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Matrix metalloproteinase-9 (MMP-9) is an extracellularly operating endopeptidase, which cleaves extracellular matrix proteins and plays an important role in synaptic plasticity, learning and memory. It is expressed in neurons in many different brain structures, including the hipocampus, prefrontal cortex and amygdala. MMP-9 is involved in maintenance of long-term potentiation (LTP) in the hipocampus and prefrontal cortex. On the other hand, its role in synaptic plasticity in the amygdala is much less known. It has been shown that the MMP-9 knock-out (MMP-9 KO) mice are impaired in amygdala-dependent appetitively motivated learning. The amygdaloid complex consists of several cytoarchitectonically and functionally distinguishable nuclei. To investigate MMP-9-dependent synaptic plasticity in different amygdalar nuclei, we studied MMP-9 role in LTP evoked in the central (CE), basal (BA) and lateral (LA) nuclei of the amygdala. In our in vitro extracellular recordings we used slices from MMP-9 KO and control mice. LTP in the BACE and LA-BA pathways was induced at the same level in the MMP-9 KO and control slices but it was disrupted several minutes after induction. In contrast, LTP in the external capsule-LA pathway was not disturbed in MMP-9 KO. These data suggests that MMP-9 is involved in stabilization but not in induction of LTP only in particular nuclei of the amygdala.
Matrix metalloproteinases (MMPs) form an enzyme family which, by mainstream research, is implicated in extracellular matrix processing in physiological and pathophysiological conditions. Some of these proteins termed gelatinases, in particular MMP-2 and MMP-9, cleave gelatin as an artifi cial substrate. Surprisingly, a number of studies have revealed the presence of gelatinolytic activity in the cell nucleus. Although the phenomenon appears not to be artifactual, neither the identity nor the role of nuclear gelatinases has been established unequivocally. In the nervous system, nuclear gelatinolysis is detectable in normal conditions, yet it is induced by seizures, and stroke. We studied nuclear gelatinolytic activity by high resolution in situ zymography (ISZ) in sections of alcohol-fi xed, polyester wax-embedded normal rat brain. Ubiquitously distributed among the major brain areas the ISZ signal was present mainly in neurons. At high magnifi cation, our study revealed previously unrecognized mesh-like pattern of nuclear gelatinolytic which, by counterstaing with fl uorescent DNA-binding dye, represents an interchromatin space. The ISZ signal colocalized with the ribonucleoprotein compartment enriched in splicing components, identifi ed using an immunoreactivity of spliceosome assembly factor SC-35. This suggesting a function for MMPs in processes of gene-expression and/or RNA-processing and hypothetically involvement in remodeling of chromosome territories.
Matrix metalloproteinase-9 (MMP-9) is an extracelularly operating protein, capable to cleave several components of extracellular matrix (ECM). It is expressed in neurons in many brain structures. It has been shown to be important for maintenance of LTP in hipoocampal CA3 to CA1 pathway (Nagy et al. 2006) as well as in the prefrontal cortex (Okulski et al. 2007). Amygdaloid body is a small heteromeric structure, important for regulation of memory and autonomic as well as endocrine responses. In the present study, we have examined if LTP is MMP-9-dependent in the pathway from basolateral to central amygdala. The basolateral nucleus of amygdala (BLA) was theta burst-stimulated using a bipolar electrode, and EPSPs were collected from CE. We have found that in slices from MMP-9 knock out mice the late phase of LTP is abolished. The same effect was obtained when inhibitor of MMP-9 was used in rat amygdala slices where LTP lasted for only 30 min after its induction. Finally, we have checked LTP in slices from the transgenic rats with neuron-specifi c MMP-9 overexpression, driven by Synapsin I promoter. LTP in these rats was lower than in control but stable. The present observation suggests that the proper level of MMP-9 expresion and activity is essential for synaptic plasticity in the BLA-CE pathway, whereas MMP-9 overexpresion may cause destabilization of neuronal environment and decreased activity-dependent strengthening of synaptic transmission.
INTRODUCTION: Social support during exposure-based psychotherapy has been suggested to have an important influence on the course of exposure treatment, however some clinical trials show that individual therapy may be more effective than group therapy. The mechanisms of social influence on fear extinction remain unknown. METHOD(S): To study neuronal correlates of social buffering in fear extinction, we have developed a rat model. In our model, rats showed a significant lowering of fear response during fear extinction when exposed to fear‑associated stimuli with a companion. The buffering magnitude depended on familiarity and physical similarity of the tested animals but not on their emotional status; the fear‑conditioned partners were as effective as naïve ones. However, the effect was transient and disappeared when rats were tested individually the next day. To test whether social buffering shares neuronal mechanisms with fear extinction, we measured activation of fear regulating neuronal circuits. Lower fear response during exposure with a partner was associated with lower activation of the infralimbic (IL), prelimbic (PL), and anterior cingulate (ACC) cortices. However, although optogenetic blocking of the IL increased fear response in rats tested separately, it left the social buffering effect intact. RESULTS: Analyzing inputs to the cortex from the ventral hippocampus (vHIPP) and basolateral amygdala (BL), we found significantly more vHIPP innervated neurons activated in the PL but not IL or ACC of the socially buffered rats. CONCLUSIONS: The results show that fear memory suppression by the presence of a companion is transient and relies, at least partially, on different neuronal circuits than fear extinction.
INTRODUCTION: Encephalization, i.e., the amount of brain mass related to an animal’s total body mass is increased in homeotherms comparing to ectotherms. A larger brain offers behavioral advantages, but also means energy expenditures that are an order of magnitude higher than in ectotherms. What are the benefits of larger, energetically expensive brains that allowed them to evolve? The ‘Expensive Tissue’ hypothesis links evolution of enlarged brain to increased cognitive skills that improve foraging performance. AIM(S): We aim at testing the ET hypothesis using two lines of mice bred for low and high basal metabolic rate (BMR). METHOD(S): Low (L-BMR) and high (H-BMR) lines of Swiss Webster mice were selected reaching 40% between-line difference in BMR. The weight of their internal organs, including the brain, their cognitive abilities and neural plasticity were measured. The cognitive abilities of the mice were tested in IntelliCage system which allows for assessment of learning of individual mice living in the social group. To test the brain plasticity-related differences between the lines we used a model of neural plasticity, CA3-CA1 hippocampal long-term potentiation (LTP). RESULTS: The weight of internal organs differed, with H-BMR mice organs being heavier. We found increased exploration of the environment in H-BMR mice, which also showed higher motivation to obtain the reward and faster learning of the reward’s position. In line with learning results, we found that LTP was induced at significantly higher level in H-BMR mice, suggesting higher neural plasticity in this line. CONCLUSIONS: Together, our results suggest that higher BMR is associated with more efficient exploration of the environment, higher motivation and better place learning. Increased cognitive skills, probably mediated by enhanced neuroplasticity, allow for improved foraging performance, in line with the ET hypothesis. FINANCIAL SUPPORT: Project is financed by the National Science Centre grant (NCN 2015/17/B/NZ8/02484).
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