The vagus nerve supplies low-threshold chemo- and mechanosensitive afferents to the mucosa of the proximal gastrointestinal (GI) tract. The absence of a full characterization of the morphology and distributions of these projections has hampered comprehensive functional analyses. In the present experiment, dextran (10K) conjugated with tetramethylrhodamine and biotin was injected into the nodose ganglion and used to label the terminal arbors of individual vagal afferents of both rats and mice. Series of serial 100-µm thick sections of the initial segment of the duodenum as well as the pyloric antrum were collected and processed with diaminobenzidine for permanent tracer labeling. Examination of over 400 isolated afferent fibers, more than 200 from each species, indicated that three vagal afferent specializations, each distinct in morphology and in targets, innervate the mucosa of the proximal GI tract. One population of fibers, the villus afferents, supplies plates of varicose endings to the apical tips of intestinal villi, immediately subjacent to the epithelial wall. A second type of afferent, the crypt afferent, forms subepithelial rings of varicose processes encircling the intestinal glands or crypts, immediately below the cryptvillus junction. Statistical assessment of the isolated fibers indicated that the villus arbors and the crypt endings are independent, issued by different vagal afferents. A third vagal afferent specialization, the antral gland afferent, arborizes along the gastric antral glands and forms terminal concentrations immediately below the luminal epithelial wall. The terminal locations, morphological features, and regional distributions of these three specializations provide inferences about the sensitivities of the afferents.

In vivo microdialysis was used to estimate extracellular concentrations of methionine-enkephalin in 19 brain sites for 5 h on each of three consecutive days (trials) in six conscious ewes. Following control procedures on d 1, ewes were completely isolated from other sheep for 60 min on d 2 (psychological stress). Physical stress was imposed on d 3 and consisted of continuous pinching of the skin for 60 min during the middle of the 5-h experimental period. Imposition of both physical and psychological stress rapidly increased serum concentrations of cortisol, and the induced increase persisted for at least 30 min after termination of the stress. Psychological stress of isolation initially increased cortisol to a greater extent than the physical stress of skin pinch, but this difference disappeared after 30 min of stress exposure. Psychological stress also transiently increased serum concentrations of beta-endorphin/beta-lipotropin, whereas physical stress did not. Average concentrations of methionine-enkephalin in dialysate ranged between 1.52 and 1.85 ng/mL when the intracerebral probes were placed into the caudate nucleus, the preoptic area of the hypothalamus, or the thalamus. The concentration of methionine-enkephalin was consistently less than 1.0 ng/mL when probes were placed into major fiber tracts of the brain (corpus callosum, internal capsule). Potassium-induced depolarization around the probe tip located in the caudate nucleus increased dialysate concentrations of methionine-enkephalin by 2.7-fold. Imposition of physical or psychological stress did not consistently increase or decrease dialysate concentrations of methionine-enkephalin in any of the brain sites studied.(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

Ovine antiserum against a conjugate of porcine neuropeptide Y (NPY) with bovine thyroglobulin was infused repeatedly into one lateral ventricle of five ovariectomized (ovx) ewes before and after subcutaneous injection of estradiol-17 beta (E beta). Serum concentrations of LH, growth hormone (GH), and prolactin (PRL) were measured at 10-min intervals before E beta and at approximately hourly intervals 8 to 18 h after E beta injection. Control ewes were infused with ovine serum from animals immunized against bovine thyroglobulin. Basal episodic profiles (pre-E beta) of LH, GH, and PRL were similar in ovx ewes infused with control or anti-NPY serum. Injection of E beta induced a surge-like increase of serum LH, which began at 12.6 h after E beta in ewes infused with anti-NPY and at 14.4 h after E beta in ewes infused with control antiserum (P < .05). The magnitude of the E beta-induced surge of LH was not different between treatments. In addition to initiating a surge-like release of LH over the period 12 to 18 h after E beta, serum GH was transiently increased during the period between 10 and 15 h after E beta. In contrast, serum PRL was increased during the entire period between 8 and 18 h after E beta. Based on the effects of immunoneutralization, endogenous NPY in the brain of E beta-treated ovx ewes seems to restrain or delay the onset of the surge-like secretion of LH and probably GnRH, but endogenous NPY does not affect the episodic pulsatile releases of LH characteristic of ovx ewes.(ABSTRACT TRUNCATED AT 250 WORDS)

Previous work established that intravenous administration of the opioid receptor antagonist naloxone abruptly increased release of luteinizing hormone (LH) and decreased release of prolactin (PRL) in suckled anestrous ewes and also increased LH release in cyclic luteal ewes. The goal of the present research was to identify brain sites at which local unilateral infusions of naloxone would consistently duplicate the previously noted effects of intravenous naloxone. Intracerebral guide tubes were surgically implanted into the brain of 13 nonpregnant and 16 pregnant ewes at least 4 weeks prior to experimentation. Intracerebral infusion (20–40 µl each through an inner cannula) was performed once daily during postpartum anestrus in suckled fall-lambing ewes and during recurring luteal states of the estrous cycle. Naloxone infusion (n = 142) usually consisted of 50 or 100 µg naloxone, although 5 ewes received 200 and 400 µg per infusion. Control infusions (n = 103) consisted of the vehicle for naloxone (i.e., 0.9% NaCl). Serum concentrations of LH and PRL were quantified at 10-min intervals from 90 min before to 100 min after infusion. Hormone data from individual ewes were grouped for least-squares analysis of variance based upon postmortem neuroanatomical identification of each infusion site. Unilateral intracerebral administration of naloxone consistently induced an increase in LH release within 20 min in the following two neuroanatomical groups: basal forebrain (n = 9 ewes) and chiasmatic area (n = 4 ewes). These naloxone-sensitive brain areas constituted an apparent continuum of tissue sites located as far rostral as ventrolateral septum, diagonal band of Broca and nucleus accumbens and continuing caudally into the preoptic area in and around the organum vasculosum of the lamina terminalis. Brain sites at which the present unilateral infusions of naloxone did not consistently stimulate release of LH included those hypothalamic areas caudal to the preoptic area such as anterior, ventromedial and lateral hypothalamic area including the arcuate nucleus and third ventricle. Therefore, neuroanatomical sites at which local unilateral infusion of naloxone stimulated (i.e., disinhibited) release of LH were very similar to the location of LH-releasing hormone (LHRH) perikarya reported by others for the ovine brain and quite distant from the pituitary gland. Although intravenous naloxone was shown previously to decrease PRL release in suckled anestrous ewes, the present infusion of naloxone did not consistently affect PRL release in such ewes. In summary, local unilateral antagonism of opioid receptors in the vicinity of LHRH perikarya was sufficient to disinhibit release of LHRH/LH, but opioid mechanisms stimulatory to PRL release were not antagonized by intracerebral infusions of naloxone.