Appetitive motivational states differ in their ability to augment aversive fear conditioning in rats (Rattus norvegicus).

Maren, Stephen; Fanselow, Michael S.

doi:10.1037/0097-7403.24.3.369

Cited by 9 publications

(6 citation statements)

References 26 publications

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“…, 2002). Our data do not readily fit this description, although the precise involvement of the hippocampus in contextual freezing still remains controversial (Maren & Fanselow, 1998; Gewirtz et al. , 2000).…”

Section: Discussioncontrasting

confidence: 60%

Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs

Yee

Singer

Chen

et al. 2007

Eur J of Neuroscience

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The neuromodulator adenosine fulfills a unique role in the brain affecting glutamatergic neurotransmission and dopaminergic signaling via activation of adenosine A1 and A2A receptors, respectively. The adenosine system is thus ideally positioned to integrate glutamatergic and dopaminergic neurotransmission, which in turn could affect behavior and cognition. In the adult brain, adenosine levels are largely regulated by its key metabolic enzyme adenosine kinase (ADK), which may assume the role of an 'upstream regulator' of these two neurotransmitter pathways. To test this hypothesis, transgenic mice with an overexpression of ADK in brain (Adk-tg), and therefore reduced brain adenosine levels, were evaluated in a panel of behavioral and psychopharmacological assays to assess possible glutamatergic and dopaminergic dysfunction. In comparison to non-transgenic control mice, Adk-tg mice are characterized by severe learning deficits in the Morris water maze task and in Pavlovian conditioning. The Adk-tg mice also exhibited reduced locomotor reaction to systemic amphetamine, whereas their reaction to the non-competitive N-methyl-d-aspartate receptor antagonist MK-801 was enhanced. Our results confirmed that ADK overexpression could lead to functional concomitant alterations in dopaminergic and glutamatergic functions, which is in keeping with the hypothesized role of ADK in the balance and integration between glutamatergic and dopaminergic neurotransmission. The present findings are of relevance to current pathophysiological hypotheses of schizophrenia and its pharmacotherapy.

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Section: Discussioncontrasting

confidence: 60%

Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs

Yee

Singer

Chen

et al. 2007

Eur J of Neuroscience

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“…Shams showed significant tone-induced freezing that was greater than pretone freezing, but sham-unpaired did not, indicating that increased freezing was not attributable to a sensitization effect. freezing (Maren and Fanselow, 1998). The recovery of extinguished fear we observed could slow extinction rates in animals tested over many days (Morgan et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

et al. 2000

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Conditioned fear responses to a tone paired with footshock extinguish when the tone is presented repeatedly in the absence of shock. Rather than erase the tone-shock association, extinction is thought to involve new learning accompanied by inhibition of conditioned responding. Despite much interest in extinction from a clinical perspective, little is known about the neural circuits that are involved. Although the prefrontal cortex has a well established role in the inhibition of inappropriate behaviors, previous reports have disagreed as to the role of the ventromedial prefrontal cortex (vmPFC) in extinction. We have reexamined the effects of electrolytic vmPFC lesions made before training on the acquisition, extinction, and recovery of conditioned fear responses in a 2 d experiment. On Day 1 vmPFC lesions had no effect on acquisition or extinction of conditioned freezing and suppression of bar pressing. On Day 2 sham rats recovered only 27% of their acquired freezing, whereas vmPFC-lesioned rats recovered 86%, which was indistinguishable from a control group that never received extinction. The high recovery in lesioned rats could not be attributed to decreased motivation or altered sensitivity to footshock. vmPFC lesions that spared the caudal infralimbic (IL) nucleus had no effect. Thus, the vmPFC (particularly the IL nucleus) is not necessary for expression of extinction, but it is necessary for the recall of extinction learning after a long delay. These data suggest a role of the vmPFC in consolidation of extinction learning or the recall of contexts in which extinction took place.Key words: extinction; infralimbic; prelimbic; fear conditioning; amygdala; inhibition Prefrontal cortex has long been implicated in inhibition of inappropriate responses. Lesions of medial prefrontal cortex (mPFC) cause perseverative responding in animals and humans and cause deficits in reversal tasks (for review, see Kolb, 1984;Fuster, 1997). Perseverative responding in prefrontal animals was extended to conditioned fear when it was shown that rats with mPFC lesions could acquire freezing responses to a tone paired with a footshock, but they required many more days to extinguish those responses when the tone was presented alone (Morgan et al., 1993). More recent data support the hypothesis that mPFC is involved in the inhibition of fear responses (Bremner et al., 1999;Herry et al., 1999;Morrow et al., 1999), and it has been suggested that deficits in extinction of conditioned fear may cause certain anxiety disorders (Charney and Deutch, 1996;Pitman, 1997).Many questions remain, however, concerning the role of the ventromedial prefrontal cortex (vmPFC) in extinction of fear. Following the original report by Morgan et al. (1993), Gewirtz et al. (1997 found no effect of vmPFC lesions on extinction of conditioned fear responses. To explain this discrepancy, Gewirtz et al. (1997) suggested that the prolonged extinction might have been attributable to increased acquisition in the lesioned animals, which was masked by asymptotic freezi...

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“…In vertebrates, several studies have revealed that ANGII plays a role in memory modulation (reviewed in Wright & Harding, 2004) and that water shortage both triggers brain ANGII (reviewed in Fitzsimons, 1998 and Takei, 2000) and facilitates contextual fear conditioning in rats (Maren et al. , 1994; Maren & Fanselow, 1998). However, our work provides the first experimental evidence that water shortage, through the action of angiotensins, induces memory facilitation (Delorenzi et al.…”

Section: Discussionmentioning

confidence: 99%

Memory strengthening by a real‐life episode during reconsolidation: an outcome of water deprivation via brain angiotensin II

Frenkel

Maldonado

Delorenzi

2005

Eur J of Neuroscience

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A considerable body of evidence reveals that consolidated memories, recalled by a reminder, enter into a new vulnerability phase during which they are susceptible to disruption again. Consistently, reconsolidation was shown by the amnesic effects induced by administration of consolidation blockers after memory labilization. To shed light on the functional value of reconsolidation, we explored whether an endogenous process activated during a concurrent real-life experience improved this memory phase. Reconsolidation of long-term contextual memory has been well documented in the crab Chasmagnathus. Previously we showed that angiotensin II facilitates memory consolidation. Moreover, water deprivation increases brain angiotensin and improves memory consolidation and retrieval through angiotensin II receptors. Here, we tested whether concurrent water deprivation improves reconsolidation via endogenous angiotensin and therefore strengthens memory. We show that memory reconsolidation, induced by training context re-exposure, is facilitated by a concurrent episode of water deprivation, which induces a raise in endogenous brain angiotensin II. Positive modulation is expressed by full memory retention, despite a weak training, 24 or 72 but not 4 h after memory reactivation. This is the first evidence that memory can be positively modulated during reconsolidation through an identified endogenous process triggered during a real-life episode. We propose that the functional value for reconsolidation would be to make possible a change in memory strength by the influence of a concurrent experience. Reconsolidation improvement would lead to memory re-evaluation, not by altering memory content but by modifying the behaviour as an outcome of changing the hierarchy of the memories that control it.

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Appetitive motivational states differ in their ability to augment aversive fear conditioning in rats (Rattus norvegicus).

Cited by 9 publications

References 26 publications

Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs

Transgenic overexpression of adenosine kinase in brain leads to multiple learning impairments and altered sensitivity to psychomimetic drugs

The Role of Ventromedial Prefrontal Cortex in the Recovery of Extinguished Fear

Memory strengthening by a real‐life episode during reconsolidation: an outcome of water deprivation via brain angiotensin II

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