Table 1.
Over-representation of human amygdaloid proteins in specific-neuronal processes by Reactome pathway analysis.
| Name of the event | Amygdaloid proteins in each event | Total number of proteins in each event | p-value |
|---|---|---|---|
| Axon guidance | 67 | 277 | 1.0e–12 |
| L1CAM interactions | 37 | 107 | 2.2e–12 |
| Transmission across chemical synapses | 45 | 191 | 1.6e–08 |
| GABA synthesis, release, reuptake, and degradation | 12 | 19 | 2.0e–08 |
| Release of GABA at the synapse | 9 | 13 | 4.2e–07 |
| GABA loaded synaptic vesicle docking and priming | 9 | 13 | 4.2e–07 |
| Membrane trafficking | 41 | 192 | 1.2e–06 |
| Serotonin neurotransmitter release cycle | 8 | 12 | 3.0e–06 |
| Dopamine neurotransmitter release cycle | 8 | 12 | 3.0e–06 |
| Dopamine synaptic vesicle docking and priming | 8 | 12 | 3.0e–06 |
| Release of docked dopamine loaded synaptic vesicle | 8 | 12 | 3.0e–06 |
| Release of docked serotonin loaded synaptic vesicle | 8 | 12 | 3.0e–06 |
| Serotonin loaded synaptic vesicle docking and priming | 8 | 12 | 3.0e–06 |
| Trafficking of AMPA receptors | 12 | 30 | 1.2e–05 |
| Glutamate binding, activation of AMPA receptors and synaptic plasticity | 12 | 30 | 1.2e–05 |
| Assembly in clathrin-coated vesicles (CCVs) | 9 | 18 | 1.8e–05 |
| Opioid Signaling | 21 | 80 | 2.0e–05 |
| Formation of clathrin coated vesicle | 7 | 11 | 2.0e–05 |
| Loading of GABA into clathrin sculpted GABA transport vesicle lumen | 6 | 8 | 2.1e–05 |
| Trafficking of GluR2-containing AMPA receptors | 8 | 16 | 5.4e–05 |
| Retrograde neurotrophin signaling | 7 | 13 | 8.8e–05 |
| Neuronal system | 48 | 292 | 2.3e–04 |
| Sema3A PAK dependent axon repulsion | 7 | 15 | 2.8e–04 |
| Trafficking of GluR2-containing AMPA receptors to extrasynaptic sites | 7 | 15 | 2.8e–04 |
| Norepinephrine neurotransmitter release cycle | 6 | 12 | 4.9e–04 |
| Endocytosis of Ca impermeable AMPA receptors | 6 | 12 | 4.9e–04 |
| Axonal growth inhibition (RHOA activation) | 5 | 9 | 8.2e–04 |
| Glutamate synaptic vesicle docking and priming | 5 | 9 | 8.2e–04 |
| release of L-glutamate at the synapse | 5 | 9 | 8.2e–04 |
| Acetylcholine synaptic vesicle docking and priming | 5 | 9 | 8.2e–04 |
| Release of acetylcholine at the synapse | 5 | 9 | 8.2e–04 |
| Release of noradrenaline at the synapse | 5 | 9 | 8.2e–04 |
| Noradrenalin synaptic vesicle docking and priming | 5 | 9 | 8.2e–04 |
| Neurofascin binds contactin-1:CASPR complex | 3 | 3 | 9.5e–04 |
| AGRN binds NCAM1, PTPRS | 3 | 3 | 9.5e–04 |
| Axonal transport of NGF:Trk complexes | 5 | 10 | 1.5e–03 |
| p75NTR regulates axonogenesis | 5 | 10 | 1.5e–03 |
| Regulation of Insulin Secretion by acetylcholine | 5 | 10 | 1.5e–03 |
| Glutamate neurotransmitter release cycle | 6 | 15 | 2.1e–03 |
| NCAM signaling for neurite out-growth | 15 | 68 | 2.1e–03 |
| Acetylcholine neurotransmitter release cycle | 5 | 11 | 2.6e–03 |
| NCAM1:pFAK:Grb2:Sos-mediated nucleotide exchange of Ras | 6 | 16 | 3.0e–03 |
| NGF signaling via TRKA from the plasma membrane | 32 | 201 | 4.1e–03 |
| Signaling by NGF | 42 | 283 | 4.2e–03 |
| Unblocking of NMDA receptor | 6 | 17 | 4.3e–03 |
| Unblocking of NMDA receptor, glutamate binding, and activation | 6 | 17 | 4.3e–03 |
| DARPP-32 events | 7 | 24 | 6.8e–03 |
| Sema4D induced cell migration and growth-cone collapse | 7 | 24 | 6.8e–03 |
| Neurotransmitter receptor binding. Transmission in the post-synaptic cell | 23 | 137 | 7.4e–03 |
| Activation of NMDA receptor upon glutamate binding and post-synaptic events | 9 | 37 | 8.3e–03 |
| glutamate uptake by astrocytes | 2 | 2 | 9.7e–03 |
| Interaction of NCAM1 with Neurocan | 2 | 2 | 9.7e–03 |
| Interaction of NCAM1 with major prion protein (PrP) | 2 | 2 | 9.7e–03 |
| Interaction of NCAM1 with agrin | 2 | 2 | 9.7e–03 |
| Enzymatic degradation of dopamine by COMT | 2 | 2 | 9.7e–03 |
| Enzymatic degradation of dopamine by monoamine oxidase | 2 | 2 | 9.7e–03 |
| Metabolism of serotonin | 2 | 2 | 9.7e–03 |
| Serotonin clearance from the synaptic cleft | 2 | 2 | 9.7e–03 |
| Degradation of GABA | 2 | 2 | 9.7e–03 |
P-value indicates the probability that the association between amygdaloid proteins and the molecular event is explained by chance (only p < 0.01 were considered). See Supplementary Table 8 to show the specific proteins in each event.