Membrane potential and input resistance in acinar cells from cat and rabbit submaxillary glands <i>in vivo</i>: effects of autonomic nerve stimulation

SUMMARY1. Intraneural electrical stimuli (0-3-1P2 mA, 0-2 ms) were delivered via a tungsten microelectrode inserted into a cutaneous fascicle in the median nerve at the wrist in twenty-eight normal subjects. The effects on sweat glands within the innervation zone were monitored as changes of skin resistance and water vapour partial pressure (WVPP). Regional anaesthesia of the brachial plexus in the axilla eliminated spontaneous sympathetic activity and reflex effects.2. At stimulation frequencies of 041 Hz each stimulus evoked a transient skin resistance reduction, the amplitude of which varied initially but reached a steady state of less than 10 kQ after, on average, nine responses. If preceded by stimulationfree intervals of 5 min or more, up to fifteen stimuli were required before the first response occurred. With higher frequencies individual responses started to merge, skin resistance levels decreased successively and levelled off around 10 Hz. The total change of resistance (0-10 Hz) was 101 + 46 (n = 9) kQ and the higher the prestimulus level, the larger the reduction (r = 0-68, P < 0 05).3. Stimulus-response latencies to the onset of a skin resistance reduction (single stimuli or trains of six impulses/20 Hz given at 0 1 Hz) shortened initially but reached steady-state values after on average nine to twelve impulses. Average conduction velocity between stimulating electrode and skin resistance recording site was 0-78 m/s and average time for electrical neuroeffector transfer in sweat glands was estimated to be 348 ms.4. In addition to direct stimulation-induced resistance responses there were also small spontaneous reductions of resistance. They were seen in all subjects and at all frequencies but were more common in some subjects and occurred predominantly at the beginning of stimulation or at changes of frequency. They occurred independently at two skin sites in the same subject and disappeared during stimulation-free periods and after atropine.5. With train stimulation (six impulses/20 Hz) at 0-1 Hz, each train evoked transient increases of WVPP of 1 mmHg or less in some subjects (latency around 1'6 s). After averaging weak increases were seen also after single stimuli in two subjects. Increases of stimulation current or frequency led to slowly developing sustained increases of WVPP concomitant with decreases in skin resistance. MS 9170M. KUNIMOTO AND OTHERS 6. Responses in skin resistance and WVPP to train stimulation at 0X1 Hz were suppressed in a dose-dependent way by i.v. injections of atropine. The cumulative dose necessary for complete inhibition of stimulus-induced responses (0-32 mg or less) had only weak effects on skin resistance responses to arousal stimuli in the opposite, non-anaesthetized hand.7. We conclude that the intraneural electrical stimulation evoked sweating mainly by direct excitation of cholinergic sudomotor nerve fibres but that a minor addition of sweat was produced by a local mechanism in sweat glands and/or terminal nerve fibres. The delayed development of skin resistance ...

Section: Spontaneous Skin Resistance Changesmentioning

confidence: 52%

Neuroeffector characteristics of sweat glands in the human hand activated by regular neural stimuli.

Kunimoto

Kirnö

Elam

et al. 1991

“…Small spontaneous potentials sometimes appeared, as has also been seen in submandibular glands of cats (Lundberg, 1955;Kagayama & Nishiyama, 1974). Since they hadthe same direction as potentials evoked by auriculo-temporal nerve stimulation and, like these, were abolished by atropine, they were assumed to be due to spontaneous release of acetylcholine from the parasympathetic nerves.…”

Section: Discussionmentioning

confidence: 82%

Sympathetically evoked secretory potentials in the parotid gland of the cat.

Emmelin¹,

Grampp²,

Thesleff³

1980

SUMMARY1. In cats under chloralose anaesthesia micro-electrodes were inserted into parotid gland cells.2. The average resting potential was found to be -356 + 4.7 (S.D.) mV. 3. Stimulation of the auriculo-temporal nerve caused hyperpolarizing, or occasionally depolarizing, secretary potentials of 5-10 mV, which were abolishable with atropine.4. Stimulation of the cervical sympathetic trunk regularly caused, after long latency (several seconds), slow depolarizations of 15-20 mV, accompanied by a decrease in input resistance. They were antagonized by practolol and therefore assumed to be mediated bv fl1-adrenoceptors. Occasionally hyperpolarization, ascribed to an effect on x-adrenoceptors, was observed.5. In many units the slow depolarization on sympathetic stimulation was preceded by short-lasting hyperpolarizing (sometimes depolarizing) transients. They resembled the evoked cholinergic responses but could be abolished not only by atropine but also by guanethidine.

“…In some cases a monophasic depolarization was observed. (Kagayama & Nishiyama, 1974). Rabbit and cat submaxillary glands…”

Section: Resultsmentioning

confidence: 99%

Membrane potential and resistance measurement in acinar cells from salivary glands in vitro: effect of acetylcholine

Nishiyama¹,

Petersen²

1974

Self Cite

SUMMARY1. Cell membrane potential and input resistance measurements were made on segments of submaxillary glands from mice, rabbits or cats placed in a tissue bath, which was perfused with physiological salt solutions.2. During exposure to a standard Krebs-Henseleit solution, ACh stimulation always evoked a marked decrease in input resistance and time constant. The change in potential evoked by ACh stimulation was either a monophasic hyperpolarization (low resting potential) or a depolarization followed by hyperpolarization (high resting potential).3. Increasing [Ca]o from 2-56 to 10 mm resulted in an enhanced input resistance. Under this condition it was sometimes possible to obtain current-voltage relations. The relationship was linear in the range -50 to -10 mV. In the absence of extracellular Ca the resting potential was reduced and ACh mostly evoked hyperpolarizations. In those cases when the resting potential remained high biphasic potentials were still observed.4. During exposure to Na-free solutions the resting potential was either unchanged or slightly enhanced. ACh never evoked biphasic potentials, but always large hyperpolarizations.5. In the first period (1 hr) after exposure to a K-free solution ACh normally evoked very large hyperpolarizationrs, often to more than -100 mV. After several hours of exposure to K-free solution the input resistance gradually increased and ACh evoked a tremendous fall in input resistance and time constant with only a small potential change. Re 7. It is concluded that ACh evokes a marked increase in surface cell membrane permeability of salivary acinar cells. The ACh evoked hyperpolarization is due to an increase in PK: the depolarization frequently preceding the hyperpolarization is probably mainly related to an increase in PNa. The membrane Na-K pump can act electrogenically at least under conditions of Na loading.