Step-like shifts of membrane potential in the stretch receptor neuron of the crayfish (Astacus fluviatilis) at high temperatures

1979 ◽  
Vol 133 (4) ◽  
pp. 257-265 ◽  
Author(s):  
H. Moser ◽  
D. Ottoson ◽  
B. Rydqvist
Keyword(s):  
Membrane Potential ◽  
High Temperatures ◽  
Stretch Receptor ◽  
Receptor Neuron ◽  
Astacus Fluviatilis

Central modulation of stretch receptor neurons during fictive locomotion in lamprey

1996 ◽  
Vol 76 (2) ◽  
pp. 1224-1235 ◽  
Author(s):  
L. Vinay ◽  
J. Y. Barthe ◽  
S. Grillner
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Receptor Antagonist ◽  
Chloride Ions ◽  
Stretch Receptor ◽  
Fictive Locomotion ◽  
Gamma Aminobutyric Acid ◽  
Potential Oscillations ◽  
Receptor Neurons ◽  
Membrane Potential Oscillations

1. In lamprey, stretch receptor neurons (SRNs), also referred to as edge cells, are located along the lateral margin of the spinal cord. They sense the lateral movements occurring in each swim cycle during locomotion. The isolated lamprey spinal cord in vitro was used to investigate the activity of SRNs during fictive locomotion induced by bath-applied N-methyl-D-aspartate (NMDA). Intracellular recordings with potassium acetate filled electrodes showed that 63% of SRNs had a clear locomotor-related modulation of their membrane potential. 2. Of the modulated SRNs, two-thirds had periods of alternating excitation and inhibition occurring during the ipsilateral and the contralateral ventral root bursts, respectively. The phasic hyperpolarization could be reversed into a depolarizing phase after the injection of chloride ions into the cells; this revealed a chloride-dependent synaptic drive. The remaining modulated SRNs were inhibited phasically during ipsilateral motor activity. 3. Experiments with barriers partitioning the recording chamber with the spinal cord into three pools, allowed an inactivation of the locomotor networks within one pool by washing out NMDA from the pool in which the SRN was recorded. This resulted in a marked reduction, but not an abolishment, of the amplitude of the membrane potential oscillations. Both the excitatory and the inhibitory phases were reduced, resulting from removal of input from inhibitory and excitatory interneurons projecting from the adjacent pools. If the glycine receptor antagonist strychnine (1 microM) was applied in one pool, the phasic hyperpolarizing phase disappeared without affecting the excitatory phase. 4. Bath application of the gamma-aminobutyric acid (GABA)A receptor antagonist, bicuculline (50-100 microM) blocked the spontaneous large unitary inhibitory postsynaptic potentials, which occurred without a clear phasic pattern. Bicuculline had no significant effect on the peak to peak amplitude of the locomotor-related membrane potential oscillations. The inhibition in SRNs therefore has a dual origin: glycinergic interneurons provide phasic inhibition, while the GABA system can exert a tonic inhibition via GABAA receptors. 5. These data show that, in addition to the stretch-evoked excitation, which SRNs receive during each locomotor cycle, most of them also receive excitation from the central pattern generator network during the ipsilateral contraction, which may ensure a maintained high level of sensitivity to stretch during the shortening phase of the locomotor cycle. This arrangement is analogous to the efferent control of muscle spindles exerted by gamma-motoneurons in mammals, which as a rule are coactivated with alpha-motoneurons to the same muscle (alpha-gamma linkage).

scholarly journals Effects of Lithium on Different Membrane Components of Crayfish Stretch Receptor Neurons

1968 ◽  
Vol 51 (5) ◽  
pp. 635-654 ◽  
Author(s):  
Shosaku Obara ◽  
Harry Grundfest
Keyword(s):  
Significant Role ◽  
Specific Effect ◽  
Stretch Receptor ◽  
Receptor Neuron ◽  
Generator Potential ◽  
Crayfish Stretch Receptor ◽  
Soma Membrane ◽  
Receptor Neurons ◽  
Membrane Components

Unlike several other varieties of input membrane, that of the crayfish stretch receptor develops a generator potential in response to stretch when all the Na of the medium is replaced with Li. However, Li depolarizes the receptor neuron, the soma membrane becoming more depolarized than that of the axon. During exposure to Li the cell usually fires spontaneously for a period, and when it becomes quiescent spike electrogenesis fails in the soma but persists in the axon. These effects are seen in the rapidly adapting as well as the slowly adapting cells. The block of spike electrogenesis of the soma membrane is only partly due to the Li-induced depolarization and a significant role must be ascribed to a specific effect of Li.

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