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Competitive plasticity via intrinsic GABAergic circuits in the developing visual cortex
S325
EXPRESSION OF NEURONAL GROWTH ASSOCIATED PROTEIN GENE IN SENSITIVE PERIOD CAT VISUAL CORTEX AND LGN.
744
PETER A. KAUB’.*, KAZUYUKI IMAMURA1.2, NOBUKO MATAGA3, HIROSHI MORIP.4, NOZOMU MORP4, YASUYOSHI WATANABE’.2. CREST, JST, *Dept. Neurosci., Osaka Biosci. Inst., Furuedai, Suita-shi, Osaka 565-0874, 3Neuronal Circuit Devel. Lab., Br. Sci. Inst., RIKEN, Wako-shi, Saitama 351-01, “Dept. Molec. Gen., NILS, Oobu, Aichi 474-8522, JAPAN. Neuronal growth associated proteins (N-GAPS), including SCGlO, are implicated in the regulation of functional reorganisation of neuronal networks. The visual cortex of 4-6 week old kitten is extremely plastic and monocular deprivation during this sensitive period induces marked changes in the development of ocular dominance columns. We examined the expression of SCGlO mRNA in kitten visual cortex and LGN by Northern blotting, using rat SCGlO cDNA probe. Expression of SCGlO mRNA in the visual cortex was found to peak at around postnatal 1 week and rapidly declined to the adult level within 3 months. To induce visual cortical reorganisation, 4 week old kittens were monocularly deprived by suturing one eye closed for one week, then reversing this condition for a further week. In 6 week old reverse sutured kitten, expression of SCGlO mRNA was raised markedly in visual cortex and slightly in LGN, compared to controls, indicating that reorganisation of the cortical network enhanced SCGlO expression. In order to determine further the role of SCGlO in plasticity regulation of kitten visual cortex, cat SCGlO specific cDNA was cloned and characterised using a unique combination of RT-PCR and the Touchdown protocol, with primers to rat SCGlO specific cDNA sequence.
745
COMPETITIVE PLASTICITY VIA INTRINSIC GABAERGIC CIRCUITS IN THE DEVELOPING VISUAL CORTEX
TAKAO
K. HENSCH’, MICHELA
FAGIOLINI’,
NOBUKO MATAGA’,
STEINUNN
BAEKKESKOV*,
‘Lab for Neuronal Circuit Development, Brain Science Institute, RIKEN, Saitama 351-0198 *Hormone Research Institute, University of California, San Francisco, CA 94143 USA
AND SHERA F. KASH*
JAPAN,
Connections serving the two eyes compete within developing visual cortex, ultimately wiring together those inputs that fire together with their target cells. We have identified an animal model that fails to functionally refine the developing visual cortex in response to sensory experience. Targeted disruption of the 65kDa isoform of the glutamic acid decarboxylase (GAD65) gene significantly reduced stimulated GABA release in the binocular zone of mouse primary visual cortex. Under such conditions, the normal loss of deprived-eye input accompanying a brief period of monocular deprivation was entirely prevented. Activity-dependent plasticity in vivo could be fully restored by concurrent enhancement of post-synaptic GABA, receptor currents with benzodiazepine infusion into the ventricles or visual cortex. By contrast, correlation-based homosynaptic modifications of visual cortex in vitro, such as Long-Term Potentiation (LTP) and Depression (LTD), did not differ from wild type and failed to predict the plasticity defect in vivo. Experience-dependent development thus appears to be driven primarily by the detection and integration of competing inputs via inhibitory circuits intrinsic to visual cortex, especially those connections mediated by GABA, receptors.
746
EFFECTS OFEXTERNAL POTENTIATION
CATION CONCENTRATIONS ON THE INDUCTION AT VISUAL CORTICAL INHIBITORY SYNAPSES.
YUKIO KOMATSU and YUMIKO
OF LONG-TERM
YOSHIMURA
Department of Visual Neuroscience. 464-8601, Japan.
Research
Institute
of Environmental
Medicine.
Nagoya
University.
Nagoya
High-frequency stimulation (HFS) of presynaptic fibers could produce long-term potentiation (LTP) at visual cortical inhibitory synapses. In the present study. we examined the effects of external cation concentrations on LTP in developing rat visual cortical slices. Inhibitory postsynaptic potentials evoked by layer IV stimulation were intracellularly recorded from layer V cells under a blockade of ionotropic glutamate receptors. HFS of layer IV failed to induce LTP when slices were perfused with a control solution containing 2.4 mM Ca”, 1.3 mM Mg2+ and 6.2 mM K’. LTP was consistently produced when [Ca”], was increased to 4 mM or [Mg”], was increased to 2.9 mM. An increase of [Ca”], or [Mg”], is known to shift the voltage dependence of ion channels in the positive direction. The incidence of LTP was also increased by reducing [cl,, which produces membrane hyperpolar;zation. In addition, LTP was induced in most of tested cells when 1 mM Cs’, which is known to block K’ channels, was added to the control solution. We have previously demonstrated that the induction of LTP is independent of postsynaptic membrane potentials. Thus, it is likely that presynaptic voltage-dependent channels, which are gated near resting membrane potentials, regulate the induction of LTP.
EXPRESSION OF NEURONAL GROWTH ASSOCIATED PROTEIN GENE IN SENSITIVE PERIOD CAT VISUAL CORTEX AND LGN.
744
PETER A. KAUB’.*, KAZUYUKI IMAMURA1.2, NOBUKO MATAGA3, HIROSHI MORIP.4, NOZOMU MORP4, YASUYOSHI WATANABE’.2. CREST, JST, *Dept. Neurosci., Osaka Biosci. Inst., Furuedai, Suita-shi, Osaka 565-0874, 3Neuronal Circuit Devel. Lab., Br. Sci. Inst., RIKEN, Wako-shi, Saitama 351-01, “Dept. Molec. Gen., NILS, Oobu, Aichi 474-8522, JAPAN. Neuronal growth associated proteins (N-GAPS), including SCGlO, are implicated in the regulation of functional reorganisation of neuronal networks. The visual cortex of 4-6 week old kitten is extremely plastic and monocular deprivation during this sensitive period induces marked changes in the development of ocular dominance columns. We examined the expression of SCGlO mRNA in kitten visual cortex and LGN by Northern blotting, using rat SCGlO cDNA probe. Expression of SCGlO mRNA in the visual cortex was found to peak at around postnatal 1 week and rapidly declined to the adult level within 3 months. To induce visual cortical reorganisation, 4 week old kittens were monocularly deprived by suturing one eye closed for one week, then reversing this condition for a further week. In 6 week old reverse sutured kitten, expression of SCGlO mRNA was raised markedly in visual cortex and slightly in LGN, compared to controls, indicating that reorganisation of the cortical network enhanced SCGlO expression. In order to determine further the role of SCGlO in plasticity regulation of kitten visual cortex, cat SCGlO specific cDNA was cloned and characterised using a unique combination of RT-PCR and the Touchdown protocol, with primers to rat SCGlO specific cDNA sequence.
745
COMPETITIVE PLASTICITY VIA INTRINSIC GABAERGIC CIRCUITS IN THE DEVELOPING VISUAL CORTEX
TAKAO
K. HENSCH’, MICHELA
FAGIOLINI’,
NOBUKO MATAGA’,
STEINUNN
BAEKKESKOV*,
‘Lab for Neuronal Circuit Development, Brain Science Institute, RIKEN, Saitama 351-0198 *Hormone Research Institute, University of California, San Francisco, CA 94143 USA
AND SHERA F. KASH*
JAPAN,
Connections serving the two eyes compete within developing visual cortex, ultimately wiring together those inputs that fire together with their target cells. We have identified an animal model that fails to functionally refine the developing visual cortex in response to sensory experience. Targeted disruption of the 65kDa isoform of the glutamic acid decarboxylase (GAD65) gene significantly reduced stimulated GABA release in the binocular zone of mouse primary visual cortex. Under such conditions, the normal loss of deprived-eye input accompanying a brief period of monocular deprivation was entirely prevented. Activity-dependent plasticity in vivo could be fully restored by concurrent enhancement of post-synaptic GABA, receptor currents with benzodiazepine infusion into the ventricles or visual cortex. By contrast, correlation-based homosynaptic modifications of visual cortex in vitro, such as Long-Term Potentiation (LTP) and Depression (LTD), did not differ from wild type and failed to predict the plasticity defect in vivo. Experience-dependent development thus appears to be driven primarily by the detection and integration of competing inputs via inhibitory circuits intrinsic to visual cortex, especially those connections mediated by GABA, receptors.
746
EFFECTS OFEXTERNAL POTENTIATION
CATION CONCENTRATIONS ON THE INDUCTION AT VISUAL CORTICAL INHIBITORY SYNAPSES.
YUKIO KOMATSU and YUMIKO
OF LONG-TERM
YOSHIMURA
Department of Visual Neuroscience. 464-8601, Japan.
Research
Institute
of Environmental
Medicine.
Nagoya
University.
Nagoya
High-frequency stimulation (HFS) of presynaptic fibers could produce long-term potentiation (LTP) at visual cortical inhibitory synapses. In the present study. we examined the effects of external cation concentrations on LTP in developing rat visual cortical slices. Inhibitory postsynaptic potentials evoked by layer IV stimulation were intracellularly recorded from layer V cells under a blockade of ionotropic glutamate receptors. HFS of layer IV failed to induce LTP when slices were perfused with a control solution containing 2.4 mM Ca”, 1.3 mM Mg2+ and 6.2 mM K’. LTP was consistently produced when [Ca”], was increased to 4 mM or [Mg”], was increased to 2.9 mM. An increase of [Ca”], or [Mg”], is known to shift the voltage dependence of ion channels in the positive direction. The incidence of LTP was also increased by reducing [cl,, which produces membrane hyperpolar;zation. In addition, LTP was induced in most of tested cells when 1 mM Cs’, which is known to block K’ channels, was added to the control solution. We have previously demonstrated that the induction of LTP is independent of postsynaptic membrane potentials. Thus, it is likely that presynaptic voltage-dependent channels, which are gated near resting membrane potentials, regulate the induction of LTP.