Non-NMDA and NMDA receptors are involved in suprathreshold excitation of network of frog tectal neurons by a single retinal ganglion cell

NMDA receptors play an important functional role in the neuron excitability and plasticity. The conditions and consequences of their activation are of interest for many neuroscientists. This investigation was designed to explore an activation of the NMDA receptors of frog tectal neurons in vivo by a burst of spikes of individual retinotectal fiber. We show that: (1) the NMDA receptors of tectal neurons can be activated by an intense burst discharge of an individual ganglion cell (likely darkness detector) at physiological conditions. (2) Activation of the NMDA receptors is achieved, primarily, due to temporal summation and frequency facilitation of the fast non-NMDA synaptic potentials. However, it is very likely that spatial summation of the fast retinotectal synaptic potentials with excitatory synaptic potentials of recurrent connections contributes to elicit the NMDA response. (3) The activation of NMDA receptors causes a higher level of activity of tectal neuron network. The suprathreshold excitation of efferent tectal neurons is characteristic for this level. Therefore, the burst discharge of only single retinal ganglion cell can activate the tectobulbospinal tract and lead to the motor reaction.     

Single retinal ganglion cell evokes the activation of L-type Ca(2+)-mediated slow inward current in frog tectal pear-shaped neurons

The dendrites of neurons from many regions of the nervous system contain voltage-sensitive channels that generate persistent inward currents. We have recently suggested that a slow negative wave (sNW), extracellularly observed in the frog tectum during the burst discharge of a single retinal ganglion cell, can be generated as a result of the persistent inward current in dendrites of tectal pear-shaped neurons. The aim of this study is to substantiate this hypothesis by simulation using a quasi-reconstructed pear-shaped neuron with bistable dendrites and experimental investigation of the sNW. In the experiments, the discharge of a single retinal ganglion cell was elicited by an electrical stimulation of the retina. The evoked electrical activity of the tectum was recorded using a carbon-fiber microelectrode inserted into tectum layer F. We found the following: (1) Slow inward current or plateau potential in bistable dendrites is reflected in the extracellular space as a sNW. (2) The sNW evoked by the burst discharge of a single retinal ganglion cell projecting to frog tectum layer F is generated by the activation of L-type calcium channels in the dendrites of pear-shaped neurons. (3) A few pear-shaped neurons may be suprathresholdly excited during the development of the sNW.     

Abolition of CA1 population spike by sensory stimulation

Summary The effect of sensory stimulation, such as stroking of the animals' fur, on activation of the hippocampal CA1 field was studied in paralyzed and locally anaesthetized rats. CA1 population responses evoked either monosynaptically (ipsilateral CA3 stimulation) or trisynaptically (perforant pathway stimulation) decreased markedly when sensory stimulation was applied, and CA1 population spikes were absent during most periods of sensory stimulation. These results demonstrate the strong modulatory role of sensory inputs on hippocampal circuits.     

The effects of cAMP on the excitability and responses of defensive behavior command neurons in the common snail evoked by sensory stimuli

Experiments on snails showed that extracellular application of dibutyryl-cAMP (db-cAMP) or intracellular application of cAMP for 30 min evoked increases in excitability and synaptic facilitation in responses to sensory stimulation of defensive behavior command neurons LP11 and RP11. Extitability increased 45–60 min after the start of addition of db-cAMP or cAMP and remained elevated until the end of the experiment (3–4h). Synaptic facilitation started 50–60 min after the onset of extracellular application of db-cAMP and remained detectable in the responses of neurons to tactile stimulation of the head for 1 h and to application of dilute quinine solution for 2–4 h. Application of db-cAMP produced no changes in responses to tactile stimulation of the foot or mantle ridge. Intracellular injection of cAMP induced facilitation of neuron responses only to weak quinine solutions. The responses of neurons to tactile stimulation of the head, foot, and mantle ridge did not change after injections of cAMP. It is suggested that cAMP is involved in the mechanisms controlling the excitability of neurons LP11 and RP11. In addition, cAMP is selectively involved in the postsynaptic mechanism inducing the transient stage of long-term facilitation of synaptic “inputs”, which mediates excitation evoked by chemical stimuli. This set of effects of cAMP is similar to effects arising during the development of nociceptive sensitization and in response to serotonin. Translated from Rossiiskii Fiziologicheskii Zhurnal imeni I. M. Sechenova, Vol. 85, No. 2, pp. 237–245, February, 1999.