Epithalamic and ventral tegmental contributions to avoidance behavior in rats.

Abstract

Active-and passive-avoidance performance were examined in rats with lesions in the interpeduncular nucleus, ventral tegmentum, combined interpeduncular nucleus and ventral tegmentum, and the stria medullaris-habenula. Impaired passive-avoidance performance was noted in all groups with lesions, whereas only the groups with lesions in the interpeduncular nucleus and stria medullaris-habenular nucleus had facilitated active-avoidance performance. The results suggest that the stria medullaris tract, habenular nucleus, habenulopeduncular tract, and interpeduncular nucleus serve as significant anatomical pathways concerned with the acquisition of both active-and passive-avoidance performance, whereas pathways traveling in the ventral tegmental area dorsal to the interpeduncular nucleus arc involved only in passive-avoidance responding.Since McCleary's (1961) analysis of avoidance performance following septal lesions, a number of investigators have attempted to specify the anatomical pathways associated with the behavioral changes observed after this lesion. Since it is often assumed that limbic midbrain pathways are disrupted following septal lesions, it is important to ask which pathways are pertinent in avoidance performance, and whether the disruption of a given septal pathway leads to behavioral changes characteristic of subjects with septal lesions on all tasks, or on only some.Recently, Van Hoesen, MacDougall, and Mitchell (1969) found that active-and passive-avoidance performance were selectively affected following the disruption of pathways carrying septal fibers. Complete or partial fimbria-dorsal fornix tractotomy facilitated active-avoidance performance, but produced no passive-avoidance deficit

Differential Neuromodulation of Acquisition and Retrieval of Avoidance Learning by the Lateral Habenula and Ventral Tegmental Area

“…On the one hand, habenula lesions had no effect on learning a standard one-way active avoidance task, but they impaired performance when training was made more difficult and stressful (Thornton and Bradbury, 1989). On the other hand, habenula lesions markedly enhanced learning of a standard two-way active avoidance task (Van Hoesen et al, 1969;Wilson et al, 1972), but under very difficult training parameters, learning enhancement was minimal and limited to the second training session (Vale-Martínez et al, 1997). The reason for the discrepant lesion effects in one-versus two-way active avoidance is unclear, but it is noteworthy that studies that used two-way active avoidance with training parameters similar to ours found lesion effects opposite to our stimulation effects (Van Hoesen et al, 1969;Wilson et al, 1972).…”

“…To test this idea, we implanted stimulating electrodes in either the VTA or LHb of gerbils engaged in two-way active avoidance learning, a task that shows learning-associated dopamine changes (Stark et al, 1999(Stark et al, , 2000(Stark et al, , 2001(Stark et al, , 2004 and that is acquired faster following LHb lesions (Wilson et al, 1972). In addition to Stark et al (1999Stark et al ( , 2000Stark et al ( , 2001Stark et al ( , 2004, several other studies from our laboratory have demonstrated the suitability of gerbils for the investigation of learning mechanisms (Scheich et al, 1993;Ohl et al, 2001;Wetzel et al, 2008).…”

Habenular lesions and avoidance learning deficits in albino rats

“…Davis et al (1966), using a step-down task, found that rats with lesions were better at passively avoiding shock than were controls (i.e., they stayed on the platform longer). However, Van Hoesen et al (1969) and Wilson et al (1972) reported impairment in passive avoidance of shock paired with food consumption (l.e., rats with habenular lesions continued to eat after being shocked while eating). The inhibition hypothesis can account for both find ings on the basis of a tendency to continue ongoing behavior, although one must specify which of the two incompatible responses (stepping down or staying on the platform ; eating or not eating) is to be considered as prepotent or ongoing in each situation.…”

“…On the other hand , Van Hoesen and his coworkers (Van Hoesen, MacDougall, & Mitchell , 1969 ;Wilson, Mitchell, & Van Hoesen, 1972) reported that habenular lesions impaired food-related passive avoidance , while enhancing two-way shuttle box avoidance perform ance. Large medial thalamic lesions, which included damage to the habenula, have been found to severely impair one-way active avoidance acquisition (Delacour, ' 1971 ;Vanderwolf, 1967Vanderwolf, , 1971, although Delacour (1971) stated that lesions limited to the habenular complex did not result in impairment in this task.…”

Long-Lasting Enhancement of Glutamatergic Synaptic Transmission by Acetylcholine Contrasts with Response Adaptation after Exposure to Low-Level Nicotine

“…The MHN-IPN pathway is part of the limbic system thought to be involved in arousal and reinforcement (Wilson et al, 1972;Wirtshafter, 1981). Glutamate serves as the excitatory transmitter at MHN-IPN synapses (Brown et al, 1983;McGehee et al, 1995).…”