Neuroscience
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Previous research in our laboratory has shown that damage to the amygdala in neonatal rhesus monkeys profoundly alters behaviors associated with fear processing, while leaving many aspects of social development intact. Little is known, however, about the impact of neonatal lesions of the amygdala on later developing aspects of social behavior. A well-defined phenomenon in the development of young female rhesus monkeys is an intense interest in infants that is typically characterized by initiating proximity or attempting to hold them. ⋯ However, following the birth of the infants, the amygdala-lesioned females showed significantly less interest in the infants than did control or hippocampus-lesioned females. They directed fewer affiliative vocalizations and facial expressions to the mother-infant pair compared to the hippocampus-lesioned and control females. These findings suggest that neonatal damage to the amygdala, but not the hippocampus, impairs important precursors of non-human primate maternal behavior.
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The encoding of reward-predictive stimuli by neurons in the nucleus accumbens (NAcc) depends on integrated synaptic activity from the basolateral amygdala (BLA) and medial prefrontal cortex (mPFC) afferent inputs. In a previous study, we found that single electrical stimulation pulses applied to the BLA facilitate mPFC-evoked spiking in NAcc neurons in a timing-dependent manner, presumably by a fast glutamatergic mechanism. In the present study, the ability of repetitive BLA activation to modulate synaptic inputs to NAcc neurons through dopamine- or N-methyl-D-aspartate (NMDA)-dependent mechanisms is characterized. ⋯ This was not attributable to mechanisms involving NMDA or dopamine D1, D2, D3 or D5 receptors, since blockade of these receptors did not affect the BLA-mediated depression. BLA-mediated depression was only evident when the BLA stimulation evoked spikes in the recorded neuron; thus, depolarization of the recorded neuron may be critical for this effect. The ability of the BLA to suppress mPFC-to-NAcc signaling may be a mechanism by which normal or pathologically heightened emotional states disrupt goal-directed behavior in favor of emotionally-driven responses.
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Classical conditioning of the eye-blink reflex in the rabbit is a form of motor learning that is uniquely dependent on the cerebellum. The cerebellar learning hypothesis proposes that plasticity subserving eye-blink conditioning occurs in the cerebellum. The major evidence for this hypothesis originated from studies based on a telecommunications network metaphor of eye-blink circuits. ⋯ A possible solution to this problem is offered by several promising new approaches that minimize the effects of experimental interventions on spontaneous neuronal activity. Results from these studies indicate that plastic changes underlying eye-blink conditioning are distributed across several cerebellar and extra-cerebellar regions. Specific input interactions that induce these plastic changes as well as their cellular mechanisms remain unresolved.
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Internal models are a key feature of most modern theories of motor control. Yet, it has been challenging to localize internal models in the brain, or to demonstrate that they are more than a metaphor. In the present review, I consider a large body of data on the cerebellar floccular complex, asking whether floccular output has features that would be expected of the output from internal models. ⋯ If we consider the brainstem circuits and eyeball as a more broadly conceived "oculomotor plant," then the output from the floccular complex could be the manifestation of an inverse model of "plant" dynamics. (3) Floccular output reflects an internal model of the physics of the orbit where head and eye motion sum to produce gaze motion. The effects of learning on floccular output suggest that it is modeling the interaction of the visually-guided and vestibular-driven components of eye and gaze motion. Perhaps the insights from studying oculomotor control provide groundwork to guide the analysis of internal models for a wide variety of cerebellar behaviors.
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To determine whether there are non-motor regions of cerebellum in which sizeable infarcts have little or no impact on motor control. ⋯ These findings demonstrate that cerebellar stroke does not always result in motor impairment, and they provide clinical evidence for topographic organization of motor versus nonmotor functions in the human cerebellum.