Radio-frequency identification tracking shows individual free-range laying hens vary in range use, with some never going outdoors. The range is typically more environmentally complex, requiring navigation to return to the indoor resources. Outdoor-preferring hens may have improved spatial abilities compared to indoor-preferring hens. Experiment 1 tested 32 adult ISA Brown hens in a T-maze learning task that showed exclusively-indoor birds were slowest to reach the learning success criterion (p < 0.05). Experiment 2 tested 117 pullets from enriched or non-enriched early rearing treatments (1 pen replicate per treatment) in the same maze at 15–16 or 17–18 weeks. Enriched birds reached learning success criterion faster at 15–16 weeks (p < 0.05) but not at 17–18 weeks (p > 0.05), the age that coincided with the onset of lay. Enriched birds that were faster to learn the maze task showed more range visits in the first 4 weeks of range access. Enriched and non-enriched birds showed no differences in telencephalon or hippocampal volume (p > 0.05). Fear may reduce spatial abilities but further testing with more pen replicates per early rearing treatments would improve our understanding of the relationship between spatial cognitive abilities and range use.
In laboratory studies, the assessment of memory is typically associated with overt behavioral responses. Thus, it has been difficult to determine whether the enhancement of hippocampal sensory‐evoked potentials that often accompany memory formation are the neurophysiological manifestation of a memory “trace” or are a secondary product of the behavioral expression of the memory. We addressed this issue by examining changes in evoked hippocampal field potentials during sensory preconditioning, a form of behaviorally silent relational learning that requires an intact hippocampus for execution. Rats were exposed to presentations of a white noise (S1) that terminated with a tone (S2). These pairings of ostensibly “neutral” stimuli supported no change in the behavior elicited by the noise. However, if the tone was subsequently paired with mild footshock (US), suppression of ongoing licking behavior (indicative of fear) was elicited by the noise, indicating that the animal had associated the noise with tone (S1‐S2), and had represented the noise‐tone‐shock (S1‐S2‐US) relationship. Pre‐training neurotoxic lesions of the hippocampus had no effect on conditioned suppression to tone after tone‐shock (S2‐US) pairings, but disrupted the expression of continued suppression to noise (S1) after tone‐shock pairings. In a second experiment, sensory‐evoked field potentials in the dorsal hippocampus were recorded with extracellular electrodes. No changes in the hippocampal response evoked by white noise were observed after pairings of noise and tone, i.e., no evidence for a memory trace could be detected. In contrast, after tone was paired with footshock, two short‐latency negative potentials within the noise‐evoked field response increased in amplitude, a response often presumed to reflect a neurophysiological correlate of memory storage. In total, these results suggest that although the hippocampus critically contributes to the processing of a behaviorally silent associative memory, there may be no role for changes in the amplitude of hippocampal sensory‐evoked field potentials in storing representations of the relationships between sensory experiences. Hippocampus 2002;12:648–656.
This study addressed the neural mediation of discriminative avoidance learning, wherein rabbits step in a wheel apparatus in response to an acoustic conditional stimulus, the CS+, to avoid a foot shock, and they learn to ignore a different stimulus, the CS−, not followed by foot shock. Previously, muscimol-induced inactivation of the amygdala in the first session of training prevented learning during the inactivation and permanently blocked the development of discriminative training-induced neuronal activity (TIA) in the medial division of the medial geniculate nucleus (MGm). These results suggested that amygdalar neurons induce discriminative TIA in the MGm via basolateral (BL) amygdalar axonal projections to the auditory cortex. To test this hypothesis, the activity of neurons in the MGm was recorded during learning in rabbits with lesions of the auditory cortex. Recordings were also made in the lateral and BL amygdalar nuclei and in the cingulate cortex. In support of the hypothesis, discriminative learning in rabbits with lesions was impaired significantly during early training sessions 1–4; in these same sessions, discriminative TIA was abolished in the MGm, the BL nucleus, and the anterior cingulate cortex. The lesions also blocked posterior cingulate cortical discriminative TIA in training sessions 1–2 but spared TIA in sessions 3–7. Lateral amygdalar neurons showed gradual development of discrimination that was not significantly affected by the lesions. The results demonstrate a critical role of auditory cortex in early discriminative learning and in the production of early discriminative TIA in multiple areas.