1972
DOI: 10.1016/0031-9384(72)90305-8
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Neocortical lesions and pavlovian conditioning

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Cited by 136 publications
(57 citation statements)
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“…Pavlov (1927) coined the term "trace conditioning" from the assumption that the ability to learn despite the stimulus-free trace interval implies the existence of a stimulus memory trace within the brain that outlasts the CS and overlaps in time with the US. Together with previous work (Clark et al 2002;;Kalmbach et al 2009Kalmbach et al , 2010 In addition to supporting Pavlov's original insight, this suggests a relatively simple explanation for the necessity of forebrain structures for trace but not delay eyelid conditioning (Clark et al 2002;Mauk and Thompson 1987;Flores and Disterhoft 2009;Kalmbach et al 2009;Oakley and Russell 1972;Powell et al 2001;Solomon et al 1986;Steinmetz et al 1989;Takehara et al 2003;Weible et al 2000). Both forms of learning are abolished by lesions of the cerebellum (Kalmbach et al 2009;Takehara et al 2003;Woodruff-Pak et al 1985), whereas trace eyelid conditioning has attracted considerable interest following observations that it is impaired by lesions of the hippocampus or mPFC (Clark et al 2002;Kalmbach et al 2009;Kim et al 1995;Kronforst-Collins and Disterhoft 1998;Moyer et al 1990;Powell et al 2001;Solomon et al 1986;Takehara et al 2003;Weible et al 2000).…”
Section: Discussionsupporting
confidence: 62%
“…Pavlov (1927) coined the term "trace conditioning" from the assumption that the ability to learn despite the stimulus-free trace interval implies the existence of a stimulus memory trace within the brain that outlasts the CS and overlaps in time with the US. Together with previous work (Clark et al 2002;;Kalmbach et al 2009Kalmbach et al , 2010 In addition to supporting Pavlov's original insight, this suggests a relatively simple explanation for the necessity of forebrain structures for trace but not delay eyelid conditioning (Clark et al 2002;Mauk and Thompson 1987;Flores and Disterhoft 2009;Kalmbach et al 2009;Oakley and Russell 1972;Powell et al 2001;Solomon et al 1986;Steinmetz et al 1989;Takehara et al 2003;Weible et al 2000). Both forms of learning are abolished by lesions of the cerebellum (Kalmbach et al 2009;Takehara et al 2003;Woodruff-Pak et al 1985), whereas trace eyelid conditioning has attracted considerable interest following observations that it is impaired by lesions of the hippocampus or mPFC (Clark et al 2002;Kalmbach et al 2009;Kim et al 1995;Kronforst-Collins and Disterhoft 1998;Moyer et al 1990;Powell et al 2001;Solomon et al 1986;Takehara et al 2003;Weible et al 2000).…”
Section: Discussionsupporting
confidence: 62%
“…Inc. 335 mals with prior ablations of the hippocampus (Solomon & Moore, 1975) or neocortex (Oakley & Russell, 1972) are able to learn the standard short-delay CR relatively normally. In fact, rabbits with all brain tissue above the level of the thalamus removed are able to learn the short-delay CR (NM response; see Enser, Note 1), as are decerebrate cats (eyeblink; see Norman, Buchwald, & Villablanca, 1977).…”
mentioning
confidence: 99%
“…For example, electrolytic or chemical lesions of the interpositus nucleus have been shown to permanently prevent conditioning or abolish learning . Conversely, decerebrations or decortications that include all cerebral cortical tissue have proven to have little effect on delay eyeblink conditioning (e.g., Mauk & Thompson, 1987;Oakley & Russell, 1972).…”
Section: Lesion Studies Of Lobule Hvi: 1) Aspiration and Electrolyticmentioning
confidence: 99%