Medial auditory thalamic nuclei are necessary for eyeblink conditioning.

Abstract

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...

Central cannabinoid receptors modulate acquisition of eyeblink conditioning

“…The CB1Rs are very dense in the hippocampus and disrupting hippocampal activity can impair delay conditioning (Solomon et al 1983). Disruption of auditory system function could also impair acquisition as well (Halverson and Freeman 2006). Low levels of CB1Rs are found in the red nucleus (Herkenham et al 1991), but alterations in magnocellular neuronal function could impair CR performance by affecting excitatory input to the facial motor nucleus, which produces the blink response (Trigo et al 1999).…”

Stimulation of the lateral geniculate, superior colliculus, or visual cortex is sufficient for eyeblink conditioning in rats

“…Recent studies using lesions, inactivation, stimulation, and neural tract tracing have provided evidence that the auditory CS pathway that is necessary for acquisition and retention of eyeblink conditioning is comprised of converging inputs to the medial auditory thalamic nuclei (MATN), and a direct ipsilateral projection from the MATN to the PN (Halverson and Freeman 2006;Campolattaro et al 2007;Freeman et al 2007;Halverson et al 2008). Unilateral lesions of the MATN, contralateral to the conditioned eye, block acquisition of eyeblink CRs to a tone CS but have no effect on conditioning with a light CS (Halverson and Freeman 2006).…”

Functional Magnetic Resonance Imaging of Delay and Trace Eyeblink Conditioning in the Primary Visual Cortex of the Rabbit

“…Notably, no activity was detected in either the LGN or superior colliculus at any stage during these experiments, although a number of previous studies have demonstrated a role for the subcortical structures of the sensory systems in classical conditioning. Lesions of the auditory (LeDoux et al, 1986;Halverson and Freeman, 2006) and visual (Koutaldis et al, 1988) thalamic nuclei have been shown to inhibit classical conditioning. Electrophysiological recordings have demonstrated that classical conditioning induces retuning of the auditory thalamic nuclei (Edeline and Weinberger, 1992).…”