Effects of MSH and Related Peptides on Avoidance Behavior in Rats

Greidanus, T B Wimersma

doi:10.1159/000400358

Cited by 38 publications

(9 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to the important role of the antero-dorsal hippocampus [44], of the septal region [42,49] and of the parafascicular area [43,47,48] in the effect of vasopressin and ACTH on avoidance extinction we now report an essential function of the amygdaloid complex in this respect. This does not necessarily mean that the amygdaloid complex is the site of action of these neuropeptides in relation to avoidance behavior.…”

Section: Discussionmentioning

confidence: 61%

“…These peptides are supposed to be involved in retrieval rather than in storage processes. They affect active and passive avoidance behavior [39,42], reversal learning performance [31], approach behavior, conditioned taste aversion [28], sexual excitement, etc., and generally these effects are of short term nature.…”

mentioning

confidence: 99%

“…Lesion studies however indicated that this parafascicular area is less essential for vasopressin in relation to its inhibitory effect on avoidance extinction than for ACTH4_., [48]. Subsequent experiments in which additional limbic structures were destroyed such as the rostral septal area [42,49] and the dorsal hippocampal complex [44] revealed that these structures are important for the behavioral effects of vasopressin and ACTH4-1o. From these data it has been suggested that the limbic system needs to be intact in order to allow the neuropeptides vasopressin and ACTH4-10 to display their inhibitory action on active avoidance extinction.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Greidanus

Croiset

Bakker

et al. 1979

Physiology & Behavior

View full text Add to dashboard Cite

VAN WlMERSMA GREIDANUS, T. B., G. CROISET, E. BAKKER AND H. BOUMAN. Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4_m) on avoidance behavior. PHYSIOL. BEHAV. 22(2) 291-295, 1979.-Lesions in the amygdaloid complex result in an increased activity of rats in open field behavior in that generally more exploration and rearing is observed as compared with sham-operated animals. No effect of the lesion was observed on acquisition and extinction of an active avoidance response, but the amygdala lesions block the inhibitory effect of the neuropeptides vasopressin and ACTH4_~,, on extinction of a conditioned avoidance response. Searching for the CNS sites of action of these neuropeptides in relation to avoidance behavior several brain areas appear to be involved in their inhibitory effects on extinction of an active avoidance response. Implantation studies point to the posterior thalamic area including the parafascicular nuclei as a site of action of ACTH [43] as well as vasopressin [47]. Lesion studies however indicated that this parafascicular area is less essential for vasopressin in relation to its inhibitory effect on avoidance extinction than for ACTH4_., [48]. Subsequent experiments in which additional limbic structures were destroyed such as the rostral septal area [42,49] and the dorsal hippocampal complex [44] revealed that these structures are important for the behavioral effects of vasopressin and ACTH4-1o. From these data it has been suggested that the limbic system needs to be intact in order to allow the neuropeptides vasopressin and ACTH4-10 to display their inhibitory action on active avoidance extinction.Since the amygdaloid complex is an essential part of the limbic system the present study was performed in which the effects of the behaviorally active vasopressin analogue desglycinamide-lysine-8-vasopressin (DG-LVP) [40] and of ACTH4_,, on extinction of an active avoidance response were studied in animals with lesions in the amygdala nuclei. In addition the effect of the amygdaloid lesion itself was studied on exploratory behavior. METHOD AnimalsMale rats of an inbred Wistar strain weighing 130-150 g were used for the experiments. Stereotaxic lesions were made bilaterally in the amygdaloid complex using radiofrequency lesioning. The procedure in the sham-operated rats was identical to that in the amygdaloid lesioned animals except for the current. In the lesioned rats bilateral electrolytic lesions were placed in the baso-lateral amygdala by passing a 2 mA anodal current through the uninsulated 0.5 mm tip of a stainless steel electrode for 40 sec. A rectal cathode completed the circuit. With the incisor bar set 5 mm above the interaural plane and using bregma at the zero point, the following coordinates were employed: posterior -1.0 ram, lateral 4.7 mm and ventral -8.5 mm. ProcedureAfter recovery from the operation, which usually took

show abstract

Section: Discussionmentioning

confidence: 61%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Greidanus

Croiset

Bakker

et al. 1979

Physiology & Behavior

View full text Add to dashboard Cite

show abstract

“…Melanocyte-stimulating hormone (MSH) and related peptides are known to affect brain function both in man and ex~e~me~tal animals 12,11,28,291. While it is generally accepted that these melanotropic peptides are produced by the pituitary gland bioassayable MSH and immunoreactive MSH peptides have been found in different regions of the brain and shown to persist after removal of the pituitary [S, 14, 1.5, 17, 18,2%23].…”

Section: ~Er~~r~~~in~mentioning

confidence: 99%

Plasma and cerebrospinal fluid α-MSH levels in the rat after hypophysectomy and stimulation of pituitary α-MSH secretion

Thody

Rotte

Greidanus

1979

Brain Research Bulletin

View full text Add to dashboard Cite

This lack of correlation between a-MSH levels in the CSF and plasma suggests that the systemic circulation does not deliver u-MSH to the CSF. The apparently normal levels of u-MSH in the hypothalamus after hypophysectomy suggests that this tissue is able to synthesize u-MSH and it is possible that the hypothalamus is a source of the a-MSH in the CSF.Cerebrospinal fluid a-MSH ~ER~~R~~~IN~ FLXJED fCSF3 is likely to serve as an important route for many hormones that modulate bmin function. A number of deferent peptide hormones have been found in the CSF [l, 3, 5-7, 9, 12, 241 and while those of hy~~thal~ic origin such as vasopressin, oxytocin and the releasing hormones enter the CSF directly, the way in which pituitary hormones such as ACTS reach the CSF is not yet clear.weight. ~y~~hy~ctorny was performed by the pam~h~~ge~ approach and con&met3 at autopsy by examination of the seUa turcia.Melanocyte-stimulating hormone (MSH) and related peptides are known to affect brain function both in man and ex~e~me~tal animals 12, 11, 28, 291. While it is generally accepted that these melanotropic peptides are produced by the pituitary gland bioassayable MSH and immunoreactive MSH peptides have been found in different regions of the brain and shown to persist after removal of the pituitary [S, 14, 1.5, 17, 18,2%23]. This suggests that the brain, as weif as the pituitary, is capable of producing MSH peptides. fn this study we report the presence of ~mmunnrea~tive cu-MSH in the CSF of the rat and present data which suggest that at teast some of this peptide is of brain rather t.han pituitary origin.Rats were anaesthetized with urethane (1.1 g/Kg IP) and polyethylene cannulae inserted into the cistema magna for the withdrawal of CSF [7]. Approximately SO-100 1,t1 CSF were wi~d~aw~~ centrifuged and stored at -20°C until assayed.(1) Polyethylene cannulae were inserted into the jugular vein and advanced to the heart. Approximately 500 ~1 blood were withdrawn and replaced by an equal votume of 0.5% salineiheparin solution.(2) In experiment 2 {see below) the rats were decapitated and trunk blood collected into tubes containing lithium sequestrene,.All blood samples were centrifuged and the plasma stored at -20°C. METHODMale Wistar rats were obtained from TNO, Zeist, The Rats were decapitated and the brain immediately reNetherlands or bred in the Depa~ment of Dermatology, moved. The hypothalamus was dissected and this and the Newcastle, and were used when approximately 180 g in remainder of the brain minus the olfactory lobes were rinsed

show abstract

“…post-i.c.v. injection in rats [27,28] and man [14].The second problem, and a matter of recurrent contro versy [I. 10, 20.…”

mentioning

confidence: 99%

Extrahypothalamic Corticotropin and <i>α</i>-Melanotropin in Human Brain

Kleber¹,

Gramsch²,

Höllt³

et al. 1980

Neuroendocrinology

View full text Add to dashboard Cite

The distribution of corticotropin (ACTH) and α-melanotropin (α-MSH) in human brain was investigated by radioimmunoassay using an antiserum which recognized h-ACTH_1-39 and α-MSH to an equal degree on a molar basis. Significant amounts of material, which migrated on calibrated Sephadex G-50 columns as synthetic h-ACTH_1-39 and synthetic α-MSH, were detected in distinct brain areas. The highest concentrations of ACTH and α-MSH were found in the diencephalon (hypothalamus 4.2 and 12.5 pmol/g wet weight, respectively) and in midbrain (periaqueductal gray 0.5 and 1.7 pmol/g, respectively) and smaller quantities in the rhombencephalon and telencephalon. The ACTH concentration in human pituitary (adenohypophysis) was 10⁴-fold greater than that in the hypothalamus. α-MSH was confined to the midpart and/or stalk region of the pituitary.

show abstract

Effects of MSH and Related Peptides on Avoidance Behavior in Rats

Cited by 38 publications

References 0 publications

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Amygdaloid lesions block the effect of neuropeptides (vasopressin, ACTH4–10) on avoidance behavior

Plasma and cerebrospinal fluid α-MSH levels in the rat after hypophysectomy and stimulation of pituitary α-MSH secretion

Extrahypothalamic Corticotropin and <i>α</i>-Melanotropin in Human Brain

Contact Info

Product

Resources

About