Effects of corticotropin releasing factor on locomotor activity in hypophysectomized rats

Eaves, Maryruth; Thatcher-Britton, Karen; Rivier, Jean; Vale, Wylie; Koob, George F.

doi:10.1016/0196-9781(85)90323-7

Cited by 139 publications

(53 citation statements)

References 9 publications

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“…The increase in behavioural activity, especially locomotor and grooming activities, as a result of the CRH infusion in the CeA in the rats' home cage, is consistent with observations that CRH administered both ICV (Diamant & De Wied, 1991;Eaves et al, 1985;Sutton et al, 1982) and locally into the CeA produces behavioural activation in the rat (Lee & Sung, 1989;Lee & Tsai, 1989;Wiersma et al, 1993). However, CRH infusion in the CeA, in a dose five times lower as the dose used in the present study, did not result in an excessive grooming response (Wiersma et al, 1993).…”

Section: Discussionsupporting

confidence: 73%

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Wiersma

Baauw

Bohus

et al. 1995

Psychoneuroendocrinology

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SUMMARYThe central nucleus of the amygdala (CeA) is known to be involved in the regulation of autonomic, neuroendocrine, and behavioural responses in stress situations. The CeA contains large numbers of corticotropin-releasing hormone (CRH)-containing cell bodies and terminals. In the present study we examined (by continuous behaviour observations) the effects of a high close of CRH (150 rig) and two doses of the CRH-receptor antagonist (a-hCRH: 1.0 and 0.1 p,g) after microinfusion into the CeA in freely moving male Wistar rats under stress-flee conditions. In comparison with control, a-hCRH infusion did not cause any behavioural activation. In contrast CRH-infusion revealed a long-lasting increase in grooming and exploration with a concomitant decrease in behaviours specified as resting. These results indicate that the CRH system in the CeA does not seem to be activated in stress-free conditions, but its activation is of importance for active behavioural responses.Keywords--Central nucleus of the amygdala (CeA); Stress-free conditions; Corticotropin-releasing hormone (CRH); a-Helical CRH (CRH-receptor antagonist).

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Section: Discussionsupporting

confidence: 73%

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Wiersma

Baauw

Bohus

et al. 1995

Psychoneuroendocrinology

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“…Importantly, anxiety-like behavioral and autonomic effects after centrally administered CRF are not dependent on CRF-induced HPA-released ACTH or corticosteroids, because these anxiety-related outcomes persist in hypophysectomized rats (Eaves et al, 1985) and in mice conditionally knocked out for CRF 1 (Müller et al, 2003). Bremner et al (1997) reported higher levels of CRF (137%) in CSF of patients diagnosed with chronic combat-related posttraumatic stress disorder versus CS-F-CRF in comparison subjects (100%).…”

Section: Discussionmentioning

confidence: 99%

Corticotropin-Releasing Factor and Urocortin I Modulate Excitatory Glutamatergic Synaptic Transmission

Liu¹,

Yu²,

Neugebauer³

et al. 2004

J. Neurosci.

134

137

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Corticotropin-releasing factor (CRF)-related peptides serve as hormones and neuromodulators of the stress response and play a role in affective disorders. These peptides are known to alter complex behaviors and neuronal properties, but their receptor-mediated effects at CNS synapses are not well described. Here we show that excitatory glutamatergic transmission is modulated by two endogenous CRFrelated peptide ligands, corticotropin-releasing factor [CRF rat/human (r/h)] and Urocortin I (Ucn I), within the central nucleus of the amygdala (CeA) and the lateral septum mediolateral nucleus (LSMLN). These limbic nuclei are reciprocally innervated, are involved in stress and affective disorders, and have high densities of the CRF receptors CRF 1 and CRF 2 . Activation of these receptors exerts diametrically opposed actions on glutamatergic transmission in these nuclei. In the CeA, CRF(r/h) depressed excitatory glutamatergic transmission through a CRF 1 -mediated postsynaptic action, whereas Ucn I facilitated synaptic responses through presynaptic and postsynaptic CRF 2 -mediated mechanisms. Conversely, in the LSMLN, CRF caused a CRF 1 -mediated facilitation of glutamatergic transmission via postsynaptic mechanisms, whereas Ucn I depressed EPSCs by postsynaptic and presynaptic CRF 2 -mediated actions. Furthermore, antagonists of these receptors also affected glutamatergic neurotransmission, indicating that endogenous ligands tonically modulated synoptic activity at these synapses.These data show that CRF receptors in CeA and LSMLN synapses exert and maintain a significant synaptic tone and thereby regulate excitatory glutamatergic transmission. The results also suggest that CRF receptors may provide novel targets in affective disorders and stress.

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“…In addition to this role, CRF also acts as an extra-hypothalamic neuromodulator and neurotransmitter, mediating adaptive behavioral responses to stress, including increased arousal, suppression of appetitive and reproductive behaviors and an increase in defensive responding and avoidance behaviors (Brown and Fisher 1985;Dunn and Berridge 1990;Owens and Nemeroff 1993;Spina et al 1996;Spina et al 2000). These behavioral activating effects have been shown to be independent of HPA axis activation, and thus represent extra-hypothalamic actions of CRF in the CNS (Britton et al 1986;Eaves et al 1985).…”

Section: Introductionmentioning

confidence: 99%

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

et al. 2008

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Rationale-Central administration of corticotropin-releasing factor (CRF) elicits a specific pattern of behavioral responses resembling a stress-like state, and is anxiogenic in rodent models of anxiety.Objectives-Specific behaviors evoked by the administration of CRF were measured. The roles of CRF receptor subtypes and that of serotonergic and noradrenergic systems in mediating these responses were studied.Methods-Burying, grooming and head shakes were quantified in rats following intracerebroventricular administration of CRF and urocortin II and after pretreatment with antagonists. The role of forebrain norepinephrine in the behavioral responses to CRF (0.3 μg) was examined following pretreatment with the neurotoxin DSP-4 and that of serotonin after depletion using systemic administration of para-chlorophenylalanine (p-CPA).Results-CRF at 0.3 and 3.0 μg caused robust increases in burying, grooming and head shakes, but urocortin II was ineffective. Pretreatment with either antalarmin or propranolol significantly attenuated the CRF-evoked behaviors. Destruction of forebrain NE pathways blocked spontaneous burying behavior elicited by CRF and conditioned burying directed towards an electrified shock probe. In contrast, depletion of 5-HT selectively attenuated CRF-evoked grooming.Conclusions-Overt behavioral responses produced by CRF, burying, grooming, and head shakes, appeared to be mediated through the CRF 1 receptor. Spontaneous burying behavior evoked by CRF or conditioned burying directed towards a shock probe were disrupted by lesion of the dorsal noradrenergic bundle and may represent anxiety-like behavior caused by CRF activation of the LC. In contrast, CRF-evoked increases in grooming were dependent on serotonin.

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Effects of corticotropin releasing factor on locomotor activity in hypophysectomized rats

Cited by 139 publications

References 9 publications

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Behavioural activation produced by crh but not α-helical CRH (CRH-receptor antagonist) when microinfused into the central nucleus of the amygdala under stress-free conditions

Corticotropin-Releasing Factor and Urocortin I Modulate Excitatory Glutamatergic Synaptic Transmission

Differential blockade of CRF-evoked behaviors by depletion of norepinephrine and serotonin in rats

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