Different disruptive effects on the acquisition and expression of conditioned taste aversion by blockades of amygdalar ionotropic and metabotropic glutamatergic receptor subtypes in rats
Department of Behavioral Physiology, Faculty of Human Sciences, Osaka University, 1-2 Yamadaoka, Suita, 565-0871, Osaka, Japan. Brain Research
(Impact Factor: 2.84).
07/2000; 869(1-2):15-24. DOI: 10.1016/S0006-8993(00)02397-0
Conditioned taste aversion (CTA) is based on the gustatory long-term memory established after association of the taste of food (conditioned stimulus, CS) with visceral signals of poisoning (unconditioned stimulus, US). After the acquisition of CTA, hedonics of the taste CS changes from positive to negative as indicated by reduced ingestive and increased aversive taste reactivities in response to re-exposures to the CS. We examined the effects of reversible and selective blockades of the amygdalar glutamate receptor subtypes, AMPA, NMDA and metabotropic glutamate receptors, on the formation of CTA. Blockades of each of the three receptor subtypes between ingestion of saccharin (CS) and malaise-inducing LiCl (US) disrupted the acquisition of CTA. After the acquisition of CTA, however, blockades of only AMPA receptors, but not NMDA or metabotropic receptors, impaired the expression of CTA. This effect was seen only during the period when the antagonistic action to AMPA receptors lasted. These results indicate that both ionotropic and metabotropic glutamate receptor subtypes in the amygdala are indispensable for the acquisition of CTA, but that the expression of acquired CTA is mediated only by AMPA receptors. The present results also suggest that the amygdalar glutamatergic neural transmission is involved in the formation and storage of long-term gustatory memory associated with the altered hedonics from positive to negative.
Available from: Kobi Rosenblum
- "Conceptually, on the one hand, our short-trace CTA complies with the commonly held assumption of neuroscience theories of associative learning that convergence of CS and US information onto particular cells/circuits leads to changes in synaptic strength at the synapses mediating the CS input to those commonly activated cells/circuit and that it underlies association formation, i.e. Hebbian plasticity (NMDAR-CaMKII-AMPARs in the IC probably in co-ordination with the amygdala;Yasoshima et al., 2000;Ferreira et al., 2005;Hashikawa et al., 2013). On the other hand, the long-trace CTA challenges this assumption, and it is possible that because of the multi-channeled background information with an increasing time interval as discussed above, homeostatic plasticity may play a crucial role to encode multiple memory traces via coordinating several brain structures such as the IC, amygdala, hippocampus, prefrontal cortices in the long-trace CTA (Vitureira et al., 2012;Turrigiano, 2012;Pozo and Goda, 2010). "
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ABSTRACT: Events separated in time are associatively learned in trace conditioning, recruiting more neuronal circuits and molecular mechanisms than in delay conditioning. However, it remains unknown whether a given sensory memory trace is being maintained as a unitary item to associate. Here, we used conditioned taste aversion learning in the rat model, wherein animals associate a novel taste with visceral nausea, and demonstrate that there are two parallel memory traces of a novel taste: a short-duration robust trace, lasting approximately 3h, and a parallel long-duration weak one, lasting up to 8h, and dependent on the strong trace for its formation. Moreover, only the early robust trace is maintained by a NMDAR-dependent CaMKII- AMPAR pathway in the insular cortex. These findings suggest that a memory trace undergoes rapid modifications, and that the mechanisms underlying trace associative learning differ when items in the memory are experienced at different time points.
Available from: Federico Bermúdez-Rattoni
- "Concerning the neurotransmission associated to memory formation, glutamatergic transmission has been implicated in http://dx.doi.org/10.1016/j.bbr.2015.02.020 0166-4328/© 2015 Elsevier B.V. All rights reserved. different types of learning     . Glutamate receptors have been classified as ionotropic or metabotropic (mGluR) receptors . "
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ABSTRACT: Cortical glutamatergic activity is known to be important for memory formation in different learning tasks. For example, glutamate activity in the insular cortex plays an important role in aversive taste memory formation by signaling the unconditioned stimulus. However, the role of glutamate in the insular cortex in appetitive taste learning has remained poorly studied. Therefore, we considered the function of glutamate in attenuation of neophobia, a model of appetitive taste recognition memory. For this purpose, we performed infusions of vehicle, glutamate, a specific mGluR1 antagonist (AIDA) or a combination of glutamate and AIDA at 0 or 30minutes, and glutamate or vehicle at 60minutes after novel saccharin consumption. Glutamate infusion impaired appetitive taste recognition memory when infused at 0 or 30minutes, whereas, AIDA infusions produced enhanced appetitive memory at the same infusion times. Furthermore, when glutamate and AIDA were infused together no effect on attenuation of neophobia was observed. As opposed to shorter infusion times, the administration of glutamate 60minutes after the presentation of the saccharin consumption was ineffective in the impairment of the appetitive taste memory. These results are discussed in view of the effect of glutamate and its mGluR1 during the appetitive taste recognition memory formation in the insular cortex.
Copyright © 2015. Published by Elsevier B.V.
Available from: Timothy J Jarome
- "Consistent with the evidence from the broad spectrum inhibitors, several studies have implicated a role for specific intracellular signaling molecules thought to be “upstream” of protein synthesis in LTM formation and storage (Johansen et al., 2011). For example, inhibition of NMDA receptor (NMDAR) function impairs the consolidation of auditory delay fear and contextual fear memories, fear potentiated startle, and conditioned taste aversion memories in the amygdala (Walker and Davis, 2000; Yasoshima et al., 2000; Rodrigues et al., 2001), auditory trace and contextual fear memories in the prefrontal cortex (Gilmartin and Helmstetter, 2010; Gilmartin et al., 2013a), contextual fear memories, MWM and objection recognition spatial memories in the hippocampus (Liang et al., 1994; Izquierdo et al., 1999; Czerniawski et al., 2012; Da Silva et al., 2013; Warburton et al., 2013), and conditioned taste aversion memories in the insular cortex (Escobar et al., 1998). Inhibition of signaling molecules thought to be downstream of NMDAR activity but upstream of protein synthesis such as Protein Kinase A, ERK-MAPK, and CaMKII impairs memory consolidation for auditory fear memories, contextual fear memories, inhibitory avoidance memories, MWM spatial memories, and conditioned taste aversion memories (Schafe and Ledoux, 2000; Schafe et al., 2000; Sacchetti et al., 2001; Koh et al., 2002; Quevedo et al., 2004; Rodrigues et al., 2004; Leon et al., 2010; Ota et al., 2010; Chen et al., 2012; Halt et al., 2012). "
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ABSTRACT: Long-term memory (LTM) formation requires transient changes in the activity of intracellular signaling cascades that are thought to regulate new gene transcription and de novo protein synthesis in the brain. Consistent with this, protein synthesis inhibitors impair LTM for a variety of behavioral tasks when infused into the brain around the time of training or following memory retrieval, suggesting that protein synthesis is a critical step in LTM storage in the brain. However, evidence suggests that protein degradation mediated by the ubiquitin-proteasome system may also be a critical regulator of LTM formation and stability following retrieval. This requirement for increased protein degradation has been shown in the same brain regions in which protein synthesis is required for LTM storage. Additionally, increases in the phosphorylation of proteins involved in translational control parallel increases in protein polyubiquitination and the increased demand for protein degradation is regulated by intracellular signaling molecules thought to regulate protein synthesis during LTM formation. In some cases inhibiting proteasome activity can rescue memory impairments that result from pharmacological blockade of protein synthesis, suggesting that protein degradation may control the requirement for protein synthesis during the memory storage process. Results such as these suggest that protein degradation and synthesis are both critical for LTM formation and may interact to properly “consolidate” and store memories in the brain. Here, we review the evidence implicating protein synthesis and degradation in LTM storage and highlight the areas of overlap between these two opposing processes. We also discuss evidence suggesting these two processes may interact to properly form and store memories. LTM storage likely requires a coordinated regulation between protein degradation and synthesis at multiple sites in the mammalian brain.
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