Synaptic Transmission In Sympathetic Ganglia Research Articles

Roles of cyclic nucleotides in the synaptic transmission in sympathetic ganglia of rabbits

1. Two kinds of slow postsynaptic potentials can be elicitable in the rabbit superior cervical ganglion: a dopaminergic hyperpolarizing (slow IPSP) one and a muscarinic depolarizing (slow EPSP) one, respectively. 2. Cyclic AMP may not be involved in the generation of slow IPSP, whereas it certainly mediates the dopamine-induced enduring modulatory enhancement of the slow EPSP response. 3. Cyclic GMP appears to mediate at least one of the components in the mechanism underlying the slow EPSP by generating a depolarization with no change in membrane conductance. 4. Cyclic GMP does additionally regulate the dopamine (or cyclic AMP)-induced modulatory enhancement of the slow EPSP by antagonizing it in a uniquely time-dependent fashion.

Histamine H1 and H2-receptors at a ganglionic synapse.

MANY humoral agents are capable of modulating synaptic transmission in sympathetic ganglia and it has been proposed that a variety of receptors are present at the ganglionic synapse (see Haefely1). There are thus many possible modulatory mechanisms at this synapse, some of which have a dual nature, the same substance being able both to facilitate and to depress ganglionic transmission by an action on two different populations of receptors. We wish to present evidence that histamine, like the catecholamines2 and 5-hydroxytryptamine (serotonin)3, has a dual action at the ganglionic synapse.

Action of dopamine and noradrenaline on synaptic transmission in sympathetic ganglia of brown fat

Action of dopamine and noradrenaline on synaptic transmission in sympathetic ganglia of brown fat

Electrical impedance and vasomotor changes accompanying synaptic transmission in sympathetic ganglia

Electrical impedance changes within the superior cervical sympathetic ganglion of the cat were recorded at 17.5 kc under various conditions at rest and during synaptic activity. Local blood flow changes in the ganglion were also assessed from the pulsatile component of the impedance bridge output. The following impedance baseline changes were obtained with the ganglion at rest: a decrease after electrode insertion and hypoventilation, and an increase with hyperventilation, asphyxia, and barbiturate anesthesia. Synaptic activity typically gave rise to an initial drop in impedance followed by a prolonged rise. The falling phase of impedance, resistant to hypoxia, fatigue, and hexamethonium, has been tentatively related to presynaptic events, and the rising phase, from similar evidence, to postsynaptic activity. All observed impedance changes were interpreted in terms of changes in relative size of the extracellular fluid compartment. Although small and short-lasting increases in blood flow with synaptic transmission were observed, blood flow changes were not found to be a necessary accompaniment of synaptic activity.

Effects of anesthetics on oxygen consumption and on synaptic transmission in sympathetic ganglia.

Effects of anesthetics on oxygen consumption and on synaptic transmission in sympathetic ganglia.