Rat Sympathetic Preganglionic Neurons Research Articles

Subtypes of glutamate receptors mediate fast and slow excitatory potentials in neonate rat sympathetic preganglionic neurones in vitro

Subtypes of glutamate receptors mediate fast and slow excitatory potentials in neonate rat sympathetic preganglionic neurones in vitro

Excitation and inhibition of rat sympathetic preganglionic neurones by catecholamines

The actions of microiontophoretically applied catecholamines on antidromically identified sympathetic preganglionic neurones (SPN) in the upper thoracic spinal cord of the anaesthetized rat were investigated. Noradrenaline (NA) excited the majority of neurones (50/71), however, a significant number were inhibited by the catecholamine (17/71). Adrenaline excited 4/9 SPN and inhibited 2/9. Dopamine had excitatory actions on SPN (3/3). Dual actions of NA on the same SPN were demonstrated, with the actions of the catecholamine being modulated by excitatory amino acids. NA was also shown to induce burst firing in 21% of SPN.

APV-sensitive dorsal root afferent transmission to neonate rat sympathetic preganglionic neurons in vitro

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices from neonate (12- to 22-day-old) rats. 2. Electrical stimulation of dorsal roots or dorsal root entry zone elicited in SPNs an excitatory postsynaptic potential (EPSP) or multiple EPSPs of varying latencies. The EPSP could be graded by varying the stimulus intensity and, on reaching the threshold, discharged an action potential. 3. The dorsal root-evoked EPSPs had a mean synaptic latency of 2.6 ms (range: 1.2-11 ms), suggesting a polysynaptic pathway. The EPSPs were characteristically slow in onset with a mean rise time and half-decay time of 8.3 and 23 ms, respectively. 4. At the resting membrane potential of -50 to -60 mV, the amplitude of EPSPs recorded in normal (1.3 mM Mg2+) Krebs solution was reduced by membrane hyperpolarization or depolarization. In Mg2(+)-free solution, EPSPs were potentiated and reached threshold for spike discharge. 5. The EPSPs were suppressed by the nonselective glutamate receptor antagonist kynurenic acid (0.1-0.5 mM) and by the N-methyl-D-aspartate (NMDA) receptor antagonists D-2-amino-5-phosphonovaleric acid (APV; 1-10 microM) and ketamine (5-10 microM), but not by the quisqualate (QA)/kainate (KA) receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX, 1-10 microM). The latter depressed the EPSPs elicited by stimulation of lateral funiculus in the same SPNs. 6. NMDA applied by pressure elicited a depolarization in the SPNs. In normal Krebs solution the response was voltage dependent with the peak amplitude occurring around -60 mV; conditioning depolarization or hyperpolarization diminished the response.(ABSTRACT TRUNCATED AT 250 WORDS)

Morphology of sympathetic preganglionic neurons in the neonatal rat spinal cord: An intracellular horseradish peroxidase study

Understanding the central neural control of autonomic functions requires a knowledge of the morphology of the preganglionic neurons, for the location of the dendritic arborizations of these neurons will indicate which central pathways may have access to them. In the present study, individual sympathetic preganglionic neurons in the neonatal rat spinal cord have been examined by the intracellular injection of horseradish peroxidase (HRP) in an in vitro preparation. Seventeen HRP-labeled preganglionic neurons in thoracic segments T1-T3 were examined in detail; of these, 12 somata were located in the intermediolateral cell column (IML), one in the lateral funiculus (LF), two in the intercalated nucleus (IC), and two at the border between IML and IC. All of the neurons had extensive dendritic arborizations arising from an average of six primary dendrites; the average total dendritic length for these cells was 2,343 microns. The morphology of preganglionic neurons differed depending on the location of their cell bodies. Preganglionic neurons located in the IML were essentially two-dimensional: the cells had some dendrites that coursed rostrocaudally for 300-500 microns within the IML and others that coursed mediolaterally, extending to the lateral surface of the cord and close to the central canal. Axons of these cells coursed ventrally from the cell body and exited from the spinal cord at the first ventral root caudal to the cell body. No intraspinal axon branches were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Neonate rat sympathetic preganglionic neurons intracellularly labelled with lucifer yellow in thin spinal cord slices

Sympathetic preganglionic neurons and interneurons were intracellularly labelled with lucifer yellow in thin transverse spinal cord slices of neonatal rats. Preganglionic neurons had spindle or oval shape somata and were located in the intermediolateral nucleus. The axons of these neurons coursed ventrally along the border of gray matter and exited the ventral horn; two to four long dendrites projected medially to the central canal and several relatively short dendrites oriented toward the lateral white matter. Interneurons were generally multipolar and located outside the immediate area of intermediolateral nucleus; their axons could sometimes be traced to the ventral funiculus. Interestingly, dye-coupled preganglionic neurons were observed for the first time. Our findings suggest that the dendritic domain of neonatal rat sympathetic preganglionic neurons is out-reaching and may represent potential sites of interaction with incoming segmental and/or descending inputs. In addition, the observation of dye-coupled preganglionic neurons raises the possibility that these neurons may have the capability of recruiting and/or synchronizing sympathetic outflow.

Excitatory and inhibitory effects of epinephrine on neonatal rat sympathetic preganglionic neurons in vitro

Current and voltage recordings were made from antidromically identified sympathetic preganglionic neurons (SPNs) in transverse thoracolumbar spinal cord slices removed from neonatal rats. When applied by either pressure ejection or superfusion, epinephrine (Epi) caused a slow depolarization or an inward current in 62 SPNs (42%) and a slow hyperpolarization or an outward current in 21 SPNs (14%). The responses persisted in low calcium- or tetrodotoxin-containing media. The Epi-induced depolarization or inward current was associated with increased membrane resistance; it was reduced by membrane hyperpolarization and nullified at a membrane potential of about −100 mV; a clear reversal however was not observed at more negative potential levels. In a number of SPNs the Epi-induced depolarization was accompanied by small inhibitory postsynaptic potentials. The latter were eliminated by a low calcium solution and by the glycine antagonist strychnine, suggesting that they were caused by glycine or a glycine-like substance released from interneurons subsequent to activation by Epi. The Epi-induced hyperpolarization or outward current was associated with decreased membrane resistance, and nullified around −100 mV. The α-adrenergic antagonist, dihydroergotamine, andα 1-antagonist, prazosin, reversibly blocked the excitatory, whereas theα 2-antagonist, yohimbine, abolished the inhibit response, respectively. It is concluded that Epi acting onα 1-andα 2-adrenergic receptors depolarizes and hyperpolarizes the r SPNs by decreasing or increasing membrane conductances to potassium ions.

In vitro effects of substance P on neonatal rat sympathetic preganglionic neurones.

1. Intracellular recordings were made from antidromically identified sympathetic preganglionic neurones (SPNs) in thin transverse neonatal rat thoracolumbar spinal cord slices. 2. Applied either by pressure ejection or superfusion, substance P (SP) caused a slow, monophasic depolarization in 60% of sympathetic preganglionic neurones; a biphasic response consisting of an initial hyperpolarization followed by a depolarization was observed in a few neurones. In addition, SP induced the occurrence of repetitive inhibitory postsynaptic potentials (IPSPs) in about 20% SPNs. 3. Low-Ca2+ or tetrodotoxin (TTX)-containing Krebs solution abolished the hyperpolarizing phase of the biphasic response and the small IPSPs, thereby augmenting the depolarizing response of SP. 4. SP-induced depolarizations were often associated with a moderate increase in membrane resistance. Generally, the response was made smaller on hyperpolarization and reversed at the membrane potential between -90 and -100 mV. These findings suggest that a reduction of membrane K+ conductance may underlie the depolarizing action of SP. 5. Subthreshold fast, excitatory postsynaptic potentials (EPSPs) evoked by stimulation of dorsal rootlets were consistently augmented during SP-induced depolarization, leading to cell discharge. 6. Focal stimulations elicited, in addition to a fast EPSP, a slow EPSP in about 40% of SPNs. The slow EPSP was often associated with an increased membrane resistance and became smaller on hyperpolarization. 7. In 15% of SPNs that generated a slow EPSP, the latter was reversibly abolished during SP-induced depolarization; the blockade persisted when the membrane potential was restored to the resting level by hyperpolarizing current. 8. It is concluded that SP is excitatory to SPNs and that its synaptic release may initiate a slow EPSP which serves to augment impulse transmission through SPNs. Further, it appears that inhibitory interneurones may also be sensitive to SP and their activation may provide a negative feed-back mechanism which can limit excessive excitation of SPNs by the peptide.

Excitatory postsynaptic potentials in neonatal rat sympathetic preganglionic neurons: possible mediation by NMDA receptors

Excitatory postsynaptic potentials (EPSPs) evoked in antidromically identified sympathetic preganglionic neurons (SPNs) and membrane depolarizations induced by N- methyl- d-aspartate (NMDA) applied by pressure ejection were increased by removing Mg ions from the perfusing media and blocked by d-2-amino-5-phosphonovalerate (APV), dl-APV and ketamine. Further, the amplitude of EPSPs and NMDA-induced depolarizations were decreased and increased by membrane hyperpolarization in Krebs solution with and without Mg 2+, respectively. These findings indicate that the excitatory amino acid receptor mediating the EPSPs in SPNs may be of the NMDA subtype.

Excitation of lateral horn neurons of the neonatal rat spinal cord by 5-hydroxytryptamine

The effects of 5-hydroxytryptamine (5-HT) on lateral horn cells contained in thin in vitro slices of neonatal rat spinal cord were investigated by means of intracellular recording techniques. Superfusion of 5-HT (1–100 μM) to lateral horn cells caused a concentration-dependent membrane depolarization leading to, in some instances, repetitive cell discharges. A number of lateral horn cells could be activated antidromically by stimulating the ventral rootlets. The conduction velocity of the antidromic spikes was estimated to be 0.3–2 m/s which corresponds to that of the axons of rat sympathetic preganglionic neurons reported by others. The 5-HT depolarization evoked in neurons that could be activated antidromically was similar to that elicited from unindentified lateral horn cells. The depolarization induced by 5-HT could be partially eliminated by low Ca/high Mg solution or tetrodotoxin in a portion of lateral horn cells and was accompanied by an increase in membrane resistance. The response was nullified near the membrane potential at which the spike afterhyperpolarization was abolished; a clear reversal of polarity was not observed at a more negative potential level. The 5-HT depolarization was reversibly blocked by methysergide and cyproheptadine and enhanced by fluoxetine, a 5-HT-uptake inhibitor. The results indicate that the indoleamine primarily exerted an excitatory action on lateral horn cells, including those tentatively identified as sympathetic preganglionic neurons, by a direct depolarization which appears to be mediated by decrease of a voltage-sensitive K conductance and partly by an indirect effect via the release of an excitatory substance(s).

Chemical Nature of Synaptic Transmission in Vertebrates

Chemical Nature of Synaptic Transmission in Vertebrates

INFLUENCE OF DISCHARGE OF MOTONEURONS UPON EXCITATION OF NEIGHBORING MOTONEURONS

INFLUENCE OF DISCHARGE OF MOTONEURONS UPON EXCITATION OF NEIGHBORING MOTONEURONS