The auditory conditioned stimulus (CS) pathway that is necessary for delay eyeblink conditioning was investigated with induced lesions of the medial auditory thalamus contralateral to the trained eye in rats. Rats were given unilateral lesions of the medial auditory thalamus or a control surgery followed by twenty 100-trial sessions of delay eyeblink conditioning with a tone CS and then five sessions of delay conditioning with a light CS. Rats that had complete lesions of the contralateral medial auditory thalamic nuclei, including the medial division of the medial geniculate, suprageniculate, and posterior intralaminar nucleus, showed a severe deficit in conditioning with the tone CS. Rats with complete lesions also showed no cross-modal facilitation (savings) when switched to the light CS. The medial auditory thalamic nuclei may modulate activity in a short-latency auditory CS pathway or serve as part of a longer latency auditory CS pathway that is necessary for eyeblink conditioning.
Keywordseyelid; learning; medial geniculate; posterior intralaminar nucleus; suprageniculate Pavlovian conditioning paradigms are optimal for establishing the neural structures that are necessary and sufficient for learning (Thompson, 1976). The amygdala and cerebellum have been implicated as sites of learning-induced plasticity that form associations among stimuli during fear and eyeblink conditioning, respectively (Fanselow & Poulos, 2005;Thompson, 2005). These learning centers receive converging information from both conditioned stimuli (CSs) and unconditioned stimuli (USs) to form the association that is necessary for producing a conditioned response (CR). Stimulus information is thought to be relayed to learning centers by neural pathways that are distinct for different types of CRs.Neural pathways for an auditory CS in fear-motivated conditioning include the medial division of the medial geniculate nucleus (MGm), posterior intralaminar nucleus (PIN), suprageniculate nucleus (SG), and their projections to the lateral and basolateral amygdala (Bordi & LeDoux, 1994;Campeau & Davis, 1995;Edeline & Weinberger, 1992;Gabriel, Saltwick, & Miller, 1975;LeDoux, Farb, & Ruggiero, 1990;LeDoux, Sakaguchi, & Reis, 1983;McCabe, McEchron, Green, & Schneiderman, 1993;McEchron, McCabe, Green, Llabre, & Schneiderman, 1995;Supple & Kapp, 1989). The MGm is also involved in appetitive conditioning (Birt & Olds, 1981;Olds, Disterhoft, Segal, Kornblith, & Hirsh, 1972). The medial auditory thalamic nuclei (MGm, PIN, and SG) provide CS input to the amygdala but are also activated by aversive USs (Bordi & LeDoux, 1994;Edeline & Weinberger, 1992;Lennartz & Weinberger, 1992
NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript related facilitation of neuronal activity in the MGm, which might be due to convergence of CS and US inputs in the MGm (Birt & Olds, 1981;Bordi & LeDoux, 1994;Edeline & Weinberger, 1992;Gabriel et al., 1975;Lennartz & Weinberger, 1992;Love & Scott, 1969;McEchron et al., 1995;Ryugo & Weinberger, 1978;S...