scholarly journals Physiological role of dendrotoxin sensitive k channels in the rat cerebellar Purkinje neurons

2007 ◽  
pp. 807-813 ◽  
Author(s):  
H Haghdoust ◽  
M Janahmadi ◽  
G Behzadi
Keyword(s):  
Action Potentials ◽  
Physiological Role ◽  
Neuronal Firing ◽  
Purkinje Neurons ◽  
Repetitive Firing ◽  
Neuronal Membrane ◽  
K Channels ◽  
Type K ◽  
Cerebellar Purkinje Neurons

To understand the contribution of potassium (K+) channels, particularly alpha-dendrotoxin (D-type)-sensitive K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits), to the generation of neuronal spike output we must have detailed information of the functional role of these channels in the neuronal membrane. Conventional intracellular recording methods in current clamp mode were used to identify the role of alpha-dendrotoxin (alpha-DTX)-sensitive K+ channel currents in shaping the spike output and modulation of neuronal properties of cerebellar Purkinje neurons (PCs) in slices. Addition of alpha-DTX revealed that D-type K+ channels play an important role in the shaping of Purkinje neuronal firing behavior. Repetitive firing capability of PCs was increased following exposure to artificial cerebrospinal fluid (aCSF) containing alpha-DTX, so that in response to the injection of 0.6 nA depolarizing current pulse of 600 ms, the number of action potentials insignificantly increased from 15 in the presence of 4-AP to 29 action potentials per second after application of DTX following pretreatment with 4-AP. These results indicate that D-type K+ channels (Kv.1, Kv1.2 or Kv1.6 subunits) may contribute to the spike frequency adaptation in PCs. Our findings suggest that the activation of voltage-dependent K+ channels (D and A types) markedly affect the firing pattern of PCs.

scholarly journals Reduced K+ Channel Inactivation, Spike Broadening, and After-Hyperpolarization in Kvβ1.1-Deficient Mice with Impaired Learning

1998 ◽  
Vol 5 (4) ◽  
pp. 257-273 ◽  
Author(s):  
Karl Peter Giese ◽  
Johan F. Storm ◽  
Dirk Reuter ◽  
Nikolai B. Fedorov ◽  
Li-Rong Shao ◽  
...  
Keyword(s):  
Pyramidal Neurons ◽  
Physiological Role ◽  
Neuronal Firing ◽  
Repetitive Firing ◽  
K Channel ◽  
Frequency Dependent ◽  
Channel Inactivation ◽  
Type K ◽  
Preference Task ◽  
Deficient Mice

A-type K+ channels are known to regulate neuronal firing, but their role in repetitive firing and learning in mammals is not well characterized. To determine the contribution of the auxiliary K+ channel subunit Kvβ1.1 to A-type K+ currents and to study the physiological role of A-type K+ channels in repetitive firing and learning, we deleted the Kvβ1.1 gene in mice. The loss of Kvβ1.1 resulted in a reduced K+ current inactivation in hippocampal CA1 pyramidal neurons. Furthermore, in the mutant neurons, frequency-dependent spike broadening and the slow afterhyperpolarization (sAHP) were reduced. This suggests that Kvβ1.1-dependent A-type K+ channels contribute to frequency-dependent spike broadening and may regulate the sAHP by controlling Ca2+ influx during action potentials. The Kvβ1.1-deficient mice showed normal synaptic plasticity but were impaired in the learning of a water maze test and in the social transmission of food preference task, indicating that the Kvβ1.1 subunit contributes to certain types of learning and memory.

Differential Role of KIR Channel and Na+/K+-Pump in the Regulation of Extracellular K+ in Rat Hippocampus

2002 ◽  
Vol 87 (1) ◽  
pp. 87-102 ◽  
Author(s):  
Raimondo D'Ambrosio ◽  
David S. Gordon ◽  
H. Richard Winn
Keyword(s):  
High Frequency ◽  
Physiological Role ◽  
Neuronal Firing ◽  
Neuronal Membrane ◽  
High Frequency Stimulation ◽  
Kir Channels ◽  
Frequency Stimulation ◽  
Rate Of Recovery ◽  
Selective Blocker

Little information is available on the specific roles of different cellular mechanisms involved in extracellular K+ homeostasis during neuronal activity in situ. These studies have been hampered by the lack of an adequate experimental paradigm able to separate K+-buffering activity from the superimposed extrusion of K+ from variably active neurons. We have devised a new protocol that allows for such an analysis. We used paired field- and K+-selective microelectrode recordings from CA3 stratum pyramidale during maximal Schaffer collateral stimulation in the presence of excitatory synapse blockade to evoke purely antidromic spikes in CA3. Under these conditions of controlled neuronal firing, we studied the [K+]o baseline during 0.05 Hz stimulation, and the accumulation and rate of recovery of extracellular K+ at higher frequency stimulation (1–3 Hz). In the first set of experiments, we showed that neuronal hyperpolarization by extracellular application of ZD7288 (11 μM), a selective blocker of neuronal I hcurrents, does not affect the dynamics of extracellular K+. This indicates that the K+ dynamics evoked by controlled pyramidal cell firing do not depend on neuronal membrane potential, but only on the balance between K+ extruded by firing neurons and K+ buffered by neuronal and glial mechanisms. In the second set of experiments, we showed that di-hydro-ouabain (5 μM), a selective blocker of the Na+/K+-pump, yields an elevation of baseline [K+]o and abolishes the K+ recovery during higher frequency stimulation and its undershoot during the ensuing period. In the third set of experiments, we showed that Ba2+ (200 μM), a selective blocker of inwardly rectifying K+channels (KIR), does not affect the posttetanus rate of recovery of [K+]o, nor does it affect the rate of K+ recovery during high-frequency stimulation. It does, however, cause an elevation of baseline [K+]o and an increase in the amplitude of the ensuing undershoot. We show for the first time that it is possible to differentiate the specific roles of Na+/K+-pump and KIR channels in buffering extracellular K+. Neuronal and glial Na+/K+-pumps are involved in setting baseline [K+]o levels, determining the rate of its recovery during sustained high-frequency firing, and determining its postactivity undershoot. Conversely, glial KIR channels are involved in the regulation of baseline levels of K+, and in decreasing the amplitude of the postactivity [K+]oundershoot, but do not affect the rate of K+clearance during neuronal firing. The results presented provide new insights into the specific physiological role of glial KIR channels in extracellular K+ homeostasis.

scholarly journals The origin of physiological local mGluR1 supralinear Ca2+ signals in cerebellar Purkinje neurons

2019 ◽  
Author(s):  
Karima Ait Ouares ◽  
Marco Canepari
Keyword(s):  
Synaptic Plasticity ◽  
Metabotropic Glutamate Receptors ◽  
Purkinje Neurons ◽  
Parallel Fibre ◽  
Climbing Fibre ◽  
Metabotropic Glutamate ◽  
Type K ◽  
Cerebellar Purkinje Neurons ◽  
Crucial Parameter

SUMMARYIn Purkinje neurons, the climbing fibre (CF) input provides a signal to parallel fibre (PF) synapses triggering PF synaptic plasticity. This supralinear Ca2+ signal, co-localised with the PF Ca2+ influx, occurs when PF activity precedes the CF input. Using membrane potential (Vm) and Ca2+ imaging, we identified the biophysical determinants of these supralinear Ca2+ signals. The CF-associated Ca2+ influx is mediated by T-type or by P/Q-type Ca2+ channels, depending on whether the dendritic Vm is hyperpolarised or depolarised. The resulting Ca2+ elevation is locally amplified by saturation of the endogenous Ca2+ buffer produced by the PF-associated Ca2+ influx, in particular by the slow Ca2+ influx mediated by type-1 metabotropic glutamate receptors (mGluR1s). When the dendrite is hyperpolarised, mGluR1s boost neighbouring T-type channels providing a mechanism for local coincident detection of PF-CF activity. In contrast, when the dendrite is depolarised, mGluR1s increase dendritic excitability by inactivating A-type K+ channels, but this phenomenon is not restricted to the activated PF synapses. Thus, Vm is likely a crucial parameter in determining PF synaptic plasticity and the occurrence of hyperpolarisation episodes is expected to play an important role in motor learning.

scholarly journals The modulation of two motor behaviors by persistent sodium currents in Xenopus laevis tadpoles

2017 ◽  
Vol 118 (1) ◽  
pp. 121-130 ◽  
Author(s):  
Erik Svensson ◽  
Hugo Jeffreys ◽  
Wen-Chang Li
Keyword(s):  
Action Potentials ◽  
Sodium Current ◽  
Repetitive Firing ◽  
Sodium Currents ◽  
Spinal Neurons ◽  
Motor Behaviors ◽  
Low Concentrations ◽  
Descending Interneurons ◽  
Lateral Sclerosis

Persistent sodium currents ( INaP) are common in neuronal circuitries and have been implicated in several diseases, such as amyotrophic lateral sclerosis (ALS) and epilepsy. However, the role of INaP in the regulation of specific behaviors is still poorly understood. In this study we have characterized INaP and investigated its role in the swimming and struggling behavior of Xenopus tadpoles. INaP was identified in three groups of neurons, namely, sensory Rohon-Beard neurons (RB neurons), descending interneurons (dINs), and non-dINs (neurons rhythmically active in swimming). All groups of neurons expressed INaP, but the currents differed in decay time constants, amplitudes, and the membrane potential at which INaP peaked. Low concentrations (1 µM) of the INaP blocker riluzole blocked INaP ~30% and decreased the excitability of the three neuron groups without affecting spike amplitudes or cellular input resistances. Riluzole reduced the number of rebound spikes in dINs and depressed repetitive firing in RB neurons and non-dINs. At the behavior level, riluzole at 1 µM shortened fictive swimming episodes. It also reduced the number of action potentials neurons fired on each struggling cycle. The results show that INaP may play important modulatory roles in motor behaviors. NEW & NOTEWORTHY We have characterized persistent sodium currents in three groups of spinal neurons and their role in shaping spiking activity in the Xenopus tadpole. We then attempted to evaluate the role of persistent sodium currents in regulating tadpole swimming and struggling motor outputs by using low concentrations of the persistent sodium current antagonist riluzole.

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