Norepinephrine (NE) and dopamine (DA) concentrations in 17 individual hypothalamic nuclei and 3 other brain regions were measured in rats, acutely or repeatedly stressed by immobilization, using a microdissection technique and a radioisotopic-enzymatic assay. Following the first 20 min immobilization (IMO) a significant NE decrease in the ventromedial (NVM) and supraoptic (NSO) nuclei and a DA decrease in the arcuate nucleus (NA) as well as NE and DA increase in the dorsomedial nucleus (NDM) were seen. Repeated IMO (40 times) produced a NE increase in the NVM, NDM, NSO paraventricular nucleus (NPV) and median eminence (ME), and a DA increase in the NDM and NPV. Changes of NE and DA concentration found in some individual hypothalamic nuclei under the influence of stress indicate that catecholamines (CAs), particularly in the medial basal hypothalamus, could be involved in the regulation of some neuroendocrine processes which are being activated during stress, especially ACTH release.

The effects of acute stress on norepinephrine (NE) and dopamine (DA) concentrations and of repeated stress on tyrosine hydroxylase (TH) activity were measured in individual hypothalamic nuclei and other rat brain regions. A microdissection technique and radioisotopic enzymatic assays enabled these studies to be performed. NE and DA concentrations were reduced and TH activity increased selectively in the arcuate nucleus. These results suggest that the arcuate nucleus may be selectively involved in the stress response and support the hypothesis that catecholamìnes in the medial basal hypothalamus mediate certain of the neuroendocrine changes observed in stress.

Immobilization (IMMO) of conscious rats evokes marked increases in release of norepinephrine (NE) in the paraventricular nucleus (PVN) of the hypothalamus, consistent with a role of NE in the PVN release of corticotropin-releasing hormone and therefore in pituitary-adrenocortical activation during stress. The present study examined the effects of surgical hemisection of the brainstem between the locus ceruleus and rostral portion of the medulla on release of NE in the PVN of the hypothalamus in vivo in conscious rats, at baseline and during IMMO. Concentrations of NE, the intraneuronal NE metabolite dihydroxyphenylglycol (DHPG), and the dopamine metabolite dihydroxyphenylacetic acid (DOPAC) were measured in microdialysate samples obtained beginning 24 h after implantation of a microdialysis probe in the PVN either ipsilateral or contralateral to the hemisection. On the lesioned side, baseline levels of NE, DHPG, and DOPAC were significantly lower and IMMO-induced increases were smaller than in sham-operated rats. Contralateral to the hemisection, DOPAC levels were significantly reduced. Neither baseline levels nor IMMO-induced increases in plasma corticosterone levels differed between lesioned and sham-operated animals. The present results indicate that: (1) NE release in the PVN at baseline and during IMMO depends mainly on ascending medullary tracts from ipsilateral brainstem A1 and A2 catecholaminergic areas, with small contributions from the locus ceruleus and from contralateral medullary cells, and (2) brainstem hemisection does not influence IMMO-induced activation of the hypothalamic-pituitary-adrenocortical axis as indicated by plasma corticosterone levels in conscious rats.

No abstract

Cholecystokinin (CCK), one of the most common brain peptides, coexists with dopamine (DA) in neurons of the medial substantia nigra (SN). CCK has been shown to excite these neurons following either direct iontophoretic or systemic administration suggesting that peripherally administered CCK may cross the blood brain barrier to act directly on nigral DA cells. However, biochemical evidence suggests that CCK does not cross the blood brain barrier, and several studies have shown that the behavioral and the satiety-inducing effects of peripherally administered CCK are abolished by vagotomy. In order to test for vagal mediation of the nigral response to systemically administered CCK, we examined the effects of a series of lesions to the vagal pathways on CCK-induced excitation in the SN. Neither acute thoracic nor chronic subdiaphragmatic vagotomies had any effect on the excitatory response of nigral DA neurons to systemically administered CCK. High cervical spinal cord transections were similarly without effect. In contrast, lesions of either vagal fibers in the medulla or of the efferent pathways from the nucleus tractus solitarii, the primary sensory nucleus of the vagus, produced significant attenuations of the nigral effects of systemically administered CCK. However, neither lesion blocked effects of CCK completely. We suggest that peripherally administered CCK has two components to its excitatory action in the SN; a component probably mediated through CCK receptors in the nucleus tractus solitarii and a direct action on DA neurons.