Excitatory amino acid receptor-mediated transmission in geniculocortical and intracortical pathways within visual cortex

Abstract

1. A preparation of turtle (Chrysemys picta and Pseudemys scripta) brain in which the integrity of the intracortical and geniculocortical pathways in visual cortex are maintained in vitro has been used to differentiate the excitatory amino acid (EAA) receptor subtypes involved in geniculocortical and intracortical synapses. 2. Stimulation of the geniculocortical fibers at subcortical loci produces monosynaptic excitatory postsynaptic potentials (EPSPs) in visual cortical neurons. These EPSPs are blocked by the broad-spectrum EAA receptor antagonist kynurenate (1-2 mM) and the non-N-methyl-D-aspartate (NMDA) antagonist 6, 7-dinitroquinoxaline-2,3-dione (DNQX, 10 microM), but not by the NMDA antagonist D,L-2-amino-5-phosphonovalerate (D,L-AP-5, 100 microM). These results indicate that the geniculocortical EPSP is mediated by EAAs that access principally, if not exclusively, EAA receptors of the non-NMDA subtypes. 3. Stimulation of intracortical fibers evokes compound EPSPs that could be resolved into three components differing in latency to peak. The component with the shortest latency was not affected by any of the EAA-receptor antagonists tested. The second component, of intermediate latency, was blocked by kyurenate and DNQX but not by D,L-AP-5. The component of longest latency was blocked by kynurenate and D,L-AP-5, but not by DNQX. These results indicate that the compound intracortical EPSP is comprised of three pharmacologically distinct components that are mediated by an unknown receptor, by quisqualate/kainate, and by NMDA receptors, respectively. 4. Repetitive stimulation of intracortical pathways at 0.33 Hz produces a dramatic potentiation of the late, D,L-AP-5-sensitive component of the intracortical EPSP. 5. These experiments lead to a hypothesis about the subtypes of EAA receptors that are accessed by the geniculocortical and intracortical pathways within visual cortex.

Immunohistochemical Localization of NMDA- and AMPA-Type Glutamate Receptor Subunits in the Basal Ganglia of Red-Eared Turtles

“…Previous ligand binding and electrophysiological studies have demonstrated the presence of functional AMPA and NMDA receptors in the forebrain of turtles, but no specific information has been available on the regional or cellular localization of NMDA and AMPA subunits in the basal ganglia of reptiles [Young et al, 1990;Larson-Prior et al, 1991;Blanton and Kriegstein, 1992]. In the present study we have characterized the distribution of several AMPA and NMDA receptor type subunits in the basal ganglia of turtles.…”

“…Although we did not demonstrate the presence of NMDAR1 receptor subunits in turtle brain, several considerations argue that such subunits are present and likely to be found in the same neurons that we found to possess NMDAR2A/B subunits. First, functional NMDA receptors cannot form in the absence of the NMDAR1 subunit, and physiological and ligand binding studies demonstrate the presence of functional NMDA receptors in turtles [Young et al, 1990;Larson-Prior et al, 1991;Blanton and Kriegstein, 1992]. Secondly, an NMDAR1 subunit has been demonstrated in chick [Kurosawa et al, 1994] and in a lizard species [Rodger et al, 1999], as well as in Xenopus laevis and a teleost species [Soloviev et al, 1997;Dunn et al, 1998].…”

“…Nonetheless, because functional NMDA receptors cannot form without the NMDAR1 subunit [Seeburg, 1993;Hollman and Heinemann, 1994], because functional NMDA receptors have been demonstrated in turtle nervous system by electrophysiological means [Larson-Prior et al, 1991;Blanton and Kriegstein, 1992] and because an NR1 subunit has been demonstrated in an avian species [Kurosawa et al, 1994] and in a lizard species [Rodger et al, 1999], it seems likely that NMDAR1 subunits are present in turtle brain. Our failure to detect these subunits with a monoclonal antibody directed against rat NMDAR1 seems likely to reflect the fact that the NMDAR1 epitope against which this antibody is directed is sufficiently different in turtles that the antibody against a mammalian NMDAR1 does not recognize turtle NMDAR1.…”

“…The cortical inputs arise from the surface structure known as the dorsal cortex and from the subcortical pallial structure known as the dorsal ventricular ridge [Hall and Ebner, 1970;Brauth and Kitt, 1980;Hoogland and Vermeulen-Vanderzee, 1989;Gonzalez et al, 1990;Ulinski, 1990], whereas the thalamic inputs arise from what appear to be the nonspecific intralaminar nuclei of the dorsal thalamus in turtles and other reptiles [Parent, 1976;Balaban and Ulinski, 1981;Veenman et al, 1997]. Some prior data suggest that cortical projection neurons in turtles are glutamatergic [Larson-Prior et al, 1991;Reiner, 1991;Blanton and Kriegstein, 1992], but little is otherwise known about the presynaptic and postsynaptic neurotransmitter organization of the cortical and thalamic input to the basal ganglia in turtles. Information on the preand postsynaptic localization of glutamate and glutamate receptors in the basal ganglia projection systems in turtles is important because it provides further insight into the evolution of the basal ganglia and its afferent systems.…”

Noradrenaline Decreases Spike Voltage Threshold and Induces Electrographic Sharp Waves in Turtle Medial Cortex in vitro

“…Some of the basic anatomo-functional features of the mammalian cortex are shared by the much simpler turtle cortex [Desan, 1984;Connors and Kriegstein, 1986;Kriegstein and Connors, 1986;Larson-Prior et al, 1991;Reiner, 1993]. As in mammals, the reptilian cortex receives dense projections from extrathalamic sources.…”