Mj Brierley

Electrical activity of caudal neurosecretory neurons in seawater- and freshwater-adapted flounder: responses to cholinergic agonists

SUMMARY The caudal neurosecretory system (CNSS) of the euryhaline flounder is involved in osmoregulatory responses underlying adaptation to seawater and freshwater. This study compared electrophysiological activity and responses to cholinergic agonists in the neuroendocrine Dahlgren cells in an in vitro preparation taken from fully seawater- (SWA) or freshwater-adapted (FWA) fish. Resting membrane and action potential parameters showed few differences between SWA and FWA cells. The hyperpolarisation-activated sag potential and depolarising afterpotential were present under both conditions; however, amplitude of the latter was significantly greater in SWA cells. The proportions of cells within the population exhibiting different firing patterns were similar in both adaptation states. However, bursting parameters were more variable in FWA cells, suggesting that bursting activity was less robust. The muscarinic agonist, oxotremorine, was largely inhibitory in Dahlgren cells, but increased activity in a non-Dahlgren cell population,α neurons. Nicotine promoted bursting activity in SWA Dahlgren cells, whereas it inhibited over half of FWA cells.

Electrical activity of caudal neurosecretory neurons in seawater and freshwater-adapted Platichthys flesus, in vivo

SUMMARY This study examined the electrical firing activity of neuroendocrine Dahlgren cells in the caudal neurosecretory system (CNSS) of the euryhaline flounder in vivo. Intracellular recordings revealed generally similar activity patterns and membrane properties to those previously reported in vitro. To investigate the potential role of the CNSS in osmoregulatory adaptation, extracellular, multiunit, recordings compared the activity patterns of Dahlgren cells in fully seawater- and freshwater-adapted fish. The proportion of cells showing bursting (as opposed to phasic or tonic) activity was greater in seawater-than in freshwater-adapted fish, as was the Correlation Index, a measure of the degree of correlation between firing activities of cells recorded simultaneously from the same preparation. Acute transfer of fish from seawater to freshwater gill perfusion led to recruitment of previously silent Dahlgren cells and a reduction in Correlation Index; freshwater to seawater transfer increased the Correlation Index. Severing the spinal cord anterior to the CNSS led to an increase in overall Dahlgren cell activity. Electrical stimulation of branchial nerve branches providing input to the brainstem, or tactile (pinch) stimulation of lips or fins, led to a reduction in CNSS activity lasting up to 500 s, indicating the presence of descending modulatory pathways from the brain. These results are consistent with a role for CNSS neuropeptides, urotensins, in supporting survival in a hypertonic, seawater, environment.

Voltage- and Ca2+-dependent burst generation in neuroendocrine Dahlgren cells in the teleost Platichthys flesus.

The neuroendocrine Type 1 Dahlgren cells of the caudal neurosecretory system of the flounder display characteristic bursting activity, which may increase secretion efficiency. The firing activity pattern in these cells was voltage‐dependent; when progressively depolarized, cells moved from silent (approximately −70 mV), through bursting and phasic to tonic firing (< −65 mV). Brief (10 s) evoked bursts of spikes were followed by a slow after‐depolarization (ADP; amplitude up to 10 mV, duration 10–200 s), which was also voltage‐dependent and could trigger a prolonged burst. The ADP was significantly reduced in the absence of external Ca2+ ions or the presence of the L‐type Ca2+ channel blocker, nifedipine. BayK 8644 (which increases L‐type channel open times) significantly increased ADP duration, whereas the Ca2+‐activated nonselective cation channel blocker, flufenamic acid, had no effect. Pharmacological blockade of Ca2+‐activated K+ channels, using apamin and charybdotoxin, increased the duration of both ADP and evoked bursts. However, action potential waveform was unaffected by either apamin/charybdotoxin, nifedipine, BayK 8644 or removal of external Ca2+. The short duration (approximately 100 ms), hyperpolarization‐activated, postspike depolarizing afterpotentials (DAP), were significantly reduced by nifedipine. We propose that long duration ADPs underlie bursts and that short duration DAPs play a role in modulation of spike frequency.