Gays and Lesbians Older and Wiser (GLOW): a support group for older gay people.

Gays and Lesbians Older and Wiser (GLOW), a support group sponsored by a geriatric medical clinic in the midwest, is described. GLOW has been meeting monthly for 7 years. Scheduling, professional involvement, and special attention to social support seem critical for the group's success. Older gay men and lesbians often have unique support needs that may not be met by either general services to the elderly or by gay organizations, which typically cater to a younger population. We conclude that carefully designed support groups can meet some support needs for this older population.

Synaptic modulation of calcium-dependent potassium conductance in myenteric neurones in the guinea-pig.

1. Ganglion cells of the myentric plexus of the guinea-pig small intestine were studied with intracellular recording methods. 2. Electrical stimulation of the interganglionic connectives elicited slow synaptic excitation (slow e.p.s.p.) that was associated with an increase in the input resistance of the cell. The slow e.p.s.p.s continued for several seconds after termination of stimulation, and they occurred only in neurones in which prolonged hyperpolarizing after-potentials followed an action potential. 3. Superfusion of the neurones with solutions containing either 1-5 mM-Mn2+ or 16 mM-Mg2+ and 1 mM-Ca2+ mimicked the slow e.p.s.p. The common characteristics of Mn2+, Mg2+ and the slow e.p.s.p. were: (a) depolarization of the membrane potential, (b) increased input resistance of the cell, (c) augmented excitability, (d) blockade of post-pike hyperpolarizing potentials and (e) reversal potential between -70 and -75 mV. 4. Analyses based on the 'constant field equation' indicated that the permeability ratios of K+ to other permeant ionic species were reduced when Ca2+ influx was blocked by Mn2+ or Mg2+. 5. The organic Ca antagonist D-600 did not affect the neurones. 6. The results suggest that slow synaptic modulation of excitability within the myenteric plexus involves a reduction of both resting GK and post-spike GK which is secondary to suppression of Ca2+ influx by the neurotransmitter for the slow e.p.s.p.

Intracellular study of tonic-type enteric neurons in guinea pig small intestine.

1. Intracellular recording revealed a population of myenteric neurons with electrical behavior that appeared to be equivalent to the tonic-type mechanosensitive neurons found in earlier studies that utilized extracellular recording of single units. 2. Electrical stimulation of the interganglionic fiber tracts evoked a slowly rising excitatory postsynaptic potential (slow EPSP) that was prolonged for several seconds after termination of the stimulus in these cells. The slow EPSP was associated with increased input resistance and augmented excitability of the somal membrane. The somal membranes had relatively low excitability in the absence of fiber tract stimulation. This was indicated by: 1) failure of depolarizing current pulses to elicit spike discharge in some cells; 2) when spikes were elicited by depolarizing current pulses, one to three spikes occurred, and these were seen only at the onset of the pulse; 3) passive invasion of the soma by current from spikes in the cell's processes did not trigger spikes; 4) the spikes were followed by prolonged hyperpolarizing afterpotentials associated with decreased input resistance. 3. Characteristics of the augmented excitability during the slow EPSP were: 1) endogenous discharge of trains of spikes, 2) spike discharge throughout 200 ms duration depolarizing current pulses, 3) electrotonic spike potentials from the processes triggered somal spikes, 4) postspike afterhyperpolarization was reduced or abolished. 4. The slow EPSP was reduced or abolished in Krebs solution with 16 mM Mg+2 and in HEPES-buffered Krebs with 1 mM Mn2+. It was enhanced in Krebs solution with 3 times normal Ca2+. Spike discharge in elevated Ca2+ eliminated the increase in input resistance associated with the slow EPSP. 5. Calcium availability was an important factor in regulation of membrane conductance and excitability in the perikaryon. The slow EPSP provides a mechanism whereby the soma of a multipolar neuron gates the spread of excitation between its dendrites and axon.

Serotonergic activation of tonic-type enteric neurons in guinea pig small bowel.

1. Electrical stimulation of interganglionic fiber tracts of Auerbach's plexus released a chemical substance, which produced a slow EPSP associated with an increase in input resistance in the postsynaptic neuron. 2. This effect of fiber tract stimulation was mimicked by microiontophoretic application of serotonin (5-HT) to the neurons. Both the endogenous transmitter substance and exogenous 5-HT produced membrane depolarization, both increased the input resistance of the neuron, both reduced or abolished hyperpolarizing afterpotentials of the action potentials, and both augmented membrane excitability. 3. During tachyphylaxis to excess 5-HT (1 micron) in the perfusion solution, the response to fiber tract stimulation was also reversibly blocked. 4. Methysergide (30 micron) blocked both the response to fiber tract stimulation and to exogenous 5-HT. 5. Cholinergic agonists and antagonists did not alter the slow EPSP and the response to exogenous 5-HT. 6. The evidence suggests that 5-HT is the neurotransmitter substance that produces the slow EPSP in myenteric neurons.

Adrenergic inhibition of serotonin release from neurons in guinea pig Auerback's plexus.

1. Norepinephrine reversibly blocked both the fast and slow stimulus-evoked EPSPs in myenteric ganglion cells. This action of norepinephrine was offset by the alpha-adrenergic blocking agent, phentolamine. 2. The putative neurotransmitter for the fast EPSP is acetylcholine, and serotonin (5-HT) is the suspected transmitter for the slow EPSP. 3. Norepinephrine did not block the excitatory effect of microiontophoresis of 5-HT onto the ganglion cells. 4. Norepinephrine decreased the input resistance and suppressed neuronal excitability. This effect was reversed by addition of 5-HT to the perfusion solution and was attributed to presynaptic blockade by norepinephrine of ongoing release of 5-HT. 5. Addition of norepinephrine after the slow EPSP had been evoked did not shorten the duration of the slow EPSP. 6. The results suggested that the mechanism of the blocking action of norepinephrine was inhibition of release of the excitatory neurotransmitters form presynaptic nerve terminals. This is probably one of the mechanisms that is involved in suppression of gastrointestinal motor function during activation of the sympathetic innervation of the bowel.

The effect of motilin on the electrical activity of rabbit circular duodenal muscle.

The effect of 13-norleucine motilin on electrical activity and membrane resistance of the rabbit circular duodenal muscle was studied with intracellular recording techniques. Electrical slow waves without spikes occurred in Krebs solution made twice hypertonic by addition of sucrose. The slow waves were basic organ specific type rhythm (BOR). Their mean frequency was 18.1.min-1, the mean amplitude from trough to peak was 11.4 mV and mean membrane potential during the trough was -59.1 mV. Motilin (1.10(-7) g/ml) had the following effects: (1) The membrane depolarized by a mean of 10.9 mV. (2) Membrane resistance was reduced. (3) The BOR slow waves were either reduced or abolished. (4) Slow fluctuations of membrane potential characteristic of a minute-type rhythm (MR) appeared. (5) Trains of spikes occurred at the crests of the MR and were associated with contraction of the muscle.

Dual effects of calcium ions on pacemaker activity in guinea-pig taenia coli.

The effects of various [Ca2+]0 on membrane potential (MP), action potential (AP) frequency, and isometric tension of isolated guinea-pig taenia coli were studied using intracellular recording techniques and simultaneous tension measurement. At 5.9 mM [K+]0 the order of potency of [Ca2+]0 this order is gradually reversed since high [Ca2+]0 becomes more potent in accelerating impulse discharges. At 2.5 mM [Ca2+]0 the line relating MP to log [K+]0 is not straight; its slope for a tenfold change of [K+]0 is 21.1 mV in the range between 5.9 and 17.7 mM [K+]0, and 51.5 mV between 32.45 and 59 mM [K+]0. In general, reducing [Ca2+]0 depolarizes the membrane whereas increasing [Ca2+]0 hyperpolarizes it. The Ca2+-induced changes of MP are reduced at high [K+]0. At 2.5 and 7.5 mM [Ca2+]0 the lines relating AP frequency and tension to the MP are nearly superimposed. In contrast, at 0.83 mM [Ca2+]0 the line is shifted to lower frequency and tension for all MP values studied. In conclusion, in the range of low [Ca2+]0 the system underlying pacemaker activity seems to be dependent on Ca2+ in two ways: 1. by an indirect negative action mediated by an increase of PK+ and by hyperpolarization of the membrane; 2. by a direct positive action which is not mediated by alterations of MP. In the range of normal and high [Ca2+]0 only potential-mediated Ca2+-effects determine AP frequency. The hypothesis is put forward that Ca2+ may carry the background inward current responsible for pacemaker activity.

Properties of mechanosensitive neurons within Auerbach's plexus of the small intestine of the cat.

Three different kinds of mechanosensitive neurons were detected by direct electrical recording from Auerbach's plexus. Neurons classified as fast-adapting mechanoreceptors discharged spikes at the onset of stimulation, and the discharge stopped during a sustained stimulus of constant intensity. Slowly-adapting mechanoreceptors maintained during sustained stimulation, a steady discharge at a frequency that was a direct function of the intensity of the stimulus. Tonic type neurons responded to mechanical stimulation with a prolonged train of spikes which had a consistent pattern from preparation to preparation. Once the tonic-type cells were triggered, the discharge followed a characteristic time course that was unchanged by further increase or decrease in stimulus intensity. Tonic-type neurons are probably not first order sensory neurons, but they may be activated by input derived from primary mechanoreceptors. Frequency of discharge of slowly-adapting mechanoreceptors was increased by histamine. This appeared to be secondary to histamine-induced contractile activity of the musculature.