Passive avoidance in rats: Disruption by dopamine applied to the nucleus accumbens

Abstract

The acquisition of a one-trial step-through passive avoidance task was examined in rats following the administration of nialamide IP and dopamine (DA) or saline into the nucleus accumbens. DA-treated rats displayed impaired learning of the task as evidenced by their lower step-through latencies on a retest trial 7 days later. The specificity of this impairment was studied in a 2 x 2 design involving intracerebral injections prior to both training and testing trials. It was found that DA treatment prior to the training trial disrupted learning or memorization of the task but that DA did not affect performance or retrieval and did not induce state-dependent learning. These findings suggest that DA applied to the nucleus accumbens does not facilitate learning per se.

Spatial deficits in a mouse model of Parkinson disease

“…Taking into account that a direct comparison between these studies is limited by the use of different pharmacological manipulations of DA system, all together, these data, on the one hand, provide support to the idea that normal transmission of information through frontostriatal circuitries is necessary for normal visuo-spatial information processing (Cools et al 2002;Lewis et al 2003;Owen et al 1998;Pillon et al 1996). On the other hand, they confirm the functional specialization of the dopamine terminal regions in processing different kinds of information (Bracs et al 1984;Cools et al 2007;De Leonibus et al 2006;Smith-Roe et al 1999).…”

Hyperactivity to novelty induced by social isolation is not correlated with changes in D2 receptor function and binding in striatum

“…The enhanced dopamine release in the nucleus accumbens during footshock shown in isolated rats (Fulford and Marsden 1998) could account, at least in part, for the retention impairment assessed using the passive avoidance paradigm. In fact there is evidence showing that nucleus accumbens is involved in passive avoidance retention (Lorenzini et al 1995;Roozendaal et al 2001) and also that dopamine injected into this area of the brain can disrupt passive avoidance performance (Bracs et al 1984). Future studies will be needed to ascertain whether impaired retention indicates impaired memory and, in that case, which component of the memory process (acquisition, consolidation, retrieval) has become disrupted by the social isolation, as well as to elucidate the specific mechanisms involved.…”

Cholinergic and dopaminergic agents which inhibit a passive avoidance response attenuate the paradigm-specific increases in NCAM sialylation state

“…Neuroleptics appear to antagonize memory formation however this appears to be mediated through a presynaptic mechanism (Ichihara et al, 1988 a,b). As a general rule, neuroleptics are known to antagonize various forms of avoidance conditioning (Niemegeers et al, 1969;Castellano et al, 1991) however direct application of dopamine to the nucleus accumbens of the striatum is equally effective in inhibiting memory formation (Bracs et al, 1984). …”