The localization of two voltage-gated calcium channels in the pyloric network of the lobster stomatogastric ganglion

Gradwohl

et al. 2014

Front. Cell. Neurosci.

Professional deep sea divers experience motor and cognitive impairment, known as High Pressure Neurological Syndrome (HPNS), when exposed to pressures of 100 msw (1.1 MPa) and above, considered to be the result of synaptic transmission alteration. Previous studies have indicated modulation of presynaptic Ca2+ currents at high pressure. We directly measured for the first time pressure effects on the currents of voltage dependent Ca2+ channels (VDCCs) expressed in Xenopus oocytes. Pressure selectivity augmented the current in CaV1.2 and depressed it in CaV3.2 channels. Pressure application also affected the channels' kinetics, such as ƮRise, ƮDecay. Pressure modulation of VDCCs seems to play an important role in generation of HPNS signs and symptoms.

Section: Discussionmentioning

confidence: 99%

Selective modulation of cellular voltage-dependent calcium channels by hyperbaric pressureâ€”a suggested HPNS partial mechanism

Gradwohl

et al. 2014

Front. Cell. Neurosci.

Progress in Neurobiology

“…In a crustacean stomatogastric motor axon, L-type calcium channels convey bistable membrane behavior in the motor nerve, as a brief electrical stimulation can lead to self-sustained tonic firing for tens of seconds (Le et al , 2006). Antibody staining in the stomatogastric nervous system showed both L-type and P/Q-type channels in peripheral nerve axons (French et al , 2002). Calcium channels may also play an important role in determining excitability in en passant synapses or varicosities during repetitive activation.…”

Section: Diversity Of Axonsmentioning

confidence: 99%

Beyond faithful conduction: Short-term dynamics, neuromodulation, and long-term regulation of spike propagation in the axon

Bucher¹,

Goaillard²

2011

171

190

Most spiking neurons are divided into functional compartments: a dendritic input region, a soma, a site of action potential initiation, an axon trunk and its collaterals for propagation of action potentials, and distal arborizations and terminals carrying the output synapses. The axon trunk and lower order branches are probably the most neglected and are often assumed to do nothing more than faithfully conducting action potentials. Nevertheless, there are numerous reports of complex membrane properties in non-synaptic axonal regions, owing to the presence of a multitude of different ion channels. Many different types of sodium and potassium channels have been described in axons, as well as calcium transients and hyperpolarization-activated inward currents. The complex time- and voltage-dependence resulting from the properties of ion channels can lead to activity-dependent changes in spike shape and resting potential, affecting the temporal fidelity of spike conduction. Neural coding can be altered by activity-dependent changes in conduction velocity, spike failures, and ectopic spike initiation. This is true under normal physiological conditions, and relevant for a number of neuropathies that lead to abnormal excitability. In addition, a growing number of studies show that the axon trunk can express receptors to glutamate, GABA, acetylcholine or biogenic amines, changing the relative contribution of some channels to axonal excitability and therefore rendering the contribution of this compartment to neural coding conditional on the presence of neuromodulators. Long-term regulatory processes, both during development and in the context of activity-dependent plasticity may also affect axonal properties to an underappreciated extent.

“…For example, periodic depolarization of inferior cardiac neurons of the crab Cancer borealis upregulates the transient outward current, I A . Blocking of the Ca 2+ influx by extracellular Cd 2+ eliminates the increase of the I A current density (French et al 2002). …”

Section: Introductionmentioning

confidence: 99%

Geometry and dynamics of activity-dependent homeostatic regulation in neurons

Olypher

Prinz

2010

J Comput Neurosci

To maintain activity in a functional range, neurons constantly adjust membrane excitability to changing intra- and extracellular conditions. Such activity-dependent homeostatic regulation (ADHR) is critical for normal processing of the nervous system and avoiding pathological conditions. Here, we posed a homeostatic regulation problem for the classical Morris-Lecar (ML) model. The problem was motivated by the phenomenon of the functional recovery of stomatogastric neurons in crustaceans in the absence of neuromodulation. In our study, the regulation of the ionic conductances in the ML model depended on the calcium current or the intracellular calcium concentration. We found an asymptotic solution to the problem under the assumption of slow regulation. The solution provides a full account of the regulation in the case of correlated or anticorrelated changes of the maximal conductances of the calcium and potassium currents. In particular, the solution shows how the target and parameters of the regulation determine which perturbations of the conductances can be compensated by the ADHR. In some cases, the sets of compensated initial perturbations are not convex. On the basis of our analysis we formulated specific questions for subsequent experimental and theoretical studies of ADHR.