Amygdala interconnections with the cingulate motor cortex in the rhesus monkey.

Amygdala interconnections with the cingulate motor cortices were investigated in the rhesus monkey. Using multiple tracing approaches, we found a robust projection from the lateral basal nucleus of the amygdala to Layers II, IIIa, and V of the rostral cingulate motor cortex (M3). A smaller source of amygdala input arose from the accessory basal, cortical, and lateral nuclei, which targeted only the rostral region of M3. We also found a light projection from the lateral basal nucleus to the same layers of the caudal cingulate motor cortex (M4). Experiments examining this projection to cingulate somatotopy using combined neural tracing strategies and stereology to estimate the total number of terminal-like immunoreactive particles demonstrated that the amygdala projection terminates heavily in the face representation of M3 and moderately in its arm representation. Fewer terminal profiles were found in the leg representation of M3 and the face, arm, and leg representations of M4. Anterograde tracers placed directly into M3 and M4 revealed the amygdala connection to be reciprocal and documented corticofugal projections to the facial nucleus, surrounding pontine reticular formation, and spinal cord. Clinically, such pathways would be in a position to contribute to mediating movements in the face, neck, and upper extremity accompanying medial temporal lobe seizures that have historically characterized this syndrome. Alterations within or disruption of the amygdalo-cingulate projection to the rostral part of M3 may also have an adverse effect on facial expression in patients presenting with neurological or neuropsychiatric abnormalities of medial temporal lobe involvement. Finally, the prominent amygdala projection to the face region of M3 may significantly influence the outcome of higher-order facial expressions associated with social communication and emotional constructs such as fear, anger, happiness, and sadness.

Neurotrophic factors in the central nucleus of amygdala may be organized to provide substrates for associative learning.

The central nucleus of amygdala was examined to identify the ultrastructural distribution of neurotrophins responsible for the complex of neuronal signaling processes which regulate synaptic transmission and neuronal plasticity, and possibly underlie memory formation. We investigated at the electron microscopic level the cellular organization of brain-derived neurotrophic factor (BDNF) and its receptor, tyrosine kinase receptor B (TrkB), in the extended amygdala (CE). We also investigated the interaction between cortical inputs to CE and BDNF and TrkB. Our results indicate the presence of pro-BDNF and BDNF in terminals in the CE which show a strong association with immunoreactive postsynaptic densities. TrkB receptor immunoreactivity was localized to postsynaptic densities of asymmetric synapses on dendrites and dendritic spines. Cortical terminals formed asymmetric synapses with dendritic shafts and spines, but were not BDNF immunoreactive. TrkB receptors were observed opposed to cortical terminals. These data also suggest that one potential substrate for associative learning may be the interaction of different cortical inputs with neurotrophin-containing terminals ending on dendritic spines and other neuronal structures of CE.