The development of GABAB-mediated activity in the rat dentate gyrus.
Animals; Baclofen/analogs & derivatives/pharmacology; Electric Stimulation; Evoked Potentials/drug effects; GABA-A Receptor Antagonists; GABA-A/drug effects/physiology; GABA-B Receptor Antagonists; GABA-B/*metabolism; Hippocampus/*growth & development/*metabolism; In Vitro Techniques; Organophosphorus Compounds/pharmacology; Rats; Receptors
We examined the effects of GABAB receptor activation in the dentate gyrus of hippocampal slices prepared from 6-8-day-old rat pup. Baclofen (0.25-1.0 microM), a GABAB agonist, rapidly and potently disinhibited the developing dentate, similar to its effect in the mature organism. CGP 35348, a GABAB antagonist, quickly reversed the baclofen-induced disinhibition. However, GABAB antagonists did not reverse long-latency (500-1000 ms IPI) paired-pulse depression, suggesting that it is not caused by a late GABAB-mediated IPSP. GABAB-mediated disinhibition of the dentate gyrus can occur by postnatal day 6, providing a powerful mechanism for altering excitability in the developing hippocampus.
DiScenna P G; Nowicky A V; Teyler T J
Brain research. Developmental brain research
1994
1994-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/0165-3806(94)90206-2" target="_blank" rel="noreferrer noopener">10.1016/0165-3806(94)90206-2</a>
Endogenous mGluR activity suppresses GABAergic transmission in avian cochlear nucleus magnocellularis neurons.
2-Amino-5-phosphonovalerate/pharmacology; Amino Acids/pharmacology; Animals; Chickens/*physiology; Cochlear Nucleus/*cytology/*physiology; Electric Stimulation; Excitatory Amino Acid Antagonists/pharmacology; Excitatory Postsynaptic Potentials/physiology; GABA-B Receptor Agonists; GABA-B Receptor Antagonists; GABA-B/physiology; gamma-Aminobutyric Acid/*physiology; Glycine/analogs & derivatives/pharmacology; In Vitro Techniques; Kinetics; Membrane Potentials/drug effects; Metabotropic Glutamate/agonists/antagonists & inhibitors/*metabolism/physiology; Models; Neurological; Neurons/*physiology; Patch-Clamp Techniques; Receptors; Resorcinols/pharmacology; Synapses/physiology; Synaptic Transmission/*physiology; Xanthenes/pharmacology
GABAergic transmission in the avian cochlear nucleus magnocellularis (NM) of the chick is subject to modulation by gamma-aminobutyric acid type B (GABA(B)) autoreceptors. Here, I investigated modulation of GABAergic transmission in NM by metabotropic glutamate receptors (mGluRs) with whole cell recordings in brain slice preparations. I found that tACPD, a nonspecific mGluR agonist, exerted dose-dependent suppression on evoked inhibitory postsynaptic currents (eIPSCs) in NM neurons. At concentrations of 100 or 200 microM, tACPD increased the failure rate of GABAergic transmission. Agonists for group I (3,5-DHPG, 200 microM), group II (DCG-IV, 2 microM), and group III (L-AP4, 10 microM) mGluRs produced a significant reduction in the amplitude of eIPSCs and a significant increase in failure rate, indicating the involvement of multiple mGluRs in this modulation. The frequency, but not the amplitude, of miniature IPSCs (mIPSCs) was decreased significantly by 3,5-DHPG or DCG-IV. Neither frequency nor amplitude of mIPSCs was affected by L-AP4. mGluR antagonists LY341495 (20 microM) plus CPPG (10 microM) significantly increased the amplitude of eIPSCs, indicating that endogenous mGluR activity suppresses GABA release to NM neurons. Furthermore, blockage of mGluRs increased GABA-evoked discharges recorded under physiological Cl(-) concentrations, whereas tACPD (100 microM) eliminated them. The results indicate that mGluRs play important roles in achieving balanced excitation and inhibition in NM and preserving fidelity of temporal information encoded by NM neurons.
Lu Yong
Journal of neurophysiology
2007
2007-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/jn.00883.2006" target="_blank" rel="noreferrer noopener">10.1152/jn.00883.2006</a>