The effect of medial frontal cortex lesions on cardiovascular conditioned emotional responses in the rat

Frysztak, Robert J.; Neafsey, Edward J.

doi:10.1016/0006-8993(94)90024-8

Cited by 236 publications

(131 citation statements)

References 59 publications

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“…It is possible that increased c-fos expression within the Infra-L by ethanol-or cocaineassociated stimuli is related to conditioned autonomic responses that are typically associated with drug cue exposure in humans (Sinha et al 2000;Stormark et al 1995). Additionally, the Infra-L is implicated in regulating impulsivity (Chudasama et al 2003), and manipulations interfering with Infra-L cortex function retard extinction of conditioned fear and increases the recovery of appetitive Pavlovian responses (Frysztak and Neafsey 1994;Pratt and Mizumori 2001;Rhodes and Killcross 2004). Thus, the Infra-L cortex warrants further attention with respect to a role in conditioned drug-seeking and relapse.…”

Section: Discussionmentioning

confidence: 99%

Distinct Patterns of Neural Activation Associated with Ethanol Seeking: Effects of Naltrexone

Dayas¹,

Liu²,

Simms³

et al. 2007

Biological Psychiatry

144

133

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Background-Alcoholism, like other substance abuse disorders, is a chronically relapsing condition. Compared with other abused drugs, however, little is known about the neural mechanisms mediating ethanol (EtOH)-craving and -seeking behavior leading to relapse. This study, therefore, was conducted to identify candidate brain regions that are recruited by an EtOH-associated contextual stimulus (S + ). A secondary objective was to determine whether EtOH S + -elicited neural recruitment patterns are modified by the opiate antagonist naltrexone (NTX), a compound that reduces cueinduced craving in alcoholics and attenuates ethanol seeking in animal models of relapse.

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Section: Discussionmentioning

confidence: 99%

Distinct Patterns of Neural Activation Associated with Ethanol Seeking: Effects of Naltrexone

Dayas¹,

Liu²,

Simms³

et al. 2007

Biological Psychiatry

144

133

View full text Add to dashboard Cite

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“…Based on studies of anticipated electrical shock in healthy human subjects, preclinical lesion models, and functional connectivity, the dorsomedial (DM) and dorsal anterolateral (DAL) PFC are thought to attenuate anxiety, defensive behavior, and cardiovascular responses to stress. 42,56,57 Several PET studies have shown abnormally decreased CBF and metabolism in these regions in individuals with primary depression as well as in depressed subjects with Parkinson's disease. 54,58 -60 The dorsolateral prefrontal cortex and dorsal anterior cingulate cortex.…”

Section: Functional Anatomy Of Mood Disordersmentioning

confidence: 99%

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Carlson¹,

Singh²,

Zarate³

et al. 2006

NeuroRX

135

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Summary:Major depressive disorder and bipolar disorder are severe mood disorders that affect the lives and functioning of millions each year. The majority of previous neurobiological research and standard pharmacotherapy regimens have approached these illnesses as purely neurochemical disorders, with particular focus on the monoaminergic neurotransmitter systems. Not altogether surprisingly, these treatments are inadequate for many individuals afflicted with these devastating illnesses. Recent advances in functional brain imaging have identified critical neural circuits involving the amygdala and other limbic structures, prefrontal cortical regions, thalamus, and basal ganglia that modulate emotional behavior and are disturbed in primary and secondary mood disorders. Growing evidence suggests that mechanisms of neural plasticity and cellular resilience, including impairments of neurotrophic signaling cascades as well as altered glutamatergic and glucocorticoid signaling, underlie the dysregulation in these circuits. The increasing ability to monitor and modulate activity in these circuits is beginning to yield greater insight into the neurobiological basis of mood disorders. Modulation of dysregulated activity in these affective circuits via pharmacological agents that enhance neuronal resilience and plasticity, and possibly via emerging nonpharmacologic, circuitry-based modalities (for example, deep brain stimulation, magnetic stimulation, or vagus nerve stimulation) offers promising targets for novel experimental therapeutics in the treatment of mood disorders.

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“…29,30 In addition to demonstrating neuroendocrine changes, rats with bilateral lesions of the dorsal prelimbic and anterior cingulate cortices also show exaggerated freezing behavior and heart rate increases during exposure to fear-conditioned sensory and/or contextual stimuli. 31,32 In contrast, bilateral lesions involving both the infralimbic and the ventral prelimbic cortices result in reduced HR responses to fear-conditioned stimuli. 32 Taken together, these findings led Frysztak and Neafsey 32 to propose that the ventral prelimbic and infralimbic cortices normally act to increase heart rate during stress.…”

Section: Potential Implications Of Subgenual Pfc Dysfunctionmentioning

confidence: 99%

“…31,32 In contrast, bilateral lesions involving both the infralimbic and the ventral prelimbic cortices result in reduced HR responses to fear-conditioned stimuli. 32 Taken together, these findings led Frysztak and Neafsey 32 to propose that the ventral prelimbic and infralimbic cortices normally act to increase heart rate during stress.…”

Section: Potential Implications Of Subgenual Pfc Dysfunctionmentioning

confidence: 99%

“…26,29,30,35 Lesions of the ventromedial PFC also alter parasympathetic autonomic function in rats in a manner that shows an intriguing parallel with autonomic abnormalities reported in humans with MDD. Frysztak and Neafsey 32 found that rats with lesions of the prelimbic and infralimbic cortex show reduced beat-to-beat variability of the heart rate both at rest and during exposure to fear-conditioned stimuli. Heart rate variability (HRV) putatively reflects parasympathetic control of the sinus node via vagal nerve transmission.…”

Section: Potential Implications Of Subgenual Pfc Dysfunctionmentioning

confidence: 99%

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Neuroimaging abnormalities in the subgenual prefrontal cortex: implications for the pathophysiology of familial mood disorders

1998

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The prefrontal cortex (PFC) ventral to the genu of the corpus callosum has been implicated in the modulation of visceral responses to stressful and emotionally provocative stimuli, based upon analysis of lesion effects involving this area in humans and experimental animals. In a recent magnetic resonance imaging (MRI) study of familial mood disorders, we demonstrated that the mean grey matter volume of this cortex is abnormally reduced in subjects with major depressive disorder (MDD) and bipolar disorder, irrespective of their treatment status or current mood state. Moreover, in preliminary histopathological assessments of subgenual PFC tissue taken post mortem from subjects with MDD and bipolar disorder we obtained results suggesting that this decrement in grey matter volume is associated with a reduction in glia without an equivalent loss of neurons. The potential functional significance of these neuroimaging and microscopic abnormalities is discussed with respect to evidence that subgenual PFC dysfunction may disturb stress-related autonomic and neuroendocrine responses and reward-related mesolimbic dopamine function. These data may thus hold important implications for the development of neural models of mood disorders that can account for the abnormal hedonic, motivational, neuroendocrine, and autonomic manifestations evident in these idiopathic conditions. Keywords: anterior cingulate; glia; MRI; PET; major depression; bipolar disorder; emotionIn a recent neuroimaging study of mood disorders we reported that the grey matter volume of the prefrontal cortex (PFC) ventral to the genu of the corpus callosum is reduced in familial bipolar disorder and familial major depressive disorder (MDD). 1 The magnetic resonance imaging (MRI)-based neuromorphometric measures acquired to demonstrate this abnormality in the 'subgenual' PFC were guided by positron emission tomographic (PET) images that showed an abnormal reduction of cerebral blood flow (BF) and glucose metabolism in this area in depression. [2][3][4] Because antidepressant treatment did not reverse these physiological abnormalities, the MRI measures of grey matter volume were obtained to determine whether the decrements in regional BF and metabolism were at least partly explained by a corresponding reduction in cortex. 5 This hypothesis was confirmed, as the mean grey matter volume of the left subgenual PFC was reduced by 39% and 48% in the bipolar disordered and unipolar depressed samples, respectively, relative to the controls (F = 9.8; P Ͻ 0.0002, after covarying for age, gender and whole brain volume). 1 This volumetric Correspondence: WC Drevets, MD, B 938,

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The effect of medial frontal cortex lesions on cardiovascular conditioned emotional responses in the rat

Cited by 236 publications

References 59 publications

Distinct Patterns of Neural Activation Associated with Ethanol Seeking: Effects of Naltrexone

Distinct Patterns of Neural Activation Associated with Ethanol Seeking: Effects of Naltrexone

Neural circuitry and neuroplasticity in mood disorders: Insights for novel therapeutic targets

Neuroimaging abnormalities in the subgenual prefrontal cortex: implications for the pathophysiology of familial mood disorders

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