MK-801 protects conditioned responses from extinction in the rabbit nictitating membrane preparation
Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate defi...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Kehoe, E. James [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
1996 |
|---|
| Schlagwörter: |
|---|
| Anmerkung: |
© Psychonomic Society, Inc. 1996 |
|---|
| Übergeordnetes Werk: |
Enthalten in: Physiological Psychology - Springer-Verlag, 1973, 24(1996), 2 vom: Juni, Seite 127-135 |
|---|---|
| Übergeordnetes Werk: |
volume:24 ; year:1996 ; number:2 ; month:06 ; pages:127-135 |
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10.3758/BF03331963 |
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| 520 | |a Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. | ||
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10.3758/BF03331963 doi (DE-627)SPR037020145 (SPR)BF03331963-e DE-627 ger DE-627 rakwb eng Kehoe, E. James verfasserin aut MK-801 protects conditioned responses from extinction in the rabbit nictitating membrane preparation 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Psychonomic Society, Inc. 1996 Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. Conditioned Stimulus (dpeaa)DE-He213 Nictitate Membrane Response (dpeaa)DE-He213 Nictitate Membrane (dpeaa)DE-He213 Light Conditioned Stimulus (dpeaa)DE-He213 Conditioned Response Acquisition (dpeaa)DE-He213 Macrae, Michaela aut Hutchinson, Catherine L. aut Enthalten in Physiological Psychology Springer-Verlag, 1973 24(1996), 2 vom: Juni, Seite 127-135 (DE-627)SPR037003089 nnns volume:24 year:1996 number:2 month:06 pages:127-135 https://dx.doi.org/10.3758/BF03331963 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 24 1996 2 06 127-135 |
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10.3758/BF03331963 doi (DE-627)SPR037020145 (SPR)BF03331963-e DE-627 ger DE-627 rakwb eng Kehoe, E. James verfasserin aut MK-801 protects conditioned responses from extinction in the rabbit nictitating membrane preparation 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Psychonomic Society, Inc. 1996 Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. Conditioned Stimulus (dpeaa)DE-He213 Nictitate Membrane Response (dpeaa)DE-He213 Nictitate Membrane (dpeaa)DE-He213 Light Conditioned Stimulus (dpeaa)DE-He213 Conditioned Response Acquisition (dpeaa)DE-He213 Macrae, Michaela aut Hutchinson, Catherine L. aut Enthalten in Physiological Psychology Springer-Verlag, 1973 24(1996), 2 vom: Juni, Seite 127-135 (DE-627)SPR037003089 nnns volume:24 year:1996 number:2 month:06 pages:127-135 https://dx.doi.org/10.3758/BF03331963 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 24 1996 2 06 127-135 |
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10.3758/BF03331963 doi (DE-627)SPR037020145 (SPR)BF03331963-e DE-627 ger DE-627 rakwb eng Kehoe, E. James verfasserin aut MK-801 protects conditioned responses from extinction in the rabbit nictitating membrane preparation 1996 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Psychonomic Society, Inc. 1996 Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. Conditioned Stimulus (dpeaa)DE-He213 Nictitate Membrane Response (dpeaa)DE-He213 Nictitate Membrane (dpeaa)DE-He213 Light Conditioned Stimulus (dpeaa)DE-He213 Conditioned Response Acquisition (dpeaa)DE-He213 Macrae, Michaela aut Hutchinson, Catherine L. aut Enthalten in Physiological Psychology Springer-Verlag, 1973 24(1996), 2 vom: Juni, Seite 127-135 (DE-627)SPR037003089 nnns volume:24 year:1996 number:2 month:06 pages:127-135 https://dx.doi.org/10.3758/BF03331963 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA AR 24 1996 2 06 127-135 |
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Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. © Psychonomic Society, Inc. 1996 |
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Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. © Psychonomic Society, Inc. 1996 |
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Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement. © Psychonomic Society, Inc. 1996 |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR037020145</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519132034.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.3758/BF03331963</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR037020145</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)BF03331963-e</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Kehoe, E. James</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">MK-801 protects conditioned responses from extinction in the rabbit nictitating membrane preparation</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="500" ind1=" " ind2=" "><subfield code="a">© Psychonomic Society, Inc. 1996</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract MK-801 is a noncompetitive antagonist to N-methyl-d-aspartate (NMDA) receptors. MK-801 was given (0.05 or 0.10 mg/kg i.v.) to rabbits during extinction of a well-established conditioned response (CR) in the nictitating membrane preparation. The drug administration produced an immediate deficit in CR performance during extinction. However, when MK-801 administration was suspended, CRs reappeared immediately and showed no evidence of the previous extinction treatment. In addition, we confirmed previous findings that MK-801 impairs both the acquisition and the expression of CRs during CS—US training. A reduction in CS processing caused by MK-801 is the most parsimonious explanation of the data. There are also two-factor alternatives, which contend that MK-801 directly hinders associative formation and either directly blocks CR output or produces a state-dependent generalization decrement.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Conditioned Stimulus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nictitate Membrane Response</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Nictitate Membrane</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Light Conditioned Stimulus</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Conditioned Response Acquisition</subfield><subfield code="7">(dpeaa)DE-He213</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Macrae, Michaela</subfield><subfield code="4">aut</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hutchinson, Catherine L.</subfield><subfield code="4">aut</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="t">Physiological Psychology</subfield><subfield code="d">Springer-Verlag, 1973</subfield><subfield code="g">24(1996), 2 vom: Juni, Seite 127-135</subfield><subfield code="w">(DE-627)SPR037003089</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:24</subfield><subfield code="g">year:1996</subfield><subfield code="g">number:2</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:127-135</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://dx.doi.org/10.3758/BF03331963</subfield><subfield code="z">lizenzpflichtig</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_A</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_SPRINGER</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">24</subfield><subfield code="j">1996</subfield><subfield code="e">2</subfield><subfield code="c">06</subfield><subfield code="h">127-135</subfield></datafield></record></collection>
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