Biomedical subjects

A D Loewy

Publications and source records attributed to A D Loewy.

At least 55 records · Page 3Linked to original sources

PubMed1992

Transneuronal labeling of spinal interneurons and sympathetic preganglionic neurons after pseudorabies virus injections in the rat medial gastrocnemius muscle.

The distribution of retrogradely and transneuronally labeled neurons was studied in CNS of rats 4 days after injections of the Bartha strain of pseudorabies virus (PRV) into the medial gastrocnemius (MG) muscle. Tissue sections were processed for immunohistochemical detection of PRV. Retrogradely labeled cells were identified in the ipsilateral MG motor column in the caudal L4 and the L5 spinal segments. In order to evaluate the efficacy of PRV retrograde cell body labeling, the number of PRV retrogradely labeled neurons in the MG motor column was compared to the number labeled with two conventional retrograde cell body markers--Fluoro-Gold and cholera toxin-HRP. A ratio of 1:3 representing medium-sized (less than 30 microns) versus large neurons (greater than 30 microns) was found in the Fluoro-Gold dye experiments; a 1:2 ratio was seen in the PRV experiments. In contrast, when cholera toxin-HRP was used as a retrograde marker, mainly large neurons were labeled; the medium-to-large cell body ratio was 1:10 suggesting cholera toxin-HRP may have a greater affinity for the terminals of alpha-motoneurons as opposed to gamma-motoneurons. Transneuronally labeled cells were identified in the L1-L6 spinal gray matter, intermediolateral cell column (T11-L2), lateral spinal nucleus and medial part of lamina VII in C4 and C5 spinal segments, brainstem (caudal raphe nuclei, rostral ventrolateral medulla, A5 cell group, paralemniscal nucleus, locus coeruleus, subcoeruleus nucleus, red nucleus) and paraventricular hypothalamic nucleus. In the L5 spinal cord, transneuronally labeled neurons were seen in the ipsilateral spinal laminae I and II and bilaterally in spinal laminae IV-VIII, and X. Similar results were obtained in rats that had chronic unilateral L3-L6 dorsal rhizotomies indicating most of the labeling was due to retrograde transneuronal cell body labeling. In order to determine whether PRV was transported into the spinal cord by the dorsal root axons, the ipsilateral dorsal root ganglia (DRGs) were examined for PRV immunoreactivity; none was found. However, using the polymerase chain reaction, viral DNA was shown to be present in the ipsilateral DRGs indicating that some of spinal cord cell body labeling may have resulted from anterograde transneuronal labeling, as well.

Animals↗

PubMed1992

CNS cell groups projecting to the submandibular parasympathetic preganglionic neurons in the rat: a retrograde transneuronal viral cell body labeling study.

The retrograde transneuronal viral tracing method was used to study the CNS nuclei that innervate the parasympathetic preganglionic neurons controlling the submandibular gland in the rat. A genetically engineered beta-galactosidase expressing Bartha strain of pseudorabies virus (PRV) was injected into the submandibular gland of rats. After 4 days, PRV infected tissues were reacted with the Bluo-Gal substrate (halogenated indolyl-beta-D-galactoside) and labeled cell bodies were identified throughout the brain. In the medulla oblongata, cell body labeling was seen in the superior salivatory nucleus, and throughout the medullary reticular formation as well as in the nucleus of the solitary tract, spinal trigeminal nucleus, and deep cerebellar nuclei. In the pons, PRV labeled neurons were found bilaterally in the locus ceruleus, subceruleus region, and parabrachial complex. In the mesencephalon, labeled cells were found in the Edinger-Westphal nucleus, deep mesencephalic nucleus, and central grey matter. Several hypothalamic regions were labeled including the lateral, perifornical and paraventricular hypothalamic nuclei. In the telencephalon, PRV-positive cell bodies were observed in the substantia innominata, bed nucleus of the stria terminalis and central nucleus of the amygdala. The results suggest that widespread areas of the CNS are involved in control of salivation.

Animals↗

PubMed1991

beta-Galactosidase expressing recombinant pseudorabies virus for light and electron microscopic study of transneuronally labeled CNS neurons.

A beta-galactosidase expression pseudorabies virus (Bartha strain) was constructed, injected into the adrenal gland of rats, and subsequently shown to transneuronally label the CNS autonomic neurons that project to the sympathoadrenal preganglionic neurons. Virally infected neurons were visualized with a one-step histochemical reaction using the Bluo-Gal substrate (halogenated indolyl-beta-D-galactoside) for the localization of beta-galactosidase activity. In some infected neurons, a Golgi-like staining of the primary and sometimes secondary dendrites could be obtained. For electron microscopic studies, the Bluo-Gal substrate produces an electron-dense reaction product that is easily identified at both low and high magnification. This virus may be useful for the study of the cell architecture and synaptic organization of transneuronally labeled neurons of functionally defined neural circuits. These results also demonstrate that it is possible to deliver foreign genes into specific chains of neurons in the mammalian CNS by means of the retrograde transneuronal vial labeling method.

Adrenal Glands↗

PubMed1991

Descending input from the hypothalamic paraventricular nucleus to sympathetic preganglionic neurons in the rat.

The descending projection of the hypothalamic paraventricular nucleus (PVN) to the sympathetic preganglionic neurons (SPNs) in the upper thoracic cord of the rat was studied. PVN-fibers were labeled by anterograde transport of Phaseolus vulgaris leucoagglutinin (PHA-L), while SPNs were retrogradely labeled with cholera toxin subunit B (CTb) which was injected into the superior cervical ganglion. SPNs labeled with CTb were mainly observed in the nucleus intermediolateralis (IML) pars principalis and pars funicularis, and a small number of them were in the nucleus intercalatus (IC) and central autonomic nucleus (CA). SPNs found in the IML had dendrites that projected in various directions. Five types of dendritic projections were noted: medial, rostral, caudal, lateral (including dorsolateral) and ventral. Longitudinal dendritic bundles interconnected each cell cluster in the IML. Medial dendrites of the IML, together with dendrites of the IC and CA, formed transverse dendritic bundles extending from the IML to the central canal. The transverse dendritic bundles disentangled near the midline and formed a loose dendritic plexus in the region just dorsal to the central canal. PVN-fibers labeled with PHA-L were observed primarily in lamina I and intermediate gray (lamina VII). Although varicose PVN-fibers and SPNs coexisted in the IML, the tight packing of the dendritic bundles prevented any clear demonstration of direct contacts between them. On the other hand, PVN-fibers were occasionally found to appose and wind around the primary or secondary dendrites of some SPNs of the CA and IC. These dendrites were studied with varicosities of PVN-fibers for a short length, and terminal boutons of PVN-fibers were also seen to make contact directly with the dendrities. The results of this study substantiated a direct connection between the PVN and SPNs, using a combination of immunohistochemical techniques for PHA-L and CTb. The possible involvement of a direct pathway from the PVN to SPNs in cardiovascular regulation is discussed.

Animals↗

PubMed1991

Forebrain nuclei involved in autonomic control.

Several key regions of the forebrain are involved in regulation of autonomic functions. These areas include the several areas within the hypothalamus (viz., paraventricular hypothalamic nucleus, lateral hypothalamic area, posterior periventricular area, and zona incerta), the basal forebrain (viz., central nucleus of the amygdala and bed nucleus of the stria terminalis), and the cerebral cortex (viz., insular and medial prefrontal cortex). All these areas have been implicated on anatomical grounds to be part of a central autonomic network involving multiple interconnecting circuits. Apart from these complex interconnections, most of these areas project to the lower brain stem where they are capable of influencing the cell groups which innervate the vagal and sympathetic preganglionic neurons or in some cases, like the paraventricular hypothalamic nucleus and the lateral hypothalamic area, provide direct projections to these neurons.

Amygdala↗

PubMed1990

CNS projections to the pterygopalatine parasympathetic preganglionic neurons in the rat: a retrograde transneuronal viral cell body labeling study.

The retrograde transneuronal viral cell body labeling method was used to study the CNS nuclei that innervate the parasympathetic preganglionic neurons which project to the pterygopalatine ganglion. Small injections of a suspension of pseudorabies virus (PRV) were made in the pterygopalatine ganglion of rats and after 4 days their brains wer e processed for immunohistochemical detection of PRV. Some of the tissues were stained with a dual immunofluoresence method that permitted the visualization of PRV and neurotransmitter enzyme or serotonin immunoreactivity in the same cell. Retrograde cell body labeling was detected in the ipsilateral ventrolateral medulla oblongata in the region that has been termed the superior salivatory nucleus. This area was the same region that was retrogradely labeled after Fluoro-Gold dye injections in the pterygopalatine ganglion. Retrograde transneuronally infected cell bodies that provide putative afferent inputs to the pytergopalatine parasympathetic preganglionic neurons were mapped throughout the brain. In the medulla oblongata, transneuronally labeled neurons were seen in the nucleus tractus solitarii, dorsomedial part of the spinal trigeminal nucleus and gigantocellular reticular nucleus. In most experiments, some A1 catecholamine cells and serotonin neurons of the raphe magnus, raphe pallidus, raphe obscurus, and parapyramidal nuclei were labeled. In the pons, labeled cells were found in the parabrachial nucleus. A5 catecholamine cell group, and non-catecholamine part of the subcoeruleus region. In the midbrain, cell body labeling was located in the central gray matter and retrorubral field. In the diencephalon, labeling was found mainly in the hypothalamus. The areas included the lateral hypothalamic area, lateral preoptic area, dorsomedial and paraventricular hypothalamic nuclei, and ventral zona incerta. Contralateral second order cell body labeling was seen in the tuberomammillary nucleus of the hypothalamus. Some of these cells were histidine decarboxylase-immunoreactive. In the forebrain, the bed nucleus of the stria terminalis, substantia innominata, and an area of the cerebral cortex called the amygdalopiriform transition zone were labeled.

Animals↗

PubMed1990

L-glutamate mapping of cardioreactive areas in the rat posterior hypothalamus.

The posterior hypothalamus has long been regarded as a CNS region that provides a sympatho-excitatory influence on the cardiovascular system and functions in thermoregulation as a heat-producing center. These ideas have been based on data derived from electrical stimulation and lesion experiments. These methods are now regarded as inadequate for accurate localization of CNS functions. In order to re-examine the function of the posterior hypothalamus, a chemical stimulation study was performed. Microinjections of the excitatory amino acid L-glutamate were made in the posterior hypothalamus of pentobarbital-anesthetized rats. This method was used in combination with autoradiography to localize [3H]glutamate, which was included with the injectate. No pressor responses were elicited from any site within the posterior hypothalamus. In contrast, chemical stimulation of the posterior periventricular hypothalamus produced large decreases in blood pressure (delta BP = 25 mm Hg) and in heart rate (delta HR = 30 bpm). Injections in the posterior hypothalamic nucleus elicited small reductions in blood pressure and heart rate. Injections in the dorsal hypothalamic area produced a similar small response. Injections ventral to the periventricular zone were also weakly reactive, but a significant elevation in rectal temperature was seen. To summarize, the most cardioresponsive area was within the periventricular zone caudal to the posterior hypothalamic nucleus and was situated near the fasciculus retroflexus.

Animals↗

PubMed1990

Pseudorabies virus: a highly specific transneuronal cell body marker in the sympathetic nervous system.

The present report presents a series of experiments using Bartha's K strain of pseudorabies virus (PRV) designed to test the specificity of this virus as a retrograde transneuronal marker in the sympathetic nervous system of rats. Three experiments were performed. First, an injection of PRV was made in the anterior chamber of the eye, followed 24 hr later by an injection of WGA-HRP. PRV infected neurons in the superior cervical ganglion (SCG) always contained WGA-HRP. This dual labeling of SCG neurons suggests that the PRV cell body labeling does not nonspecifically infect nearby neurons. Second, after PRV injections into the pinna or eye, a specific segmental distribution of the transneuronal cell body labeling occurred in the intermediolateral cell column and related spinal areas. After eye injections, the majority of transneuronally labeled neurons were in the T1-T3 segments. After pinna injections, the majority of labeled cells were in the T2-T5 segments. Since the SCG cells innervating these 2 end organs lie in close proximity to each other within the ganglion, these results suggest that a specific transfer of the virus to the preganglionic neurons occurred, possibly via a transsynaptic mechanism. Third, virally infected glial cells were rarely found in the SCG or spinal cord. In summary, Bartha's K strain of PRV is a specific transneuronal retrograde grader marker in the sympathetic nervous system.

Animals↗

PubMed1989

CNS cell groups regulating the sympathetic outflow to adrenal gland as revealed by transneuronal cell body labeling with pseudorabies virus.

The CNS cell groups that innervate the sympathoadrenal preganglionic neurons of rats were identified by a transneuronal viral cell body labeling technique combined with neurotransmitter immunohistochemistry. Pseudorabies virus was injected into the adrenal gland. This resulted in retrograde viral infections of the ipsilateral sympathetic preganglionic neurons (T4-T13) and caused retrograde transneuronal cell body infections in 5 areas of the brain: the caudal raphe nuclei, ventromedial medulla, rostral ventrolateral medulla, A5 cell group, and paraventricular hypothalamic nucleus (PVH). In the spinal cord, the segmental distribution of virally infected neurons was the same as the retrograde cell body labeling observed following Fluoro-gold injections in the adrenal gland except there was almost a 300% increase in the number of cells labeled and a shift in cell group distribution. These results imply there are local interneurons that regulate the sympathoadrenal preganglionic neurons. In the medulla oblongata, serotonin (5-HT)-, substance P (SP)-, thyrotropin-releasing hormone-, Met-enkephalin-, and somatostatin-immunoreactive neurons of the raphe pallidus and raphe obscurus nuclei and the ventromedial medulla were infected. In the ventromedial and rostral ventrolateral medulla, immunoreactive phenylethanolamine-N-methyltransferase, SP, neuropeptide Y, somatostatin, and enkephalin neurons were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the hypothalamus, tyrosine hydroxylase- and SP-immunoreactive neurons of the dorsal parvocellular PVH were infected. Only a few immunoreactive vasopressin, oxytocin, Met-enkephalin, neurotensin, and somatostatin PVH neurons were labeled.

Adrenal Glands↗

PubMed1989

A general pattern of CNS innervation of the sympathetic outflow demonstrated by transneuronal pseudorabies viral infections.

Pseudorabies virus (PRV) injections of various sympathetic ganglia and the adrenal gland were made in rats. These produced immunohistochemically detectable retrograde viral infections of ipsilateral sympathetic preganglionic neurons (SPNs) and transneuronal infections of the specific sets of second order neurons in the spinal cord and brain that innervate the infected SPNs. Five cell groups in the brain appear to regulate the entire sympathetic outflow: the paraventricular hypothalamic nucleus (PVH), A5 noradrenergic cell group, caudal raphe region, rostral ventrolateral medulla, and ventromedial medulla. In addition, local interneurons in laminae VII and X of the spinal cord are also involved. Other CNS areas also became transneuronally labeled after infections of certain sympathetic ganglia, most notably the superior cervical and stellate ganglia. These areas include the central gray matter and lateral hypothalamic area. The zona incerta was uniquely labeled after stellate ganglion infections. The cell body labeling was specific. This specificity was demonstrated in the PVH where the neurons of the parvocellular PVH that form the descending sympathetic pathway were labeled in a topographic fashion. Finally, we demonstrate that the retrograde transneuronal viral cell body labeling method can be used simultaneously with either neuropeptide transmitter or transmitter synthetic enzyme immunohistochemistry.

Animals↗

PubMed1989

Cardiovascular effects produced by L-glutamate stimulation of the lateral hypothalamic area.

L-Glutamate microinjections into the tuberal region of the lateral hypothalamic area (LHAt) caused a fall in blood pressure and heart rate in pentobarbital-anesthetized rats. The bradycardia was mediated by both beta-adrenergic and muscarinic mechanisms as demonstrated with pharmacological blockade. The hypotension was due to a decrease in cardiac output, not a decrease in total peripheral resistance. In addition, there was a reduction in coronary blood flow. If heart rate was held constant by pharmacological blockade or by electrical cardiac pacing, L-glutamate stimulation of the LHAt still caused a fall in blood pressure. When the electrically paced model was used, this hypotension was due to a fall in cardiac output. In contrast, with the pharmacological blockade of the heart, the hypotension was due to a decrease in the total peripheral resistance. The cardiac output reduction in the paced condition was not mediated solely by either beta-sympathetic or parasympathetic mechanisms as determined by pharmacological blockade. With heart rate held constant by either drugs or pacing, LHAt stimulation did not alter regional blood flow or resistance in any vascular bed, including the coronary circulation. We conclude that L-glutamate stimulation of the LHAt lowers the cardiac output and heart rate by both parasympathetic and beta-adrenergic mechanisms and elicits hypotension by lowering cardiac output in the naive and electrically paced model.

Animals↗

PubMed1988

L-glutamate stimulation of the zona incerta in the rat decreases heart rate and blood pressure.

Microinjections of L-glutamate into the zona incerta of pentobarbital anesthetized rats caused decreases in blood pressure and heart rate. The bradycardic response was reduced by approximately 70% after i.v. administration of atropine methyl nitrate. After combined muscarinic and beta-adrenergic blockade the bradycardic response was reduced to 90% of the control value. This suggests that the bradycardia was mediated primarily by activating the vagal outflow. Blood pressure decreases elicited after pharmacological blockade of the heart with both atropine and timolol were approximately 50% of the control values. This indicates that the zona incerta is also capable of altering stroke volume and/or inhibiting the sympathetic outflow controlling the peripheral blood vessels. By using an injectate containing L-glutamate mixed with [3H]L-glutamate and subsequent analysis of autoradiographic tissue sections, we have determined that the most reactive site is the region of the ventral zona incerta.

Animals↗

PubMed1988

Spinal origin of sympathetic preganglionic neurons in the rat.

The segmental distribution of sympathetic preganglionic neurons (SPNs) and dorsal root ganglion cells (DRGs) was studied after Fluoro-gold injections into the major sympathetic ganglia and adrenal gland in rats. A quantitative assessment of the segmental and nuclear locations was made. Four general patterns of innervation were apparent: (1) a large number of SPNs (1000-2000/ganglion) innervate the sympathetic ganglia which control head or thoracic organs and a relatively small number of SPNs (100-400/ganglion) innervate the sympathetic ganglia controlling the gut, kidney, and pelvic organs; this difference in density of innervation probably relates to the level of fine control that can occur in these end organs by the SPNs; (2) the reverse pattern is seen in the DRG labeling where a large number of DRGs were labeled after Fluoro-gold injections into the preaortic ganglia (celiac, superior, and inferior mesenteric) and a small number were labeled after injections into the cervical sympathetic ganglia; (3) the intermediolateral cell column is the main source of SPNs except for the inferior mesenteric ganglion which is innervated predominantly by SPNs originating in the central autonomic nucleus (75%); the lateral funiculus is a source of SPNs mainly for the cervical sympathetic ganglia; and (4) each sympathetic ganglion and the adrenal gland receives a multisegmental SPN and DRG input with one segment being the predominant source of the innervation. The adrenal gland shows an intermediate position in terms of the density of SPN input (approximately 800 cells) and dorsal root input (approximately 300 cells); it has a widespread segmental input (T4-T12) with the T8 segment being the major source.

Animals↗

PubMed1986

Descending noradrenergic pathways involved in the A5 depressor response.

The objective of the present study was to analyze the anatomical basis of the A5 depressor response and to test if the putative neurotransmitter noradrenaline is involved in the response. Two approaches were used; one was neuroanatomical and the other was pharmacological. First, the retrograde transport method in which two fluorescent markers (Fast blue and rhodamine microspheres) was used in combination with the indirect immunofluorescence technique to establish that A5 catecholamine neurons project to both the spinal cord and the region of the nucleus tractus solitarii (NTS). Second, we analyzed the effects of 6-hydroxydopamine (6-OHDA) lesions of the spinal cord and/or NTS area on the A5 depressor response. This response was elicited by a 80-nl microinjection of L-glutamate (500 mM) into the A5 region in pentobarbital anesthetized rats; it was characterized by a decrease in blood pressure and heart rate. After destruction of various noradrenergic terminal fields we have found that intraspinal injections of 6-OHDA caused a 30% reduction in the blood pressure component of the A5 depressor response and a transient depression of the bradycardic response. This result suggests that only a small portion of the A5 depressor response depends on the descending A5 spinal pathway. Injections of 6-OHDA into the NTS region caused a transient depression of the A5 depressor response, and by 7-14 days postinjection, the response returned to normal. After combined 6-OHDA injections into the spinal cord and NTS area, the blood pressure and heart rate components of the A5 depressor response were reduced to 80% of the control level at 3 days postinjection. By 14 days, even with severe depletion of noradrenaline in the spinal cord (96%) and a moderate depletion of noradrenaline in the NTS (50%), the A5 response was restored to about 80% of its original magnitude, suggesting some type of functional recovery occurs in this system. Third, the blood pressure decrease elicited by L-glutamate stimulation of the A5 cell group was unaffected by pharmacological blockade of the heart. In addition, this response appeared to be normal in rats that had both their autonomic supply to the heart blocked pharmacologically and their spinal cord noradrenaline levels depleted (14 days after intraspinal 6-OHDA injections). These data suggest that the major A5 depressor response operates mainly by inhibition of the sympathetic outflow involved in control of total peripheral resistance and that this system is controlled by a descending spinal pathway which probably does not use noradrenaline as a neurotransmitter.

Adrenergic Fibers↗

PubMed1985

LH-RH analogue acts as substance P antagonist by inhibiting spinal cord vasomotor responses.

Intrathecal injections of the luteinizing hormone-releasing hormone (LH-RH) analogue, [D-pGlu1-D-Phe2-D-Trp3,6]-LH-RH caused dose-dependent decreases in mean arterial blood pressure in anesthetized rats similar to those seen with [D-Pro4-D-Trp7,9]-substance P4-11. Similarly, intrathecal injections of either peptide reversed the pressor response elicited by application of kainic acid on the ventral surface of the medulla oblongata. Both analogues also had similar IC50 values (approximately 10(-5) M) for the inhibition of specific [3H]substance P binding in tissue-sections of the intermediolateral cell column. However, the LH-RH analogue failed to block substance P (SP)-induced contractions of the isolated guinea pig ileum and did not affect tail-flick withdrawal time in a thermal nociceptive test, whereas the SP analogue acted as an antagonist in both of these bioassays. These results suggest that [D-pGlu1-D-Phe2-D-Trp3,6]-LH-RH may act as an antagonist which can inhibit the sympathetic vasomotor outflow and potentially be a substance P-physalaemin (SP-P) receptor antagonist in the central nervous system but without effect on peripheral SP-P receptors.

Animals↗

PubMed1985

Substance P mechanisms of the spinal cord related to vasomotor tone in the spontaneously hypertensive rat.

This report deals with substance P (SP) mechanisms involved in regulation of vasomotor tone at the spinal cord levels in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Our results indicate the following. (1) Intrathecal injections of the SP antagonist, D-Pro,D-Trp-SP cause dose-dependent decreases in mean arterial pressure and heart rate in Sprague-Dawley rats, WKYs and SHRs; the maximal blood pressure decreases are equal to those seen after cervical spinal cord transection. (2) Intrathecal injections of this antagonist into the L1 spinal level in WKYs or SHRs that had previously had their C8 spinal cords transected caused a rise in blood pressure and heart rate, suggesting that intrinsic spinal SP mechanisms are probably not involved in vasomotor tone. (3) The intermediolateral cell column region (IML) of 16-week-old WKYs and SHRs has a single high affinity and saturable binding component with approximately the same dissociation constant (Kd = 1.21 nM for WKYs; Kd = 1.25 nM for SHRs); the SHRs showed a higher number of sites (Bmax = 24.5 fmol/mg protein) than WKY rats (Bmax = 19.9 fmol/mg protein). The Kd and Bmax obtained from IML sections from 4-week-old WKYs and SHRs exhibit no differences, although their binding values with 2 nM [3H]SP are higher than those obtained from the 16-week-old animals. (4) D-Pro4,D-Trp7,9-SP4-11 has the same relatively low (micromolar range) potency for displacing [3H]SP binding in the IML of WKYs and SHRs. (5) SHRs (16 weeks old) contain 20% more SP immunoreactivity in the IML than WKY rats (834 +/- 36 pg/mg protein vs 694 +/- 50 pg/mg protein); 4-week-old rats do not show such differences. The potential significance of these results is discussed in relation to the control of vasomotor tone.

Animals↗

PubMed1985

Reduction of [3H]substance P binding in the intermediolateral cell column after sympathectomy.

Guanethidine-induced destruction of sympathetic postganglionic neurons in neonatal rats leads to transneuronal degeneration of the sympathetic preganglionic neurons. Using this model, we have been able to show a approximately 35% decrease in [3H]substance P ([3H]SP) binding in the intermediolateral cell column--suggesting that sympathetic preganglionic neurons possess substance P receptors. Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons.

Animals↗

PubMed1985

Co-localization of substance P- and phenylethanolamine-N-methyltransferase-like immunoreactivity in neurons of ventrolateral medulla that project to the spinal cord: potential role in control of vasomotor tone.

Both substance P (SP)- and epinephrine-containing neurons in the rostral ventrolateral medulla have been thought to play a role in regulating vasomotor tone. The combination of retrograde transport of a fluorescent dye (Fast Blue) and immunofluorescent staining for SP- and phenylethanolamine-N-methyltransferase (PNMT)-immunoreactivity was used to determine the relationships of these two groups of ventrolateral medullary neurons which project to the spinal cord. The majority of spinally projecting neurons in the rostral ventrolateral medulla contain both PNMT-like and SP-like immunoreactivity. The presence of PNMT-immunoreactive material in a neuron implies that epinephrine is a probable neurotransmitter for such a cell. Earlier work demonstrated that epinephrine and SP have opposite effects on the firing of sympathetic preganglionic neurons. Our results raise the possibility of a novel mechanism of synaptic regulation of the sympathetic preganglionic vasomotor neurons.

Animals↗