Dopamine produces muscle contractions and modulates motoneuron-induced contractions in Aplysia gill.

1. Dopamine has been reported to exist in unusually large quantities in Aplysia gill. The physiological role of this neurotransmitter in this organ was examined. 2. The addition of dopamine to a gill perfusate results in the contractions of the lateral and medial external pinnule muscles, the circular and longitudinal muscles of the afferent vessel, and the circular muscles of the efferent vessel. 3. Dopamine-induced contractions persist after chemical synaptic transmission is eliminated in the gill. This suggests that excitatory dopamine receptors are present on gill smooth muscle fibers themselves. 4. Dopamine also potentiates the gill response to action potentials in single identified gill motoneurons. Evidence presented suggests that muscle contractions and modulation of motoneuron contractions are independent phenomena. 5. While modulation may in part be mediated by increases in excitatory junction potential (EJP) amplitude, in many cases large increases in muscle contractions occur while the enhancement of EJPs is disproportionately small. 6. Dopamine's ability to produce muscle contractions suggests that there may be dopaminergic motoneuron innervation of the gill. We suggest that dopamine's modulatory actions may be mediated via modification of excitation-contraction coupling in smooth muscle fibers.

Electrophysiological and pharmacological properties of cultured rat thyroid cells.

The electrophysiological properties of a hormone-dependent, differentiated thyroid epithelial cell strain were studied using intracellular microelectrodes. The average membrane potential of solitary, isolated cells was -78.4 +/- 1.3 mV. The membrane potential depolarized 55 mV per tenfold increase in extracellular potassium concentration. Weak electrical coupling was recorded between contiguous cells. Like thyroid cells in vivo, these cells did not generate action potentials. In some cells a spontaneous, slow transition in the membrane potential from -80mV to -30 mV was accompanied by an increase in input resistance. Membrane potential transitions could be induced by perfusing cells with isotonic Hanks solutions saturated with CO2 (pH = 5.5) or by perfusing cells with hypotonic Hanks solutions (190-290 mOsm/kg). Membrane potential transitions were due to a decreased potassium permeability. Noradrenaline elicited both a fast depolarization and a slow depolarization. The fast depolarization was due to an increase in conductance of Na+ channels and of Cl- channels. Intracellular injection of Ca++ elicited the fast depolarization. Intracellular injection of EGTA or cobalt abolished the fast depolarization. Replacement of extracellular Ca++ by Mg++ did not affect the fast depolarization. Thus, the fast depolarization was due to accumulation of intracellular Ca++. The fast depolarization was abolished by the alpha adrenergic blocker phentolamine (10(-6) M), and was not abolished by the beta adrenergic blocker propranolol (10(-5) M).

Chemosensitivity of single smooth muscle cells to acetylcholine, noradrenaline, and histamine in vitro.

Electrical responses to acetylcholine, noradrenaline, and histamine were recorded from solitary smooth muscle cells. Iontophoresis of each transmitter elicited three fast responses: a hyperpolarization, a depolarization, or a biphasic hyperpolarization-depolarization. Each transmitter activated a specific receptor since responses were specifically blocked by antagonists, two transmitters elicited different responses in solitary cells, and desensitization of response to one transmitter did not cause desensitization of responses to other transmitters. Responses were due to increased ion conductances since input resistance decreased during responses and reversal potentials were measured for depolarizing responses (-5 mV) and hyperpolarizing responses (-60 mV). Regional differences in transmitter sensitivity were mapped on solitary cells. Biphasic responses were due to simultaneous activation of receptors mediating hyperpolarizing responses and receptors mediating depolarizing responses which were segregated in the cell membrane. Noradrenaline enhanced action potential amplitude by regulation of voltage-dependent ion conductances. Finally, noradrenaline and histamine elicited periodic hyperpolarizing potentials, which may be due to increased intracellular Ca++.

Electrophysiological properties of human oviduct smooth muscle cells in dissociated cell culture.

Intracellular recordings were made from human oviduct smooth muscle maintained in cell culture. Solitary cells isolated from one another and cells in contact with one another retained electrical properties of smooth muscle in vivo. Membrane potential of solitary cells and connected cells was -35 mV. Connected cells formed electrotonic junctions which transmitted current from one cell to another. This current spread was responsible for differences in input resistance and time constant in solitary cells, 66 Momega and 96 msec, compared to connected cells, 26 Momega and 56 msec. All cells expressed delayed rectification to depolarizing current pulses. Some cells generated action potentials spontaneously or in response to intracellular current pulses. Action potentials were abolished by cobalt or by EGTA. Slow wave potentials, 5 . 20 mV in amplitude, occurred continuously once every 15 to 45 seconds in connected cells.