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Kent C. Berridge - One of the best experts on this subject based on the ideXlab platform.
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where does damage lead to enhanced Food Aversion the ventral pallidum substantia innominata or lateral hypothalamus
Brain Research, 1993Co-Authors: Howard Casey Cromwell, Kent C. BerridgeAbstract:Abstract It is well known that lesions of the lateral hypothalamus (LH) produce aphagia. Several previous studies have reported that lateral hypothalamus damage produces Food Aversion in addition to aphagia. However, damage to other regions near the LH also produce aphagia and enhanced Aversion. The purpose of this study was to resolve where the site or sites for Aversion-inducing lesions is/are located. Small, bilateral excitotoxin lesions (QUIN, 10 μg in 1 μl or IBO, 15 μg in 1 μl) or bilateral sham injections of vehicle were made into the globus pallidus (GP), the ventral pallidum/substantia innominata (VP/SI) or the lateral hypothalamus (LH). Affective reactions to taste were elicited by infusing sucrose solutions (1 M) into the mouth via chronic oral cannulae. The number of aversive responses (gapes, chin-rubbing, head-shaking and forelimb flails) emitted was tallied. Individual lesions were mapped and a single ‘necessary and sufficient’ site for damage-induced Aversion was identified (the area of overlapping damage common to all rats that showed enhanced aversive reactions). To identify the lesions, two lesion-mapping techniques were used: (1) a conventional neuron-counting procedure in which an attempt is made to count all neurons within a brain region, and (2) a new modified ‘fractionator’ procedure consisting of exhaustive 400× magnification counts at point locations within a brain region. Results indicated that aversive reactions to Food are enhanced only following bilateral neuron loss (>70%) from the caudal ventromedial VP/SI alone. This shared site has a lateral diameter of 1.0 mm, a dorsoventral diameter of 0.5 mm and a rostrocaudal diameter of 1.0 mm. Damage restricted to the LH never produced enhanced Aversion even when it produced aphagia. The crucial region for Aversion is located ventral and medial to the globus pallidus and dorsal and lateral to the lateral hypothalamus.
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where does damage lead to enhanced Food Aversion the ventral pallidum substantia innominata or lateral hypothalamus
Brain Research, 1993Co-Authors: Howard Casey Cromwell, Kent C. BerridgeAbstract:It is well known that lesions of the lateral hypothalamus (LH) produce aphagia. Several previous studies have reported that lateral hypothalamus damage produces Food Aversion in addition to aphagia. However, damage to other regions near the LH also produce aphagia and enhanced Aversion. The purpose of this study was to resolve where the site or sites for Aversion-inducing lesions is/are located. Small, bilateral excitotoxin lesions (QUIN, 10 micrograms in 1 microliter or IBO, 15 micrograms in 1 microliter) or bilateral sham injections of vehicle were made into the globus pallidus (GP), the ventral pallidum/substantia innominata (VP/SI) or the lateral hypothalamus (LH). Affective reactions to taste were elicited by infusing sucrose solutions (1 M) into the mouth via chronic oral cannulae. The number of aversive responses (gapes, chin-rubbing, head-shaking and forelimb flails) emitted was tallied. Individual lesions were mapped and a single 'necessary and sufficient' site for damage-induced Aversion was identified (the area of overlapping damage common to all rats that showed enhanced aversive reactions). To identify the lesions, two lesion-mapping techniques were used: (1) a conventional neuron-counting procedure in which an attempt is made to count all neurons within a brain region, and (2) a new modified 'fractionator' procedure consisting of exhaustive 400 x magnification counts at point locations within a brain region. Results indicated that aversive reactions to Food are enhanced only following bilateral neuron loss (> 70%) from the caudal ventromedial VP/SI alone. This shared site has a lateral diameter of 1.0 mm, a dorsoventral diameter of 0.5 mm and a rostrocaudal diameter of 1.0 mm. Damage restricted to the LH never produced enhanced Aversion even when it produced aphagia. The crucial region for Aversion is located ventral and medial to the globus pallidus and dorsal and lateral to the lateral hypothalamus.
V. P. Nikitin - One of the best experts on this subject based on the ideXlab platform.
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Changes in Amnesia Parameters over Time after Long-Term Memory Disruption with Protein Kinase Mζ Inhibitor
Bulletin of Experimental Biology and Medicine, 2019Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. KozyrevAbstract:We studied the involvement of protein kinase Mζ (PKMζ) in the mechanisms of amnesia development within 10 days after disruption of conditioned Food Aversion memory with ZIP (a PKMζ inhibitor). Repeated training performed in 3 days after amnesia induction with ZIP, led to the formation of conditioned Food Aversion memory, but the number of combined presentations of Food and reinforcer stimuli was lower than during the initial training. Repeated training performed in 10 days after amnesia induction also led to memory formation, but the number of combined presentations of the stimuli was similar to that during the initial training. It was hypothesized that at the early stages of ZIP-induced amnesia, residual memory trace can be restored and amplified during repeated training, which led to memory expression at the behavioral level. At the late stages of amnesia, this memory trace was completely erased and repeated training led to the formation of a new memory. Thus, PKMζ inhibition results in the relatively fast impairment of memory retrieval and induces long-term process of memory erasing.
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Administration of Protein Synthesis Inhibitor before Reminder Reverses Amnesia Induced by Memory Reconsolidation Impairment with 5-HT Receptors Antagonist
Bulletin of Experimental Biology and Medicine, 2019Co-Authors: V. P. Nikitin, S. A. Kozyrev, S. V. SolntsevaAbstract:Administration of 5-HT receptor antagonist to snails trained in conditioned Food Aversion prior to reminding of the conditioning stimulus caused amnesia. At the early period of amnesia (day 3), injections of protein synthesis inhibitor cycloheximide without reminder or reminder alone were ineffective. At the same time, injections of the inhibitor combined with reminder led to memory recovery; this effect in most animals persisted for at least 10 days. In the rest snails, aversive responses to presentations of the conditioning stimulus persisted for 2 days. Cycloheximide injection and reminder in 10 days after induction of amnesia did not affect its development or caused a transient memory recovery (2 days). We hypothesized that amnesia is an active process unfolding in time. One of mechanism of this process is reminder-induced and protein synthesis-depended reactivation of amnesia. Inhibitor of protein synthesis disturbed this reactivation and led to recovery of the initial memory of conditioned Food Aversion.
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Peculiarities of Participation of DNA Methyltransferases in the Mechanisms of Storage, Impairment, and Recovery of Conditioned Food Aversion Memory
Bulletin of Experimental Biology and Medicine, 2018Co-Authors: V. P. Nikitin, S. A. Kozyrev, S. V. SolntsevaAbstract:We studied the participation of DNA-methylation processes in the mechanisms of memory storage and reconsolidation, amnesia induction, and in recovery of the conditioned Food Aversion memory in edible snails. It was found that daily injections of DNA methyltransferases inhibitor over 3 days combined with a reminder of a conditioned Food stimulus did not affect memory storage. The administration of DNA methyltransferase inhibitors did not suppress induction of amnesia caused the NMDA receptor antagonist/reminder. Injections of DNA methyltransferase inhibitors combined with the reminder led to memory recovery in 3 days after amnesia induction. Thus, DNA methyltransferase inhibitors in the same doses did not affect storage and reconsolidation of memory, as well as the mechanisms of amnesia induction. At the same time, injections of inhibitors led to memory recovery, apparently, due to disruption of reactivation and amnesia development.
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Involvement of Glycogen Synthase Kinase-3 in the Mechanisms of Conditioned Food Aversion Memory Reconsolidation
Bulletin of Experimental Biology and Medicine, 2017Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. KozyrevAbstract:Experiments were performed on the snails trained in conditioned Food Aversion for 3 days. Injection of TDZD-8 (glycogen synthase kinase-3 inhibitor, 2 mg/kg) in combination with reminder (presentation of a conditioned Food stimulus) led to memory impairment developing 3 days after inhibitor/reminder exposure and followed by spontaneous recovery in 10 days. Injections of TDZD-8 in a dose of 4 or 20 mg/kg before reminder were shown to cause amnesia that persisted for more than 10 days. Memory recovery during repeated training was observed at the earlier period than after initial training. The impairment of memory reconsolidation by TDZD-8 after training of snails for 1 day was less pronounced than under standard training conditions (3 days). The effect of a glycogen synthase kinase-3 inhibitor during memory reconsolidation is probably followed by impairment of memory retrieval and/or partial loss, which can be compensated spontaneously or after repeated training.
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Different components of conditioned Food Aversion memory.
Brain Research, 2016Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. Kozyrev, P. V. Nikitin, Alexey ShevelkinAbstract:Memory reconsolidation processes and protein kinase Mzeta (PKMzeta) activity in memory maintenance and reorganization are poorly understood. Therefore, we examined memory reconsolidation and PKMzeta activity during the maintenance and reorganization of a conditioned Food Aversion memory among snails. These processes were specifically evaluated after administration of a serotonin receptor antagonist (methiothepin), NMDA glutamate receptor antagonist (MK-801), protein synthesis inhibitor (cycloheximide; CYH), or PKMzeta inhibitor (zeta inhibitory peptide; ZIP) either 2 or 10 days after Aversion training. Two days post-training, injections of MK-801 or CYH, combined with a conditioned stimulus reminder, caused amnesia development, and a second training 11 days after this induction did not lead to long-term memory formation. Interestingly, MK-801 or CYH injections and the reminder 10 days after training did not affect memory retrieval. Methiothepin and the reminder, or ZIP without the reminder, at 2 and 10 days after training led to memory impairment, while a second training 11 days after amnesia induction resulted in memory formation. These results suggest that the maintenance of a conditioned Food Aversion involves two different components with variable dynamics. One component could be characterized by memory strengthening over time and involve N-methyl-D-aspartate receptors and protein synthesis reconsolidation at early, but not late, training stages. The other memory component could involve serotonin-dependent reconsolidation and Mzeta-like kinase activity at both early and late stages after learning. Deficiencies within these two components led to various forms of memory impairment, which differed in terms of the formation of a conditioned Food Aversion during the second training.
Howard Casey Cromwell - One of the best experts on this subject based on the ideXlab platform.
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where does damage lead to enhanced Food Aversion the ventral pallidum substantia innominata or lateral hypothalamus
Brain Research, 1993Co-Authors: Howard Casey Cromwell, Kent C. BerridgeAbstract:Abstract It is well known that lesions of the lateral hypothalamus (LH) produce aphagia. Several previous studies have reported that lateral hypothalamus damage produces Food Aversion in addition to aphagia. However, damage to other regions near the LH also produce aphagia and enhanced Aversion. The purpose of this study was to resolve where the site or sites for Aversion-inducing lesions is/are located. Small, bilateral excitotoxin lesions (QUIN, 10 μg in 1 μl or IBO, 15 μg in 1 μl) or bilateral sham injections of vehicle were made into the globus pallidus (GP), the ventral pallidum/substantia innominata (VP/SI) or the lateral hypothalamus (LH). Affective reactions to taste were elicited by infusing sucrose solutions (1 M) into the mouth via chronic oral cannulae. The number of aversive responses (gapes, chin-rubbing, head-shaking and forelimb flails) emitted was tallied. Individual lesions were mapped and a single ‘necessary and sufficient’ site for damage-induced Aversion was identified (the area of overlapping damage common to all rats that showed enhanced aversive reactions). To identify the lesions, two lesion-mapping techniques were used: (1) a conventional neuron-counting procedure in which an attempt is made to count all neurons within a brain region, and (2) a new modified ‘fractionator’ procedure consisting of exhaustive 400× magnification counts at point locations within a brain region. Results indicated that aversive reactions to Food are enhanced only following bilateral neuron loss (>70%) from the caudal ventromedial VP/SI alone. This shared site has a lateral diameter of 1.0 mm, a dorsoventral diameter of 0.5 mm and a rostrocaudal diameter of 1.0 mm. Damage restricted to the LH never produced enhanced Aversion even when it produced aphagia. The crucial region for Aversion is located ventral and medial to the globus pallidus and dorsal and lateral to the lateral hypothalamus.
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where does damage lead to enhanced Food Aversion the ventral pallidum substantia innominata or lateral hypothalamus
Brain Research, 1993Co-Authors: Howard Casey Cromwell, Kent C. BerridgeAbstract:It is well known that lesions of the lateral hypothalamus (LH) produce aphagia. Several previous studies have reported that lateral hypothalamus damage produces Food Aversion in addition to aphagia. However, damage to other regions near the LH also produce aphagia and enhanced Aversion. The purpose of this study was to resolve where the site or sites for Aversion-inducing lesions is/are located. Small, bilateral excitotoxin lesions (QUIN, 10 micrograms in 1 microliter or IBO, 15 micrograms in 1 microliter) or bilateral sham injections of vehicle were made into the globus pallidus (GP), the ventral pallidum/substantia innominata (VP/SI) or the lateral hypothalamus (LH). Affective reactions to taste were elicited by infusing sucrose solutions (1 M) into the mouth via chronic oral cannulae. The number of aversive responses (gapes, chin-rubbing, head-shaking and forelimb flails) emitted was tallied. Individual lesions were mapped and a single 'necessary and sufficient' site for damage-induced Aversion was identified (the area of overlapping damage common to all rats that showed enhanced aversive reactions). To identify the lesions, two lesion-mapping techniques were used: (1) a conventional neuron-counting procedure in which an attempt is made to count all neurons within a brain region, and (2) a new modified 'fractionator' procedure consisting of exhaustive 400 x magnification counts at point locations within a brain region. Results indicated that aversive reactions to Food are enhanced only following bilateral neuron loss (> 70%) from the caudal ventromedial VP/SI alone. This shared site has a lateral diameter of 1.0 mm, a dorsoventral diameter of 0.5 mm and a rostrocaudal diameter of 1.0 mm. Damage restricted to the LH never produced enhanced Aversion even when it produced aphagia. The crucial region for Aversion is located ventral and medial to the globus pallidus and dorsal and lateral to the lateral hypothalamus.
Paul L R Andrews - One of the best experts on this subject based on the ideXlab platform.
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conditioned Food Aversion in suncus murinus house musk shrew a new model for the study of nausea in a species with an emetic reflex
Physiology & Behavior, 2001Co-Authors: Julia E Smith, Mark I Friedman, Paul L R AndrewsAbstract:Abstract The lack of a small animal model with an emetic reflex in which the relationship between conditioned Food Aversion and emesis could be investigated prompted a study of the insectivore, Suncus murinus (the house musk shrew). A novel Food (either tuna or chicken cat Food) was paired (C+) with a single exposure to either nicotine (4 mg/kg sc), motion (1 Hz, 4 cm, 10 min) or lithium chloride (100 mg/kg ip) or was paired (C−) with either saline or sham exposure to motion. Nicotine and motion both induced emesis (retching/vomiting) but lithium chloride did not. All three treatments produced a conditioned Food Aversion after a single pairing with consumption of C+ Food. When given a choice between the two Foods, S. murinus given lithium chloride, motion exposure and nicotine consumed, respectively, only 25%, 23% and 1% of their total intake from the C+ Food. This study shows that a conditioned Food Aversion can be readily induced in S. murinus and that the induction of emesis can be uncoupled from Food Aversion. S. murinus provides a promising new model in which the relationship between emesis, nausea and conditioned Food Aversion can be investigated.
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Conditioned Food Aversion in Suncus murinus (house musk shrew) — a new model for the study of nausea in a species with an emetic reflex
Physiology & Behavior, 2001Co-Authors: Julia E Smith, Mark I Friedman, Paul L R AndrewsAbstract:Abstract The lack of a small animal model with an emetic reflex in which the relationship between conditioned Food Aversion and emesis could be investigated prompted a study of the insectivore, Suncus murinus (the house musk shrew). A novel Food (either tuna or chicken cat Food) was paired (C+) with a single exposure to either nicotine (4 mg/kg sc), motion (1 Hz, 4 cm, 10 min) or lithium chloride (100 mg/kg ip) or was paired (C−) with either saline or sham exposure to motion. Nicotine and motion both induced emesis (retching/vomiting) but lithium chloride did not. All three treatments produced a conditioned Food Aversion after a single pairing with consumption of C+ Food. When given a choice between the two Foods, S. murinus given lithium chloride, motion exposure and nicotine consumed, respectively, only 25%, 23% and 1% of their total intake from the C+ Food. This study shows that a conditioned Food Aversion can be readily induced in S. murinus and that the induction of emesis can be uncoupled from Food Aversion. S. murinus provides a promising new model in which the relationship between emesis, nausea and conditioned Food Aversion can be investigated.
S. V. Solntseva - One of the best experts on this subject based on the ideXlab platform.
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Changes in Amnesia Parameters over Time after Long-Term Memory Disruption with Protein Kinase Mζ Inhibitor
Bulletin of Experimental Biology and Medicine, 2019Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. KozyrevAbstract:We studied the involvement of protein kinase Mζ (PKMζ) in the mechanisms of amnesia development within 10 days after disruption of conditioned Food Aversion memory with ZIP (a PKMζ inhibitor). Repeated training performed in 3 days after amnesia induction with ZIP, led to the formation of conditioned Food Aversion memory, but the number of combined presentations of Food and reinforcer stimuli was lower than during the initial training. Repeated training performed in 10 days after amnesia induction also led to memory formation, but the number of combined presentations of the stimuli was similar to that during the initial training. It was hypothesized that at the early stages of ZIP-induced amnesia, residual memory trace can be restored and amplified during repeated training, which led to memory expression at the behavioral level. At the late stages of amnesia, this memory trace was completely erased and repeated training led to the formation of a new memory. Thus, PKMζ inhibition results in the relatively fast impairment of memory retrieval and induces long-term process of memory erasing.
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Administration of Protein Synthesis Inhibitor before Reminder Reverses Amnesia Induced by Memory Reconsolidation Impairment with 5-HT Receptors Antagonist
Bulletin of Experimental Biology and Medicine, 2019Co-Authors: V. P. Nikitin, S. A. Kozyrev, S. V. SolntsevaAbstract:Administration of 5-HT receptor antagonist to snails trained in conditioned Food Aversion prior to reminding of the conditioning stimulus caused amnesia. At the early period of amnesia (day 3), injections of protein synthesis inhibitor cycloheximide without reminder or reminder alone were ineffective. At the same time, injections of the inhibitor combined with reminder led to memory recovery; this effect in most animals persisted for at least 10 days. In the rest snails, aversive responses to presentations of the conditioning stimulus persisted for 2 days. Cycloheximide injection and reminder in 10 days after induction of amnesia did not affect its development or caused a transient memory recovery (2 days). We hypothesized that amnesia is an active process unfolding in time. One of mechanism of this process is reminder-induced and protein synthesis-depended reactivation of amnesia. Inhibitor of protein synthesis disturbed this reactivation and led to recovery of the initial memory of conditioned Food Aversion.
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Peculiarities of Participation of DNA Methyltransferases in the Mechanisms of Storage, Impairment, and Recovery of Conditioned Food Aversion Memory
Bulletin of Experimental Biology and Medicine, 2018Co-Authors: V. P. Nikitin, S. A. Kozyrev, S. V. SolntsevaAbstract:We studied the participation of DNA-methylation processes in the mechanisms of memory storage and reconsolidation, amnesia induction, and in recovery of the conditioned Food Aversion memory in edible snails. It was found that daily injections of DNA methyltransferases inhibitor over 3 days combined with a reminder of a conditioned Food stimulus did not affect memory storage. The administration of DNA methyltransferase inhibitors did not suppress induction of amnesia caused the NMDA receptor antagonist/reminder. Injections of DNA methyltransferase inhibitors combined with the reminder led to memory recovery in 3 days after amnesia induction. Thus, DNA methyltransferase inhibitors in the same doses did not affect storage and reconsolidation of memory, as well as the mechanisms of amnesia induction. At the same time, injections of inhibitors led to memory recovery, apparently, due to disruption of reactivation and amnesia development.
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Involvement of Glycogen Synthase Kinase-3 in the Mechanisms of Conditioned Food Aversion Memory Reconsolidation
Bulletin of Experimental Biology and Medicine, 2017Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. KozyrevAbstract:Experiments were performed on the snails trained in conditioned Food Aversion for 3 days. Injection of TDZD-8 (glycogen synthase kinase-3 inhibitor, 2 mg/kg) in combination with reminder (presentation of a conditioned Food stimulus) led to memory impairment developing 3 days after inhibitor/reminder exposure and followed by spontaneous recovery in 10 days. Injections of TDZD-8 in a dose of 4 or 20 mg/kg before reminder were shown to cause amnesia that persisted for more than 10 days. Memory recovery during repeated training was observed at the earlier period than after initial training. The impairment of memory reconsolidation by TDZD-8 after training of snails for 1 day was less pronounced than under standard training conditions (3 days). The effect of a glycogen synthase kinase-3 inhibitor during memory reconsolidation is probably followed by impairment of memory retrieval and/or partial loss, which can be compensated spontaneously or after repeated training.
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Different components of conditioned Food Aversion memory.
Brain Research, 2016Co-Authors: V. P. Nikitin, S. V. Solntseva, S. A. Kozyrev, P. V. Nikitin, Alexey ShevelkinAbstract:Memory reconsolidation processes and protein kinase Mzeta (PKMzeta) activity in memory maintenance and reorganization are poorly understood. Therefore, we examined memory reconsolidation and PKMzeta activity during the maintenance and reorganization of a conditioned Food Aversion memory among snails. These processes were specifically evaluated after administration of a serotonin receptor antagonist (methiothepin), NMDA glutamate receptor antagonist (MK-801), protein synthesis inhibitor (cycloheximide; CYH), or PKMzeta inhibitor (zeta inhibitory peptide; ZIP) either 2 or 10 days after Aversion training. Two days post-training, injections of MK-801 or CYH, combined with a conditioned stimulus reminder, caused amnesia development, and a second training 11 days after this induction did not lead to long-term memory formation. Interestingly, MK-801 or CYH injections and the reminder 10 days after training did not affect memory retrieval. Methiothepin and the reminder, or ZIP without the reminder, at 2 and 10 days after training led to memory impairment, while a second training 11 days after amnesia induction resulted in memory formation. These results suggest that the maintenance of a conditioned Food Aversion involves two different components with variable dynamics. One component could be characterized by memory strengthening over time and involve N-methyl-D-aspartate receptors and protein synthesis reconsolidation at early, but not late, training stages. The other memory component could involve serotonin-dependent reconsolidation and Mzeta-like kinase activity at both early and late stages after learning. Deficiencies within these two components led to various forms of memory impairment, which differed in terms of the formation of a conditioned Food Aversion during the second training.