Clonidine in the prepyriform cortex blocked anorectic response to amino acid imbalance

Ingestion of imbalanced amino acid diets (IMB) has been associated with a decrease in norepinephrine (NE) concentration in the prepyriform cortex (PPC), an area essential for the anorectic response to IMB. Decreased NE could result from activity-induced release (and subsequent metabolism) of the transmitter. If activity of the NE system is important in the rat's anorectic response to IMB, reduced NE activity should result in increased IMB intake. Therefore, the feeding response to IMB was measured after injecting clonidine (Clon) into the PPC to inhibit NE release. At 3 and 6 h after Clon (1.0 and 1.5 micrograms/rat) injections, IMB intake was increased from 69 (the usual response to IMB in untreated animals) to > 100% of control intake. Effective injection sites did not include the gustatory neocortex, an area important for conditioned taste aversions. Thus activation of the NE system in the PPC may be associated with the initial reduced intake of IMB, suggesting that NE activity in the PPC has a role in the neural mechanisms that subserve recognition of amino acid deficiency.

Observation of neuronal activity using real-time voltage-sensitive dye imaging

Sensory systems are confronted with the problem of taking “information” in the outside world and encoding and manipulating it in forms that can be used in the neuronal world. A major challenge is to document how the transition between these worlds takes place (transduction) and, once it has taken place, how the data are manipulated by neural circuits (integration). Since the brain is an intrinsically parallel device, carrying out many functions simultaneously, it would appear as important to record brain activity in a similarly parallel manner as to record events in single cells and membranes. Optical recording of neuronal events offers a first step toward thing to observe events that are distributed among the cells and processes of a neuronal network.In the sense of smell odors appear to be encoded by activity distributed across many neurons at each level of the system studied so far, from the sensory cells in the nose to the pyramidal cells in prepyriform cortex (for review see). Thus, to elucidate how the molecular properties of odorants are represented by neurons it is probably necessary to observe the patterns of distributed activation. The distribution of activity across many neuronal elements, in contrast to representing odor molecules by dedicated “labelled lines”, confers redundancy and fault tolerance on a system that is crucial for complex behaviors that underly survival for many animals species, as well as providing flexibility for being sensitive to large numbers of compounds.

Distribution of dietary limiting amino acid injected into the prepyriform cortex

Diffusion or metabolism of the dietary limiting amino acid (DLAA) in the prepyriform cortex (PPC) may account for the time lag between injection of the DLAA into the PPC and the increase in intake of an amino acid-imbalanced diet. Results from the injection of [3H]Leu +/- [14C]Thr (DLAA) into the PPC indicated rapid (less than 15 min) and limited diffusion (85-90% of recovered label was less than or equal to 1 mm from the injection site). 3H and 14C decreased in the trichloroacetic acid (TCA)-soluble fraction and increased in the TCA-insoluble fraction during the first 1.5 h and remained constant in the TCA-insoluble fraction 1.5-6 h after injection. An increase (approximately 50%) in 3H in the TCA-insoluble fraction was found less than or equal to 30 min after injection of the DLAA. There was no affect of the DLAA on 3H in the TCA-soluble fraction. These results indicated that a change in metabolism within the PPC may be responsible for the delay in onset of the feeding response after injection of the DLAA into the PPC.

Effect of dietary limiting amino acid in prepyriform cortex on meal patterns

Microinjection of the dietary limiting essential amino acid (DLAA) into the prepyriform cortex (PPC) increased intake of a diet having an imbalance among the essential amino acids (imbalanced diet) from 50-55% of baseline, when artificial cerebrospinal fluid (aCSF) was injected, to 70-75% of baseline. The increase in intake of the imbalanced diet by DLAA injection became apparent after 3-6 h and was maintained throughout the dark period. Meal size, meal duration, and the number of meals returned to normal after bilateral injections of the DLAA into the PPC of rats fed the imbalanced diet. Injection of the DLAA 30 min before the onset of the dark phase increased intake of imbalanced diet to 70% of baseline intake. When injections of threonine or isoleucine were made 6 and 3 h, respectively, prior to onset of the dark phase, intake of imbalanced diet increased to 85% of baseline intake. Results suggest that some form of processing of the injected DLAA within the PPC is necessary to increase the intake of imbalanced diets.

Effect of dietary limiting amino acid in prepyriform cortex on food intake

The mechanisms underlying the reduced intake of an amino acid-imbalanced diet (imbalanced diet) appears to involve a decrease in the content of the dietary limiting amino acid (DLAA) in the prepyriform cortex (PPC). Intake of imbalanced diet was increased from 45-50 to 70-75% of baseline after bilateral injection of the DLAA directly into the PPC, following an inverted U-shaped dose-response curve. Injections had no effect on intake of basal diets. Injection of the DLAA into the PPC reversed the aversion to imbalanced diet in choice studies, as rats selected an imbalanced diet over protein-free diet after such injections. Intake of imbalanced diet did not increase after a nonlimiting amino acid was injected into the PPC or after injections of the DLAA into other brain areas. Results were similar when either threonine or isoleucine was the DLAA. These results confirm that the decrease in the concentration of the DLAA in the PPC is involved in the reduction in intake of imbalanced diets.