| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
1 Dept. of Biology and Volen Center for Complex Systems, Brandeis University, Waltham, MA, USA
* To whom correspondence should be addressed. E-mail: lisman{at}brandeis.edu.
CA1 pyramidal cells receive two major excitatory inputs; the perforant path (PP) terminates in the most distal dendrites whereas the Schaffer collateral (SC) terminates more proximally. We have examined the mechanism of the afterhyperpolarization (AHP) that follows single subthreshold EPSPs in these inputs. The AHPs were not reduced by a GABAA antagonist or by agents that block Ca2+ entry. Application of the Ih blocker, ZD7288 partially blocked the AHP in the PP; the substantial remaining component was blocked by 2-hydroxysaclofen, a GABAB antagonist. In contrast, the AHP in the SC depends nearly completely on Ih, with almost no GABAB component. Thus postsynaptic GABAB receptors appear to be preferentially involved at distal synapses, consistent with the spatial distribution of GABAB receptors and GIRK channels. GABAB does however play a role at proximal synapses through presynaptic suppression of glutamate release, a mechanism that is much weaker at distal synapses. Experiments were conducted to explore the functional role of the AHP in the PP, which has a higher NMDA/AMPA ratio than the SC. Blockade of the AHP converted a response that had a small NMDA component to one that had a large component. These results indicate that the Ih and postsynaptic GABAB conductances act as a brake on distally generated NMDA responses.
This article has been cited by other articles:
|
|
 |
|
  D.-P. Li, Q. Yang, H.-M. Pan, and H.-L. Pan Plasticity of pre- and postsynaptic GABAB receptor function in the paraventricular nucleus in spontaneously hypertensive rats Am J Physiol Heart Circ Physiol, August 1, 2008; 295(2): H807 - H815. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. E. Speed and L. E. Dobrunz Developmental Decrease in Short-Term Facilitation at Schaffer Collateral Synapses in Hippocampus Is mGluR1 Sensitive J Neurophysiol, February 1, 2008; 99(2): 799 - 813. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Sanhueza, C. C. McIntyre, and J. E. Lisman Reversal of Synaptic Memory by Ca2+/Calmodulin-Dependent Protein Kinase II Inhibitor J. Neurosci., May 9, 2007; 27(19): 5190 - 5199. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Fernandez de Sevilla, M. Fuenzalida, A. B. Porto Pazos, and W. Buno Selective Shunting of the NMDA EPSP Component by the Slow Afterhyperpolarization in Rat CA1 Pyramidal Neurons J Neurophysiol, May 1, 2007; 97(5): 3242 - 3255. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. K. Best, R. J. Siarey, and Z. Galdzicki Ts65Dn, a Mouse Model of Down Syndrome, Exhibits Increased GABAB-Induced Potassium Current J Neurophysiol, January 1, 2007; 97(1): 892 - 900. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. R. Proctor, L. Diao, R. K. Freund, M. D. Browning, and P. H. Wu Synaptic GABAergic and glutamatergic mechanisms underlying alcohol sensitivity in mouse hippocampal neurons J. Physiol., August 15, 2006; 575(1): 145 - 159. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Kulik, I. Vida, Y. Fukazawa, N. Guetg, Y. Kasugai, C. L. Marker, F. Rigato, B. Bettler, K. Wickman, M. Frotscher, et al. Compartment-dependent colocalization of Kir3.2-containing K+ channels and GABAB receptors in hippocampal pyramidal cells. J. Neurosci., April 19, 2006; 26(16): 4289 - 4297. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. A. Otmakhova, J. Lewey, B. Asrican, and J. E. Lisman Inhibition of Perforant Path Input to the CA1 Region by Serotonin and Noradrenaline J Neurophysiol, August 1, 2005; 94(2): 1413 - 1422. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Visit Other APS Journals Online |
