Panic disorder: Response to sodium lactate and treatment with antidepressants

ELEVATED tph2 mRNA EXPRESSION IN A RAT MODEL OF CHRONIC ANXIETY

“…Although we were not able test both SI behavior and panic-like physiological responses in the present study, panic-like physiological responses have been detected when rats of the same intra-BL UCN1-priming paradigm were infused intravenously with sodium lactate [20,25] , an agent that is also used to probe for panic disorder in human studies. [27,28,65,66] This vulnerability to panic-like responses following amygdala priming may be related to our finding that increased anxiety-like behavior was strongly correlated with elevated tph2 expression in the DRVL/VLPAG, because several other lines of evidence suggest that DRVL/VLPAG serotonergic neurons play a role in control of panic-like responses. For example, an acute challenge with panicogenic stimuli such as sodium lactate or hypercapnia, or exposure to adverse stimuli such as forced swimming in cold water, [67,68] strongly activates serotonergic neurons in the DRVL/VLPAG region, as indicated by increases in c-Fos expression.…”

“…[21][22][23][24] Repeated activation (priming) of CRF receptors within the BL with low-dose UCN1 results in a robust anxiety-like state that persists for more than 30 days in rats, [25] as confirmed by reduced social interaction (SI) time in the SI test and panic-like physiologic responses, including tachycardia and increased respiratory rate, after intravenous administration of sodium lactate, [20,25] an agent used as a research probe for panic disorder in human studies. [26][27][28] In contrast, a single injection of the same "sub-threshold" UCN1 dose is insufficient to alter the animals' emotional state, [25] indicating the need for BL-neuronal plasticity before a behavioral phenotype is evident.…”

ELEVATED tph2 mRNA EXPRESSION IN A RAT MODEL OF CHRONIC ANXIETY

“…Although we were not able test both SI behavior and panic-like physiological responses in the present study, panic-like physiological responses have been detected when rats of the same intra-BL UCN1-priming paradigm were infused intravenously with sodium lactate [20,25] , an agent that is also used to probe for panic disorder in human studies. [27,28,65,66] This vulnerability to panic-like responses following amygdala priming may be related to our finding that increased anxiety-like behavior was strongly correlated with elevated tph2 expression in the DRVL/VLPAG, because several other lines of evidence suggest that DRVL/VLPAG serotonergic neurons play a role in control of panic-like responses. For example, an acute challenge with panicogenic stimuli such as sodium lactate or hypercapnia, or exposure to adverse stimuli such as forced swimming in cold water, [67,68] strongly activates serotonergic neurons in the DRVL/VLPAG region, as indicated by increases in c-Fos expression.…”

“…[21][22][23][24] Repeated activation (priming) of CRF receptors within the BL with low-dose UCN1 results in a robust anxiety-like state that persists for more than 30 days in rats, [25] as confirmed by reduced social interaction (SI) time in the SI test and panic-like physiologic responses, including tachycardia and increased respiratory rate, after intravenous administration of sodium lactate, [20,25] an agent used as a research probe for panic disorder in human studies. [26][27][28] In contrast, a single injection of the same "sub-threshold" UCN1 dose is insufficient to alter the animals' emotional state, [25] indicating the need for BL-neuronal plasticity before a behavioral phenotype is evident.…”

Agoraphobia: a test of the separation anxiety hypothesis

“…Panic attacks commonly recur following discontinuation of these drugs. In agoraphobic or panic disorder patients, acute anxiety attacks symptomatically similar to apparently spontaneous panic episodes can be produced in the laboratory using infusions of sodium lactate or yohimbine (Rifkin. 1983;Liebowitz er al., 1983;Charney, Heninger and Redmond, 1983).…”

The Psychobiology of Emotions

“…Epidemiological studies suggest that both lactate sensitivity and panic attacks have a strong genetic predisposition. Researchers have noted a relatively high concordance rate between panic disorder patients and biological relatives who have been diagnosed with major depression or an anxiety disorder (Rifkin & Siris, 1985).…”

ELEVATED tph2 mRNA EXPRESSION IN A RAT MODEL OF CHRONIC ANXIETY

“…Although we were not able test both SI behavior and panic-like physiological responses in the present study, panic-like physiological responses have been detected when rats of the same intra-BL UCN1-priming paradigm were infused intravenously with sodium lactate [20,25] , an agent that is also used to probe for panic disorder in human studies. [27,28,65,66] This vulnerability to panic-like responses following amygdala priming may be related to our finding that increased anxiety-like behavior was strongly correlated with elevated tph2 expression in the DRVL/VLPAG, because several other lines of evidence suggest that DRVL/VLPAG serotonergic neurons play a role in control of panic-like responses. For example, an acute challenge with panicogenic stimuli such as sodium lactate or hypercapnia, or exposure to adverse stimuli such as forced swimming in cold water, [67,68] strongly activates serotonergic neurons in the DRVL/VLPAG region, as indicated by increases in c-Fos expression.…”

“…[21][22][23][24] Repeated activation (priming) of CRF receptors within the BL with low-dose UCN1 results in a robust anxiety-like state that persists for more than 30 days in rats, [25] as confirmed by reduced social interaction (SI) time in the SI test and panic-like physiologic responses, including tachycardia and increased respiratory rate, after intravenous administration of sodium lactate, [20,25] an agent used as a research probe for panic disorder in human studies. [26][27][28] In contrast, a single injection of the same "sub-threshold" UCN1 dose is insufficient to alter the animals' emotional state, [25] indicating the need for BL-neuronal plasticity before a behavioral phenotype is evident.…”

Agoraphobia: a test of the separation anxiety hypothesis

“…Panic attacks commonly recur following discontinuation of these drugs. In agoraphobic or panic disorder patients, acute anxiety attacks symptomatically similar to apparently spontaneous panic episodes can be produced in the laboratory using infusions of sodium lactate or yohimbine (Rifkin. 1983;Liebowitz er al., 1983;Charney, Heninger and Redmond, 1983).…”

The Psychobiology of Emotions

“…Epidemiological studies suggest that both lactate sensitivity and panic attacks have a strong genetic predisposition. Researchers have noted a relatively high concordance rate between panic disorder patients and biological relatives who have been diagnosed with major depression or an anxiety disorder (Rifkin & Siris, 1985).…”

ELEVATED tph2 mRNA EXPRESSION IN A RAT MODEL OF CHRONIC ANXIETY

“…Although we were not able test both SI behavior and panic-like physiological responses in the present study, panic-like physiological responses have been detected when rats of the same intra-BL UCN1-priming paradigm were infused intravenously with sodium lactate [20,25] , an agent that is also used to probe for panic disorder in human studies. [27,28,65,66] This vulnerability to panic-like responses following amygdala priming may be related to our finding that increased anxiety-like behavior was strongly correlated with elevated tph2 expression in the DRVL/VLPAG, because several other lines of evidence suggest that DRVL/VLPAG serotonergic neurons play a role in control of panic-like responses. For example, an acute challenge with panicogenic stimuli such as sodium lactate or hypercapnia, or exposure to adverse stimuli such as forced swimming in cold water, [67,68] strongly activates serotonergic neurons in the DRVL/VLPAG region, as indicated by increases in c-Fos expression.…”

“…[21][22][23][24] Repeated activation (priming) of CRF receptors within the BL with low-dose UCN1 results in a robust anxiety-like state that persists for more than 30 days in rats, [25] as confirmed by reduced social interaction (SI) time in the SI test and panic-like physiologic responses, including tachycardia and increased respiratory rate, after intravenous administration of sodium lactate, [20,25] an agent used as a research probe for panic disorder in human studies. [26][27][28] In contrast, a single injection of the same "sub-threshold" UCN1 dose is insufficient to alter the animals' emotional state, [25] indicating the need for BL-neuronal plasticity before a behavioral phenotype is evident.…”

Agoraphobia: a test of the separation anxiety hypothesis

“…Panic attacks commonly recur following discontinuation of these drugs. In agoraphobic or panic disorder patients, acute anxiety attacks symptomatically similar to apparently spontaneous panic episodes can be produced in the laboratory using infusions of sodium lactate or yohimbine (Rifkin. 1983;Liebowitz er al., 1983;Charney, Heninger and Redmond, 1983).…”

The Psychobiology of Emotions

“…Epidemiological studies suggest that both lactate sensitivity and panic attacks have a strong genetic predisposition. Researchers have noted a relatively high concordance rate between panic disorder patients and biological relatives who have been diagnosed with major depression or an anxiety disorder (Rifkin & Siris, 1985).…”