Biomedical subjects

L P Schramm

Publications and source records attributed to L P Schramm.

At least 19 recordsLinked to original sources

PubMed2001

Spinal interneurons play a minor role in generating ongoing renal sympathetic nerve activity in spinally intact rats.

The purpose of the present study was to determine whether spinal interneurons play a role in the regulation of sympathetic activity in spinally intact rats. In acutely spinally transected rats, we have described a population of spinal interneurons that, by virtue of correlations between their ongoing firing rates and the magnitude of ongoing renal sympathetic nerve activity (RSNA), are candidates for generators of sympathetic activity. Further evidence for a sympathetic role for these neurons comes from our observation that cervical spinal stimulation that reduces RSNA also reduces their discharge rates. In chloralose-anesthetized, spinally intact and spinally transected rats, we recorded ongoing RSNA and the ongoing activities of T(10) dorsal horn and intermediate zone interneurons, and we determined the incidence of sympathetically related neurons in these rats by cross-correlating their activities with RSNA. The incidence of correlated neurons was much smaller in spinally intact than in spinally transected rats. We stimulated the dorsolateral, C(2-3) spinal cord before and after acute C(1) spinal transection. Dorsolateral cervical stimulation in spinally transected rats reduced both RSNA and the activities of most T(10) interneurons, but stimulation in spinally intact rats increased RSNA while still reducing the activities of most T(10) interneurons. Both the low incidence of sympathetically correlated spinal neurons in intact rats and the dissociation between the effects of cervical stimulation on RSNA and the discharge rates of spinal interneurons argue against these neurons playing a major role in regulating sympathetic activity in intact rats.

Action Potentials↗

PubMed2000

Ongoing and stimulus-evoked activity of sympathetically correlated neurons in the intermediate zone and dorsal horn of acutely spinalized rats.

We have shown previously that in the acutely spinalized anesthetized rat the activities of many dorsal horn interneurons (DHN) at the T(10) level are correlated positively with both ongoing and stimulus-evoked renal sympathetic nerve activity (RSNA) and therefore may belong to networks generating RSNA after acute, cervical, spinal transection. In the present study, we recorded from both DHN and interneurons in the intermediate zone (IZN) of the T(10) spinal segment in acutely C(1)-transected, chloralose-anesthetized, artificially respired rats. The activities of a similar percentage of IZN and DHN were correlated positively with ongoing RSNA, but the peaks of spike-triggered averages of RSNA based on the activity of IZN were larger, relative to dummy averages, than spike-triggered averages of RSNA based on the activity of DHN. Sympathetically correlated DHN and IZN differed in their responses to noxious somatic stimuli. Most correlated DHN had relatively simple somatic fields; they were excited by noxious stimulation of the T(10) and nearby dermatomes and inhibited by stimulation of more distal dermatomes. As we have shown previously, the excitatory and inhibitory fields of these neurons were very similar to fields that, respectively, excited and inhibited RSNA. On the other hand, the somatic fields of 50% of sympathetically correlated IZN were significantly more complex, indicating a difference between either the inputs or the processing properties of IZN and DHN. Sympathetically correlated IZN and DHN also differed in their responses to colorectal distension (CRD), a noxious visceral stimulus. CRD increased RSNA in 11/15 rats and increased the activity of most sympathetically correlated T(10) IZN. On the other hand, CRD decreased the activity of a majority of sympathetically correlated T(10) DHN. These observations suggest that the same stimulus may differentially affect separate, putative, sympathoexcitatory pathways, exciting one and inhibiting the other. Thus the magnitude and even the polarity of responses to a given stimulus may be determined by the modality and location of the stimulus, the degree to which multiple pathways are affected by the stimulus, and the ongoing activity of presympathetic neurons, at multiple rostrocaudal levels, before stimulation. A multipathway system may explain the variability in autonomic responses to visceral and somatic stimuli exhibited in spinally injured patients.

Action Potentials↗

PubMed1998

Interaction between neuronal nitric oxide synthase and inhibitory G protein activity in heart rate regulation in conscious mice.

Nitric oxide (NO) synthesized within mammalian sinoatrial cells has been shown to participate in cholinergic control of heart rate (HR). However, it is not known whether NO synthesized within neurons plays a role in HR regulation. HR dynamics were measured in 24 wild-type (WT) mice and 24 mice in which the gene for neuronal NO synthase (nNOS) was absent (nNOS-/- mice). Mean HR and HR variability were compared in subsets of these animals at baseline, after parasympathetic blockade with atropine (0.5 mg/kg i.p.), after beta-adrenergic blockade with propranolol (1 mg/kg i.p.), and after combined autonomic blockade. Other animals underwent pressor challenge with phenylephrine (3 mg/kg i.p.) after beta-adrenergic blockade to test for a baroreflex-mediated cardioinhibitory response. The latter experiments were then repeated after inactivation of inhibitory G proteins with pertussis toxin (PTX) (30 microgram/kg i.p.). At baseline, nNOS-/- mice had higher mean HR (711+/-8 vs. 650+/-8 bpm, P = 0.0004) and lower HR variance (424+/-70 vs. 1,112+/-174 bpm2, P = 0.001) compared with WT mice. In nNOS-/- mice, atropine administration led to a much smaller change in mean HR (-2+/-9 vs. 49+/-5 bpm, P = 0.0008) and in HR variance (64+/-24 vs. -903+/-295 bpm2, P = 0.02) than in WT mice. In contrast, propranolol administration and combined autonomic blockade led to similar changes in mean HR between the two groups. After beta-adrenergic blockade, phenylephrine injection elicited a fall in mean HR and rise in HR variance in WT mice that was partially attenuated after treatment with PTX. The response to pressor challenge in nNOS-/- mice before PTX administration was similar to that in WT mice. However, PTX-treated nNOS-/- mice had a dramatically attenuated response to phenylephrine. These findings suggest that the absence of nNOS activity leads to reduced baseline parasympathetic tone, but does not prevent baroreflex-mediated cardioinhibition unless inhibitory G proteins are also inactivated. Thus, neuronally derived NO and cardiac inhibitory G protein activity serve as parallel pathways to mediate autonomic slowing of heart rate in the mouse.

Animals↗

PubMed1998

Ejaculatory abnormalities in mice with targeted disruption of the gene for heme oxygenase-2.

Nitric oxide (NO) is well established as a neurotransmitter in the central and peripheral nervous systems. More recently, another gas, carbon monoxide (CO) has also been implicated in neurotransmission. In the nervous system CO is formed by a subtype of heme oxygenase (HO) designated HO2. HO2 is localized to discrete neuronal populations in the brain resembling localizations of soluble guanylyl cyclase, which is activated by CO. CO may also function in the peripheral autonomic nervous system, in conjunction with NO. The majority of ganglia in the myenteric plexus possess both HO2 and neuronal NO synthase (NOS). Defects in myenteric plexus neurotransmission occur both in mice with targeted deletion of genes for HO2 and neuronal NOS. HO2 also occurs in other autonomic ganglia including the petrosal, superior cervical and nodose ganglia. Neuronal NOS is localized to neurons regulating male reproductive behavior, such as penile erection, and NOS inhibitors prevent erection. Because of the other parallels between NO and CO, we speculated that CO may play a role in male reproductive behavior. In the present study we describe HO2 localization in neuronal structures regulating copulatory reflexes. Reflex activity of the bulbospongiosus muscle, which mediates ejaculation and ejaculatory behavior, is markedly diminished in mice with targeted deletion of the gene for HO2 (HO2-).

Animals↗

PubMed1997

Origins of the sympathetic innervation of the cervical end of the uterus in the rat.

A retrograde neuronal tracer (Fast Blue) was injected in the cervical end of the uterine horn of virgin rats. The majority of the retrogradely labeled post-ganglionic sympathetic neurons were found in the sympathetic chain (74%). The superior mesenteric ganglia, inferior mesenteric ganglia and suprarenal ganglia accounted for 22, 3 and < 1%, respectively. The distribution of neurons in the sympathetic chain labeled from the uterus resembles that described for other pelvic organs.

Animals↗

PubMed1997

Pregnancy-induced uterine neuronal degeneration in the rat.

We studied the location, distribution, and density of uterine nerve bundles in virgin, full-term pregnant, and early postpartum female rats. In the virgin, a low-magnification analysis of uterine whole-mounts stained for acetylcholinesterase revealed fibers both in close association with blood vessels and coursing freely within muscle or connective tissue in the mesometrium and the uterine body. Higher magnification analysis of sections treated immunohistochemically with antibodies to the ubiquitous neuronal protein gene product 9.5, tyrosine hydroxylase, and calcitonin gene-related peptide indicated that the greatest density of nerve bundles was in the mesometrial triangle and intramyometrial region. Although the majority of bundles were associated with blood vessels, many coursed freely, particularly in the myometrial and endometrial layers. The density of innervation within the body of the uterus was heterogeneous. For instance, both innervated and noninnervated spiral arteries branched from the same innervated circumferential artery. In the term pregnant rat, we observed a profound denervation within all layers of the body of the uterus. The few remaining nerve bundles tended to be associated with blood vessels, and they were confined to the intramyometrial region. Within 48 h postpartum, both the number and density of nerve bundles increased. Long tortuous bundles, not seen in the full-term rat, were observed. The present study is the first to describe and illustrate the pattern of uterine innervation in virgin, full-term pregnant, and early postpartum rats over a wide range of magnifications.

Acetylcholinesterase↗

PubMed1997

Uterine arterial vasoconstrictions mediated by ovarian nerves in virgin and postpartum rats.

In most mammals, including humans, pregnancy results in the loss of most uterine vasomotor fibers. These experiments determined whether, despite this denervation, sympathetic nerves mediated uterine vasoconstrictions in the rat 24 h after delivery. Both virgin and uniparous postpartum rats were anesthetized with urethan. Femoral vessels were cannulated for measurement of arterial pressure and intravenous administration of fluids and drugs. Blood flow was measured in a uterine artery after ligation of all anastomotic ovarian vessels. Electrical stimulation of ovarian nerve efferents elicited frequency-dependent uterine vasoconstrictions in both virgin and postpartum rats. Vasoconstrictions in postpartum rats were not significantly different from those observed in virgins. In both virgin and postpartum rats, neurogenic vasoconstrictions were reduced by combined alpha 1- and alpha 2-adrenergic blockade. We conclude that the uterine branches of the ovarian nerve mediate adrenergic uterine vasoconstrictions. In the largely denervated uterus of the postpartum rat, these vasoconstrictions may be mediated by surviving innervation of the uterine artery and its major branches. Sympathetic vasoconstriction acting at these sites would constitute an effective defense against postpartum hemorrhage.

Adrenergic Antagonists↗

PubMed1997

Sympathetically correlated activity of dorsal horn neurons in spinally transected rats.

In mammals with an intact neuraxis, most sympathetic nerve activity is generated by brain stem systems. Therefore these systems have attracted much more attention than spinal systems that generate excitatory inputs to sympathetic preganglionic neurons. The purpose of this study was to determine whether, within hours of C1 spinal cord transection, spinal dorsal horn neurons (DHNs) play a role in generating sympathetic nerve activity. Experiments were conducted in chloralose-anesthetized rats. We recorded renal sympathetic nerve activity (RSNA) in the left renal nerve, and we recorded the activity of neurons located in the left dorsal horn at T2, T8, T10, T13, and L2. We also recorded the activity of neurons in the right dorsal horn at T10. The somatic fields and cutaneous modalities of most neurons were determined. Spike-triggered averaging was used to determine relationships between the ongoing activity of DHNs and ongoing RSNA. In the left dorsal horn, bursts of ongoing activity of 16% of DHNs at T8 and 43% of DHNs at T10 were positively correlated with bursts of ongoing RSNA at latencies of 59 +/- 8 (SE) ms. At no other level on the left side, nor in the T10 segment on the right side, was the activity of DHNs correlated with RSNA. DHNs with activity correlated with RSNA were located only in dorsal horn laminae III-V. Deeper laminae were not investigated in these experiments. The activity of all sympathetically correlated DHNs exhibited bursts of action potentials with interspike intervals of < 10 ms. All but one of the sympathetically correlated DHNs exhibited wide-dynamic-range modalities. The modalities of sympathetically uncorrelated neurons were more heterogeneous. Brief (5-10 s) noxious cutaneous stimulation of mid- and lower thoracic dermatomes on the left side excited all sympathetically correlated DHNs and simultaneously increased RSNA. The excitatory cutaneous fields of sympathetically correlated neurons were circumscribed by the excitatory fields for RSNA. The excitatory cutaneous fields of some sympathetically uncorrelated DHNs extended beyond the excitatory fields for RSNA. Noxious cutaneous stimulation of the extremities on the left side that decreased RSNA simultaneously decreased the activity of all sympathetically correlated DHNs. These data provide electrophysiological evidence that, in spinally transected rats, a population of DHNs may generate or convey excitatory input to renal sympathetic preganglionic neurons.

Action Potentials↗

PubMed1994

Processing of splanchnic and somatic input in thoracic spinal cord of the rat.

To better understand the spinal transmission of visceral afferent information, we conducted neurophysiological studies of single spinal neurons that receive input from the greater splanchnic nerve (GSN). Extracellular single-neuron recordings were made in the thoracic spinal cord of chloralose-anesthetized, paralyzed, and artificially ventilated rats, some of which had undergone acute spinal transection at C1. Neurons were divided into four classes according to their responses to GSN stimulation: one-burst excitatory, two-burst excitatory, biphasic, and inhibited. We then studied the characteristics of the convergent somatic input to each class of neurons using either natural somatic stimuli or electrical stimulation of the iliohypogastric nerve (IHN). Most splanchnic input was mediated by unmyelinated fibers, whereas somatic input was mediated by both unmyelinated and small myelinated fibers. Most of the neurons exhibited somatic receptive fields, and the majority responded to both innocuous and noxious somatic stimuli. However, a small number could be excited only by GSN stimulation. Although a careful analysis of response characteristics indicated that there was a tendency for neurons to exhibit similar responses to electrical stimulation of the GSN and the IHN, we observed many combinations of somatic and visceral responses. We suggest that visceral afferent activity, in addition to being processed via convergent somatovisceral pathways, may be processed by neurons that convey only visceral information or by neurons in which visceral and somatic information is differentially coded.

Afferent Pathways↗

PubMed1994

Splanchnic and somatic afferent convergence on cervical spinal neurons of the rat.

The rostral cervical spinal cord is increasingly being considered the source of important propriospinal regulation. To better understand the substrate for this function, we investigated the effects of stimulation of the greater splanchnic nerve (GSN) and both thoracic and cervical somatic afferents on the activity of cervical spinal neurons. Extracellular single-neuron recordings were made in the C2-C5 spinal segments of chloralose-anesthetized, paralyzed, and artificially ventilated rats. Neurons were classified according to their responses to GSN stimulation. Neurons were inhibited by this stimulation as frequently as they were excited. We then studied the characteristics of cervical and thoracic convergent somatic input to each class of neurons. Although all cervical neurons that responded to GSN stimulation responded to electrical stimulation of the iliohypogastric nerve (IHN), only the few neurons that exhibited whole body receptive fields (RF) responded to natural thoracic somatic stimuli. Responses to electrical stimulation of the GSN and IHN were similar for most neurons; most exhibited nociceptive cutaneous RFs in cervical dermatomes. These data indicate that input from cervical somatic afferents and from both thoracic visceral and thoracic somatic afferents converge on individual splanchnic-receptive cervical neurons. Although these neurons exhibited the predicted cervical somatic RFs, responses from thoracic levels did not exhibit discrete RFs, requiring instead more synchronous or more spatially convergent input.

Abdomen↗

PubMed1993

Peripheral and central pathways regulating the kidney: a study using pseudorabies virus.

We used the retrograde transneuronal transport of a neurotropic virus, pseudorabies virus (PRV), to identify the neurons in sympathetic ganglia, spinal cord and brain which regulate renal function and renal circulation. PRV was microinjected into the left kidney of 70, pentobarbital-anesthetized, male rats. After an incubation period of 1-4 days, rats were anesthetized and sacrificed. PRV-infected neurons were located immunocytochemically in pre- and paravertebral sympathetic ganglia, the intermediolateral cell column of the T10-T13 segments and several brainstem cell groups: the medullary raphe nuclei, rostral ventrolateral medulla, rostral ventromedial medulla, A5 cell group, and the paraventricular hypothalamic nucleus. In more heavily infected rats, additional labeling was found in the locus coeruleus, periaqueductal gray matter, lateral hypothalamic area, zona incerta, and anterior hypothalamic area. No infected propriospinal neurons were observed in the lateral spinal nucleus or gray matter of the caudal cervical, lumbosacral or thoracic spinal segments not containing infected putative sympathetic preganglionic neurons. The paucity of infected propriospinal neurons in the presence of infected brainstem neurons, even in lightly infected rats, is discussed in reference to the relative importance of descending vs spinal regulation of the sympathetic outflow to the kidney.

Animals↗

PubMed1992

Interaction between medullary and cervical regulation of renal sympathetic activity.

We have reported that electrical or glutamate stimulation of the dorsolateral surface of the cervical spinal cord elicits a 40-60% decrease in renal sympathetic activity (RSA) in anesthetized rats. Because evoked sympatho-inhibition was observed, however, only after transection of the cervical spinal cord at C1, we suggested that unidentified supraspinal neurons affect the regulation of RSA by cervical neurons. In the present experiments, we tested the hypothesis that the modulatory supraspinal neurons are located in the ventrolateral medulla by observing the effects of rostroventral, lateral, medullary (RVLM) injections of the GABAergic agonist, muscimol, on baseline RSA and on our ability to inhibit that activity by cervical stimulation. GABAergic inhibition in the RVLM of chlorolose anesthetized rats elicited changes in RSA that were similar to those observed after transection of the spinal cord, including a 41% decrease in mean arterial pressure and a 44% increase in RSA. Moreover, after muscimol inhibition of RVLM neurons, electrical or glutamate stimulation of the dorsolateral cervical spinal cord elicited a decrease in RSA in otherwise intact rats. These results suggest that neurons in the RVLM interact with neurons in the cervical spinal cord in the regulation of RSA.

Animals↗

PubMed1992

Role of cervical neurons in propriospinal inhibition of thoracic dorsal horn neurons.

We previously reported that electrical or glutamate stimulation of the cervical spinal cord elicits a 40-60% decrease in renal sympathetic nerve activity (RSA) in the anesthetized rats. This sympatho-inhibition was possible, however, only after transection of the spinal cord at C1 or GABAergic inhibition of neurons in the rostral ventrolateral medulla. We postulated that cervical neurons inhibit RSA by inhibiting the activity of spinal interneurons that are antecedent to sympathetic preganglionic neurons (SPNs), and that these interneurons may be, in turn, excited by afferent signals. In this study, we tested the hypothesis that cervical neurons can inhibit visceroceptive thoracic spinal neurons. We recorded the spontaneous and evoked activity of 45 dorsal horn neurons responsive to splanchnic stimulation before, during, and after chemical or electrical stimulation of the cervical spinal cord in chloralose-anesthetized spinal rats. Cervical spinal stimulation that inhibited RSA also inhibited the spontaneous and/or evoked activity of 44 dorsal horn neurons. In addition to inhibiting splanchnic-evoked neuronal responses, cervical stimulation also inhibited responses, in the same neurons, evoked by noxious heat or light brushing of receptive dermatomes. We concluded that cervical neurons participate in propriospinal inhibition of afferent transmission and that this inhibitory system may be involved in controlling the access of afferent information to SPNs.

Afferent Pathways↗

PubMed1990

Splanchnic input to thoracic spinal neurons and its supraspinal modulation in the rat.

The urinary responses of 62 T8-T11 spinal neurons were recorded extracellularly following electrical stimulation of the greater splanchnic nerve (GSN) in chloralose-anesthetized rats. Recorded neurons were found in both the dorsal and ventral horns. Fifty-seven neurons increased their firing rate in response to GSN stimulation; 8 of these exhibited biphasic responses consisting of excitations followed by inhibitions. Excitatory responses to GSN stimulation consisted of either one or two bursts with latencies consistent with activation by either A delta or C fibers. GSN stimulation inhibited 5 neurons. The effects of reversible spinalization on spontaneous activity and on both synchronous and non-synchronous (afterdischarge) GSN-evoked responses were investigated using a cooling probe on the spinal cord between C1 and C2. Of 19 neurons tested in this way, 9 exhibited opposite directional changes in their spontaneous activities and their GSN-evoked responses upon spinalization. Differential effects of cold-block on first and second bursts, or on A delta- and C-fiber mediated responses, were not usually observed. However, differential effects of cold-block on synchronous and non-synchronous portions of the overall GSN-evoked response were often observed in that their magnitudes often changed independently of one another. Supraspinal pathways contributed to GSN-evoked responses of several neurons because their responses were diminished during cooling while spontaneous activity was increased or unchanged. These decreases in the magnitude of the GSN-evoked response were not always accounted for by decreases in the synchronous portions of the responses. However, most neurons did exhibit decreases in the number of non-synchronous responses, or afterdischarges, during spinal cooling, exhibiting in some cases biphasic responses. This study provides evidence for strong supraspinal regulation of splanchnic afferent input to the spinal cord of the rat. Further, this regulation exhibits some specificity toward different portions of splanchnic-evoked responses in spinal neurons.

Afferent Pathways↗

PubMed1990

Chronic cervical spinal cord injury and autonomic hyperreflexia in rats.

Although it is well established that patients with cervical spinal cord injury are prone to acute, marked, hypertensive episodes, i.e., autonomic hyperreflexia, the specific mechanisms mediating this sometimes-fatal phenomenon are not completely understood. In this report, we describe the preparation and characterization of a rat model of chronic cervical spinal cord injury and autonomic hyperreflexia. Adult male Sprague-Dawley rats were chronically instrumented with arterial, venous, and gastric catheters. Beginning the first day after a complete cervical spinal transection (CST) and continuing for 1 wk, acute hypertensive responses to a modest increase of urinary bladder pressure (0-20 mmHg) were studied. Mean arterial pressure increased 25.9 +/- 4.8 mmHg during bladder distension the first day after CST. This response was not significantly different 3, 5, and 7 days after CST (overall average = 18.0 +/- 2.3 mmHg). The pressor response to bladder distension was completely abolished by intravesical lidocaine and autonomic ganglionic blockade (atropine + hexamethonium). Responses to bladder distension were not observed after the administration of chloralose anesthesia. We conclude that after cervical spinal transection the rat exhibits autonomic hyperreflexia similar to that seen in humans with spinal injury. Furthermore, autonomic hyperreflexia is completely established within 24 h after CST in the rat. Finally, some spinal autonomic reflexes are suppressed by chloralose anesthesia in the rat.

Animals↗

PubMed1989

Determinants of arterial pressure after chronic spinal transection in rats.

The present study was conducted to determine whether sympathetic vasoconstrictor activity is a determinant of mean arterial pressure (MAP) hours and days after cervical spinal transection (CST) in unanesthetized rats. MAP on the 2 days before CST was 107.2 +/- 3.6 and 103.3 +/- 3.0 mmHg, respectively, and fell to 77.7 +/- 1.1 mmHg on day 1 after CST. MAP returned to control levels over the course of the study and, by day 9 after CST, was not statistically different from control (98.6 +/- 3.4 mmHg). Neither autonomic ganglionic blockade nor alpha-adrenergic blockade affected MAP the 1st day after CST. Similarly, alpha-adrenergic blockade was without effect on days 3, 5, and 7 after CST. Administration of a vasopressin V1-antagonist had no effect on MAP on day 1 or day 8 after CST. However, blockade of angiotensin-converting enzyme with captopril decreased arterial pressure both on day 1 (-22.1 +/- 2.6 mmHg) and day 8 (-23.3 +/- 2.9 mmHg) after CST. We conclude that neither sympathetic nor vasopressin vasoconstrictor activity affected MAP within the 1st wk after CST. Although the vasoconstrictor actions of angiotensin II were important, these effects were not responsible for the normalization of MAP observed after CST.

Angiotensin II↗

PubMed1988

Spinal projections of renal afferent nerves in the rat.

This study was designed to describe renal afferent information with respect to its intraspinal projections, convergence with cutaneous inputs, ascending projections, and modulation by descending fiber tracts. Extracellular recordings were made from neurons in the spinal gray while electrically stimulating the renal nerves in chloralose-anesthetized, artificially ventilated rats. Almost all neurons (n = 119) were spontaneously active. Some responses consisted of high-frequency bursts while others consisted of fewer than 6 action potentials. Response onset latencies to renal nerve stimulation were consistent with activation by thinly myelinated or unmyelinated afferents. Several neurons in deeper laminae were inhibited by stimulation of renal afferents. Most neurons were located in laminae IV and V. Some were located in laminae I, VII and VIII. All neurons were located at spinal levels T10 to L1. Most neurons responded to both noxious and non-noxious mechanical cutaneous stimuli from relatively large receptive fields on the ipsilateral flank. Response latencies to cutaneous electrical stimulation were shorter than those to renal nerve stimulation. Neurons in intact and spinally transected rats responded with similar onset latencies and durations to renal nerve stimulation. However, neurons in spinally transected rats exhibited prolonged responses to cutaneous stimulation. Axons of 25% of the neurons projected through the cervical spinal cord in the ventrolateral funiculus. They had conduction velocities of 12-32 m/s. These data provide the first electrophysiological description of spinal projections of renal afferent fibers in the rat.

Afferent Pathways↗

PubMed1988

Maximum likelihood identification of neural point process systems.

Using the theory of random point processes, a method is presented whereby functional relationships between neurons can be detected and modeled. The method is based on a point process characterization involving stochastic intensities and an additive rate function model. Estimates are based on the maximum likelihood (ML) principle and asymptotic properties are examined in the absence of a stationarity assumption. An iterative algorithm that computes the ML estimates is presented. It is based on the expectation/maximization (EM) procedure of Dempster et al. (1977) and makes ML identification accessible to models requiring many parameters. Examples illustrating the use of the method are also presented. These examples are derived from simulations of simple neural systems that cannot be identified using correlation techniques. It is shown that the ML method correctly identifies each of these systems.

Action Potentials↗