Responses of cortical neurons to stimulation of corpus callosum in vitro

Abstract

1. An in vitro slice preparation of rat cingulate cortex was used to analyze the responses of layer V neurons to electrical stimulation of the corpus callosum (CC). In addition, synaptic termination of callosal afferents with layer V neurons was evaluated electron microscopically to provide a structural basis for interpreting some of the observed response sequences. 2. Layer V neurons had a resting membrane potential (RMP) of 60 +/- 0.68 (SE) mV, an input resistance of 47 +/- 4.74 M omega, a membrane time constant of 4.37 +/- 0.51 ms, an electrotonic length constant of 1.38 +/- 0.25, and produced spontaneous action potentials that were 50 +/- 0.3 mV in amplitude. Intracellular depolarizing current pulses evoked spikes that were sometimes associated with low-amplitude (2-5 mV) depolarizing (5-10 ms in duration) and hyperpolarizing (10-20 ms in duration) afterpotentials. 3. A single stimulus of increasing intensities to the CC produced one of the following response sequences: a) antidromic spike and an excitatory postsynaptic potential (EPSP), which initiated one or more spikes; b) antidromic spike, EPSP-evoked action potentials, and a hyperpolarization, which may have represented an intrinsic cell property or inhibitory synaptic activity; c) EPSP and evoked spikes only; d) high-amplitude EPSP with an all-or-none burst of action potentials. 4. Antidromically activated (AA) neurons always produced EPSPs in response to CC stimulation. When compared with nonantidromically activated neurons, AA cells had a more negative RMP, greater electrotonic length constant (LN), higher ratio of dendritic to somatic conductance (rho), and formed shorter duration, callosal-evoked EPSPs. 5. Neurons in anterior cingulate cortex produced EPSPs of longer duration than did those in posterior cortex (50 +/- 3.57 versus 26 +/- 1.56 ms, respectively). EPSPs in anterior neurons also had a higher maximum amplitude (20.5 +/- 1.0 versus 11.5 +/- 0.79 mV) and longer time to peak (11.6 +/- 2.2 versus 8.2 +/- 0.8 ms). 6. Electron microscopy of Golgi-impregnated neurons following contralateral lesions demonstrated that both pyramidal and nonpyramidal neurons received direct callosal afferents. Synaptic termination of callosal axons with the apical dendritic trees of anterior pyramidal cells was 6 times greater than it was with posterior pyramidal neurons. 7. EPSP shape differences in anterior and posterior neurons may be partially accounted for by the density and distribution of callosal afferents to these two cortices.

Mechanisms underlying potentiation of synaptic transmission in rat anterior cingulate cortex in vitro.

“…The results described in this study confirm and extend the findings of Vogt & Gorman (1982) that there is a monosynaptic, excitatory input from the corpus callosum onto layer V and layer VI pyramidal neurones in the anterior cingulate cortex. The transmitter released by this input activates both NMDA and non-NMDA glutamate receptor subtypes.…”

“…This input is preserved in a coronal slice from the cingulate cortex (Vogt & Gorman, 1982). Since the interpretation of many of the experiments on the mechanisms underlying LTP require that the synaptic potential is monosynaptic we went to considerable lengths to ensure that the EPSPs analysed in our study were monosynaptic.…”

A low-voltage activated, transient calcium current is responsible for the time-dependent depolarizing inward rectification of rat neocortical neurons in vitro

“…The mean value was found to be 1.1 +_0.4 ms. According to Rail's model of the neuron (Rall 1969(Rall , 1977, the equivalent electrotonic length (L) was calculated to be 1.13 space constants (+0.23; n = 20), suggesting that the neurons of the superficial layers of the rat frontal cortex are electrotonically compact (Vogt and Gorman 1982;Stafstrom et al 1984c). Within the potential range up to 15 mV positive to the RMP, the slope resistance increased with depolarization and there was no indication of a time-dependent event (steady state inward rectification in depolarizing direction; see Fig.…”

Nonlinear Neurovascular Coupling in Rat Sensory Cortex by Activation of Transcallosal Fibers

“…The biphasic IPSP that follows the initial EPSP is produced by activity of local inhibitory interneurons and not by release of GABA from callosal fibers (Vogt and Gorman, 1982;Carr and Sesack, 1998), since both the EPSP and the IPSP responses disappeared after local treatment with CNQX. We did not attain electrophysiologic evidence of NMDAR activity, which is difficult to record because the response is small and delayed, compared with the early and large AMPAR response.…”