold but a functional, hexamethonium-sensitive response was still elicited in spinal rats. 3. Various parameters of the defecation response were modulated by drugs (phentolamine, picrotoxin, naloxone) expected to interfere (either centrally or peripherally), with neural pathways controlling the autonomic outflow for the reflex response. 4. In capsaicin-pretreated rats (50 mg/kg s.c. on 2nd day of life, experiments performed at 2 months), daily fecal production was unchanged as compared to vehicle-treated, age-matched controls. However, under urethane-anesthesia, defecation threshold was increased at higher-than-normal values by capsaicin-pretreatment. 5. In in vitro experiments, capsaicin (1 microM) induced a transient inhibition of field stimulation-induced contractions of the rat isolated rectum. This effect was mimicked by application of calcitonin gene-related peptide (CGRP) (0.1 microM) while Substance P (0.1 microM) had an opposite effect. In preparations desensitized to exogenous CGRP, the inhibitory effect of capsaicin was almost abolished. 6. These findings indicate that in rats, reflex defecation is mainly organized at spinal level, although the participation of supraspinal centers may modify the functional response. Capsaicin-sensitive afferents may be involved in the initiation of certain forms of reflex defecation, although capsaicin-resistant mechanisms are capable of activating the normal excretory function.

Animals↗
PubMed1985

A neural pathway for the shift response in the cat.

The shift response (McIlwain effect) was elicited by moving a large grating situated greater than 15 degrees from the conventional receptive field center (RFC). We examined the change in the amplitude of the shift response induced by placing a steady target on the RFC or the RF surround. We found that appropriate stimulation of the RFC or the RF surround will increase and inappropriate stimulation will decrease the amplitude of the shift response in a graded manner. The amplitude of the shift response was not correlated with the maintained activity but was correlated with the transient peak firing rate which is evoked by flashing the enhancing stimulus. A shift stimulus which elicits a strong shift response can be blocked by inappropriate stimulation. The results suggest that the shift signal is modulating a tonic signal which is present in the RF. Because the shift response is a transient excitation, we suggest that the shift response results from a disinhibitory process. A possible neural pathway for the shift response is presented.

Animals↗
PubMed2003

Postoperative ileus is maintained by intestinal immune infiltrates that activate inhibitory neural pathways in mice.

BACKGROUND AND AIMS: Postoperative ileus after abdominal surgery largely contributes to patient morbidity and prolongs hospitalization. We aimed to study its pathophysiology in a murine model by determining gastric emptying after manipulation of the small intestine. METHODS: Gastric emptying was determined at 6, 12, 24, and 48 hours after abdominal surgery by using scintigraphic imaging. Intestinal or gastric inflammation was assessed by immune-histochemical staining and measurement of tissue myeloperoxidase activity. Neuromuscular function of gastric and intestinal muscle strips was determined in organ baths. RESULTS: Intestinal manipulation resulted in delayed gastric emptying up to 48 hours after surgery; gastric half-emptying time 24 hours after surgery increased from 16.0 +/- 4.4 minutes after control laparotomy to 35.6 +/- 5.4 minutes after intestinal manipulation. The sustained delay in gastric emptying was associated with the appearance of leukocyte infiltrates in the muscularis of the manipulated intestine, but not in untouched stomach or colon. The delay in postoperative gastric emptying was prevented by inhibition of intestinal leukocyte recruitment. In addition, postoperative neural blockade with hexamethonium (1 mg/kg intraperitoneally) or guanethidine (50 mg/kg intraperitoneally) normalized gastric emptying without affecting small-intestinal transit. The appearance of intestinal infiltrates after intestinal manipulation was associated with increased c-fos protein expression in sensory neurons in the lumbar spinal cord. CONCLUSIONS: Sustained postoperative gastroparesis after intestinal manipulation is mediated by an inhibitory enterogastric neural pathway that is triggered by inflammatory infiltrates recruited to the intestinal muscularis. These findings show new targets to shorten the duration of postoperative ileus pharmacologically.

Animals↗
PubMed1987

Neural pathways involved in the photoperiodic control of reproductive physiology and behavior in female hamsters (Mesocricetus auratus).

Female hamsters received horizontal knife cuts to investigate the role of hypothalamic connections in the photoperiodic control of female reproductive functions. Knife cuts placed ventral to or through the paraventricular nucleus (PVN), but dorsal to the suprachiasmatic nucleus (SCN), prevented photoperiod-induced acyclicity and uterine regression in animals maintained under a nonstimulatory photoperiod for 10 weeks. The animals were then ovariectomized and tested for lordosis behavior following subcutaneous injections of ovarian hormones to investigate the photoperiodic modulation of female sexual behavior. Animals exposed to a nonstimulatory photoperiod were less behaviorally sensitive to treatment with estradiol benzoate (EB) alone, but did not differ from animals maintained under a stimulatory photoperiod when EB was combined with progesterone. The effect of photoperiod and behavioral sensitivity to hormone replacement was independent of the surgical condition. The results are consistent with the hypothesis that dorsal projections from the SCN to the PVN mediate gonadal responses to short photoperiods. They also indicate that photoperiod-induced changes in behavioral sensitivity to gonadal steroids may be mediated by neural pathways distinct from those that mediate the gonadal changes.

Animals↗
PubMed1996

Carotid chemoreflex. Neural pathways and transmitters.

The chemoreceptor projection site encompasses a midline area (0-0.5 mm caudal, 0-0.5 mm lateral and 0.3-0.5 deep with respect to the calamus scriptorius) which includes the commissural subnucleus of NTS. The chemosensitive neurons located in this site fire tonically, without any rhythmic relation to the phrenic nerve bursts, and are not responsive to baroreceptor stimulation. These neurons may serve as a pre-central pattern generator for respiration. The mechanisms which mediate respiratory responses (i.e., PN responses) to carotid chemoreceptor stimulation are as follows. Activation of carotid chemoreceptors results in the release of an excitatory amino acid (probably glutamate) in the chemoreceptor projection site; both NMDA and non-NMDA receptors in this site mediate the responses to chemoreceptor stimulation. The chemosensitive neurons send projections (which have not been identified yet) to respiratory neurons. Unlike in the neonatal rat, the inspiratory drive to the phrenic motoneurons is mediated by both NMDA and non-NMDA receptors. The PN response to chemoreceptor stimulation are also mediated by NMDA and non-NMDA receptors located in the phrenic motor nucleus. Cardiovascular responses to chemoreceptor stimulation are mediated by neural pathways connecting the chemosensitive neurons to the rostral ventrolateral medullary pressor area. These projections are glutamatergic. Activation of the sympatho-excitatory neurons in the rostral ventrolateral medulla results in pressor and tachycardic responses characteristic of chemoreceptor activation.

Action Potentials↗