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1 rts of temporal, parietal, sensorimotor, and limbic cortex.
2 elective expression of VGF in the developing limbic cortex.
3 atal regions associated with association and limbic cortex.
4 prefrontal cortex and increased rates in the limbic cortex.
5 nistration produced significant decreases in limbic cortex.
6 and a significant decrease of D1 mRNA in the limbic cortex.
7 in relevant brain areas such as amygdala and limbic cortex.
8 2 included the lateral frontal and anterior limbic cortex.
9 T2 was higher in the ventral hippocampus and limbic cortex 3 days after seizure activity compared wit
11 by physical (mechanical) compression of the limbic cortex against the adjacent tympanic bulla and su
12 elencephalon, signal was abundant throughout limbic cortex and neocortex, olfactory bulb, hippocampus
13 ant human (rh) BDNF into the rodent neo- and limbic cortex and used a turkey anti-BDNF antibody to de
14 lly affects brain activity in prefrontal and limbic cortex, and speculate that dopamine's effects on
15 able to excitotoxic injury (the striatum and limbic cortex) but not in regions relatively resistant t
16 rlie a hypoglutamatergic state in regions of limbic cortex, consistent with published results from ot
17 f both interictal and PSs in acute models of limbic cortex ictogenesis induced by pharmacological man
19 istent with metabolic studies, the cingulate-limbic cortex, inducing neuroadaptation, neuropil reduct
20 injections into anterior thalamus reproduce limbic cortex injury, and GABA-receptor agonist injectio
22 viscera have a greater representation on the limbic cortex than somatic structures, and this explains
24 oses how two parallel learning pathways from limbic cortex to the SNc, one devoted to excitatory cond
25 striatum, but lacks projections to parts of limbic cortex, to nucleus accumbens, and to the amygdala
26 in a subnetwork that primarily included the limbic cortex, visual cortex, and subcortex during emoti
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