Metabolic mapping of rat forebrain and midbrain during delay and trace eyeblink conditioning

Abstract

While the essential neural circuitry for delay eyeblink conditioning has been largely identified, much of the neural circuitry for trace conditioning has yet to be determined. The major difference between delay and trace conditioning is a time gap between the presentation of the conditioned stimulus (CS) and the unconditioned stimulus (US) during trace conditioning. It is this time gap, which accounts for the additional memory component and may require extra neural structures, including hippocampus and prefrontal cortex. A metabolic marker of energy use, radioactively labeled glucose analog, was used to compare differences in glucose analog uptake between delay, trace, and unpaired experimental groups (rats, Long-Evans), to identify possible new areas of involvement within forebrain and midbrain. Here, we identify increased 2-DG uptake for the delay group compared to the unpaired group in various areas including: the medial geniculate nuclei (MGN), the amygdala, cingulate cortex, auditory cortex, medial dorsal thalamus, and frontal cortices. For the trace group, compared to the unpaired group, there was an increase in 2-DG uptake for the medial orbital frontal cortex and the medial MGN. The trace group also exhibited more increases lateralized to the right hemisphere, opposite to the side of US delivery, in various areas including: CA1, subiculum, presubiculum, perirhinal cortex, ventral and dorsal MGN, and the basolateral and central amygdala. While some of these areas have been identified as important for delay or trace conditioning, some new structures have been identified such as the orbital frontal cortex for both delay and trace groups.

Neurobehavioral assessment of maternal odor in developing rat pups: implications for social buffering

“…Brains were sectioned in a cryostat (20 μm) at −20°C. Every third section was collected on a cover slip and exposed for 5 days along with standards ( 14 C standards 10 × 0.02 mCi, American Radiolabeled Chemicals Inc., St Louis, MO) and exposed to X-ray film in a cassette (Kodak, Rochester, NY) (Boulanger Bertolus et al, 2014; Debiec & Sullivan, 2014; Plakke, Freeman, & Poremba, 2009; Sullivan & Wilson, 1995). …”

The neural circuitry and molecular mechanisms underlying delay and trace eyeblink conditioning in mice

“…However, only a few researchers pay attention to its involvement in DEC. By using the methods of lateral amygdale lesion or muscimol (MSC) injection into the lateral amygdale, Sakamoto et al found [47] that the lateral amygdale plays important roles in the acquisition and expression of DEC in mice. Similarly, metabolic and lesion studies also show that the amygdala plays a role in DEC in rats [58][59][60]. Boele et al proposed the Amygdala-CerebellumDynamic-Conditioning Model (ACDC model), which indicates that the short-latency-response (SLR), a characteristic trace of the EBC in mice, may originate from the amygdala [17].…”

Micro-Positron Emission Tomography Imaging of Rat Brain Metabolism during Expression of Contextual Conditioning

“…However, interest is growing, in part because contextual conditioning in rats serves as an animal model for human pathological anxiety such as in generalized anxiety disorder (Grillon et al, 2006;Zanoveli et al, 2007;Luyten et al, 2011b). So far, the neurocircuitry of conditioning has been studied primarily through lesion or inactivation experiments in rodents (often pretraining interventions) (Kim and Jung, 2006;Walker et al, 2009) and, to a lesser degree, using autoradiography or histochemistry techniques (Gonzalez-Lima and Scheich, 1986;Beck and Fibiger, 1995;Poremba et al, 1998;Plakke et al, 2009). To our knowledge, there are no published neuroimaging studies of conditioned rats, despite the obvious advantages of visualizing and quantifying metabolism of the intact brain in behaving animals.…”