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1 heta frequencies and drive theta activity in limbic cortex.
2  2 included the lateral frontal and anterior limbic cortex.
3 elective expression of VGF in the developing limbic cortex.
4 atal regions associated with association and limbic cortex.
5 prefrontal cortex and increased rates in the limbic cortex.
6 nistration produced significant decreases in limbic cortex.
7 and a significant decrease of D1 mRNA in the limbic cortex.
8 ttention network), with the exception of the limbic cortex.
9 rts of temporal, parietal, sensorimotor, and limbic cortex.
10 s widely connected to frontal, parietal, and limbic cortex.
11 in relevant brain areas such as amygdala and limbic cortex.
12 T2 was higher in the ventral hippocampus and limbic cortex 3 days after seizure activity compared wit
13 ducing a shift in the balance of cortical to limbic cortex activity.
14  by physical (mechanical) compression of the limbic cortex against the adjacent tympanic bulla and su
15 elencephalon, signal was abundant throughout limbic cortex and neocortex, olfactory bulb, hippocampus
16 ant human (rh) BDNF into the rodent neo- and limbic cortex and used a turkey anti-BDNF antibody to de
17  and by activation of PV interneurons in pre-limbic cortex and ventral subiculum of the hippocampus.
18 lly affects brain activity in prefrontal and limbic cortex, and speculate that dopamine's effects on
19 ity was located in the default mode network, limbic cortex, and subcortical nuclei.
20 ast, the rodent MSR receives inputs from the limbic cortex but contains well-defined nuclei, includin
21 able to excitotoxic injury (the striatum and limbic cortex) but not in regions relatively resistant t
22 rlie a hypoglutamatergic state in regions of limbic cortex, consistent with published results from ot
23 f both interictal and PSs in acute models of limbic cortex ictogenesis induced by pharmacological man
24        However, it also had connections with limbic cortex, including retrosplenial and caudal cingul
25 istent with metabolic studies, the cingulate-limbic cortex, inducing neuroadaptation, neuropil reduct
26  injections into anterior thalamus reproduce limbic cortex injury, and GABA-receptor agonist injectio
27 atively resistant to excitotoxicity (the non-limbic cortex, thalamus and white matter).
28 viscera have a greater representation on the limbic cortex than somatic structures, and this explains
29 e demonstrate two parallel pathways from the limbic cortex to the hippocampus.
30 oses how two parallel learning pathways from limbic cortex to the SNc, one devoted to excitatory cond
31  striatum, but lacks projections to parts of limbic cortex, to nucleus accumbens, and to the amygdala
32  in a subnetwork that primarily included the limbic cortex, visual cortex, and subcortex during emoti
33                Regions of the prefrontal and limbic cortex were most consistently reported in studies