Vasoactive Intestinal Polypeptide Neurons Research Articles

The synaptic relationship between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and their axon terminals in the rat small intestine: light and electron microscopic study

The present study demonstrates synaptic contacts between vasoactive intestinal polypeptide (VIP)-like immunoreactive neurons and immunoreactive axon terminals in the submucous and myenteric plexuses of the rat small intestine. Our observations suggest that VIP afferents directly affect the VIP neurons in the small intestine via synapses.

VIP neurons in the neocortex

What is the nature of the cellular actions of VIP (vasoactive intestinal polypeptide) in the neocortex? Is VIP co-localized with another neurotransmitter? Do VIP neurons interact with other cortical neurotransmitter systems? How does the intracortical VIP-containing neuronal system relate to the basic elements of cortical organization? Recent immunohistochemical and pharmacological investigations have addressed these questions and have shed some light on the possible function of VIP-containing neurons in the neocortex.

The coexistence of substance P-(SP), avian pancreatic polypeptide-(APP), and glucagon-(GLC) like immunoreactivities in the chicken retina

Vasoactive Intestinal Polypeptide (VIP) promotes the hydrolysis of 3H-glycogen newly synthesized from 3H-glucose by mouse cortical slices. This effect occurs rapidly, approximately 50% of the maximal effect being reached within one minute. The maximal effect is achieved after 5 minutes and maintained for at least 25 minutes. Furthermore the glycogenolytic effect of VIP is reversible, and pharmacologically specific. Thus several neuropeptides present in cerebral cortex such as cholecystokinin-8, somatostatin-28, somatostatin-14, met-enkephalin, leu-enkephalin, do not affect 3H-glycogen levels. VIP fragments 6–28, 16–28 and 21–28 are similarly inactive. Furthermore, among the peptides which share structural homologies with VIP, such as glucagon, secretin, PHI-27 and Gastric Inhibitory Peptide, only secretin and PHI-27 promote 3H-glycogen hydrolysis, with EC50 of 500 and 300 nM respectively, compared to an EC50 of 25 nM for VIP. Immunohistochemical observations indicate that each VIP-containing bipolar cell is identified with a unique radial cortical volume, which is generally between 15–60 μm in diameter and overlaps with the contiguous domains of neighbouring VIP-containing bipolar cells. Thus this set of biochemical and morphological observations support the notion that VIP neurons have the capacity to regulate the availability of energy substrates in cerebral cortex locally, within circumscribed, contiguous, radial domains.

Morphological and functional correlates of VIP neurons in cerebral cortex

Vasoactive Intestinal Polypeptide (VIP) promotes the hydrolysis of 3H-glycogen newly synthesized from 3H-glucose by mouse cortical slices. This effect occurs rapidly, approximately 50% of the maximal effect being reached within one minute. The maximal effect is achieved after 5 minutes and maintained for at least 25 minutes. Furthermore the glycogenolytic effect of VIP is reversible, and pharmacologically specific. Thus several neuropeptides present in cerebral cortex such as cholecystokinin-8, somatostatin-28, somatostatin-14, met-enkephalin, leu-enkephalin, do not affect 3H-glycogen levels. VIP fragments 6–28, 16–28 and 21–28 are similarly inactive. Furthermore, among the peptides which share structural homologies with VIP, such as glucagon, secretin, PHI-27 and Gastric Inhibitory Peptide, only secretin and PHI-27 promote 3H-glycogen hydrolysis, with EC 50 of 500 and 300 nM respectively, compared to an EC 50 of 25 nM for VIP. Immunohistochemical observations indicate that each VIP-containing bipolar cell is identified with a unique radial cortical volume, which is generally between 15–60 μm in diameter and overlaps with the contiguous domains of neighbouring VIP-containing bipolar cells. Thus this set of biochemical and morphological observations support the notion that VIP neurons have the capacity to regulate the availability of energy substrates in cerebral cortex locally, within circumscribed, contiguous, radial domains.

Vasoactive intestinal polypeptide (VIP)-containing neurons in the spinal cord of the rat and their projections

The distribution of vasoactive intestinal polypeptide (VIP)-like immunoreactive structures in the rat spinal cord and their projections were investigated by means of an immunofluorescent method. In the normal rat, a small number of VIP-positive fibers were observed in the superficial layer of the dorsal horn and in the lateral funiculus. With colchicine pretreatment, VIP-positive neurons were demonstrated in the lateral spinal nucleus (lsn) and in the lamina X (Rexed). Transections of the spinal cord at various levels revealed that some of the VIP neurons in the lsn might po supraspinal areas via lateral funiculus.

An immunohistochemical investigation of vasoactive intestinal polypeptide in the colon of patients with Hirschsprung's disease

The distribution of vasoactive intestinal polypeptide (VIP) in the colon of patients with Hirschsprung's disease was investigated by the peroxidase-antiperoxidase (PAP) immunohistochemical method. Three colonic segments, ganglionic, oligoganglionic and aganglionic, were stained by the unlabeled antibody enzyme method. VIP immunoreactive nerve cell bodies, nerve fibers and nerve endings were distributed throughout the ganglionic and oligoganglionic segments. In contrast, the aganglionic segment contained no VIP nerve endings and the number of fibers was reduced. These differences are thought to be a cause of construction of the colon in Hirschsprung's disease and VIP neurons are therefore believed to participate in the relaxatiion of smooth muscle.

Synaptology of three peptidergic neuron types in the central nucleus of the rat amygdala

The synaptology of neurotensin (NT)-, somatostatin (SS)- and vasoactive intestinal polypeptide (VIP)-immunoreactive neurons was studied in the central nucleus of the rat amygdala (CNA). Three types of axon terminals formed synaptic contacts with peptide-immunoreactive neurons in the CNA: Type A terminals containing many round or oval vesicles; Type B terminals containing many pleomorphic vesicles; and Type C terminals containing fewer, pleomorphic vesicles. Peptide-immunoreactive terminals were type A. All three types of terminals formed symmetrical axosomatic and asymmetrical axodendritic contacts. However, type B and peptide-immunoreactive terminals frequently formed symmetrical axodendritic synaptic contacts. VIP-immunoreactive terminals also formed asymmetrical axodendritic contacts. SS- and NT-immunoreactive terminals commonly formed symmetrical contacts on SS- and NT-immunoreactive cell bodies, respectively. VIP-immunoreactive axon terminals were postsynaptic to nonreactive terminals. Type B terminals appeared more frequently on VIP neurons than on NT or SS neurons.

Somatostatin and VIP neurons in the retina of different species.

Neurons displaying somatostatin or vasoactive intestinal polypeptide (VIP) immunoreactivity were detected among the amacrine cells in the retina of baboon, cynomolgus monkey, squirrel monkey, cow, pig, cat, rabbit, guinea-pig, rat, mouse, frog and goldfish. Generally, immunoreactive cell bodies were located in the inner nuclear layer with processes ramifying in three more or less well-defined sublayers in the inner plexiform layer. The density of the sublayers and their location varied with the peptide and species investigated. In most cases there was a sublayer in the outermost part (Ramon y Cajal's sublamina 1) of the inner plexiform layer and this sublayer was usually the best developed. In some species a few somatostatin fibres were also detected in the outer plexiform layer, suggesting that some interplexiform cells contain somatostatin. In the baboon VIP was found exclusively in interstitial amacrine cells which have their cell bodies and processes entirely within the inner plexiform layer.

Vasoactive intestinal polypeptide induces glycogenolysis in mouse cortical slices: a possible regulatory mechanism for the local control of energy metabolism.

Mouse cerebral cortex slices will synthesize [3H]glycogen in vitro. Vasoactive intestinal polypeptide (VIP) stimulates the enzymatic breakdown of this [3H]glycogen. The concentration giving 50% of maximum effectiveness (EC50) is 26 nM. Under the same experimental conditions norepinephrine also induces a concentration-dependent [3H]glycogen hydrolysis with an EC50 of 500 nM. The effect of VIP is not mediated by the release of norepinephrine because it is not blocked by the noradrenergic antagonist d-1-propranolol and is still present in mice in which an 85% depletion of norepinephrine was induced by intracisternal 6-hydroxydopamine injections. Other cortical putative neurotransmitters such as gamma-aminobutyric acid, aspartic acid, glutamic acid, somatostatin, and acetylcholine (tested with the agonist carbamylcholine) do not induce a breakdown of [3H]glycogen. This glycogenolytic effect of VIP and norepinephrine, presumed to be mediated by cyclic AMP formation, should result, at the cellular level, in an increased glucose availability for the generation of phosphate-bound energy. Given the narrow radial pattern of arborization of the intracortical VIP neuron and the tangential intracortical trajectory of the noradrenergic fibers, these two systems may function in a complementary fashion: VIP regulating energy metabolism locally, within individual columnar modules, and norepinephrine exerting a more global effect that spans adjacent columns.

Vasoactive intestinal polypeptide and cholinergic mechanisms in cat nasal mucosa: studies on choline acetyltransferase and release of vasoactive intestinal polypeptide.

Quantitative immunohistochemical analysis of the sphenopalatine ganglion in normal cats revealed that virtually all ganglion cells (98.5%) were immunoreactive to vasoactive intestinal polypeptide (VIP). After surgical removal of this ganglion, the content of both VIP and choline acetyltransferase (acetyl-CoA:choline O-acetyltransferase, EC 2.3.1.6), a specific marker for cholinergic neurons, was decreased to about 70-80% in the nasal mucosa. In contrast, in animals subjected to sympathectomy combined with sensory (trigeminal) denervation, no significant change in VIP or choline acetyltransferase was found in the nasal mucosa. The present findings strongly suggest that a large proportion of the VIP neurons in the sphenopalatine ganglion contain choline acetyltransferase. This further supports the view that VIP is present in a population of autonomic cholinergic neurons innervating exocrine glands in the cat. In contrast, the ciliary ganglion contained high levels of choline acetyltransferase but no VIP. Parasympathetic nerve stimulation (15 Hz) caused a maximal vasodilation and a 500-fold increase in VIP output from the nasal mucosa. The plasma VIP immunoreactivity eluted at the same position as porcine VIP on gel permeation chromatography. Atropine pretreatment, which is known to abolish nasal secretion, caused a further 3-fold increase in VIP output during the nerve stimulation (15 Hz). Simultaneously, a markedly prolonged duration of the vasodilatory response was observed. The increased output of VIP during parasympathetic nerve stimulation by atropine pretreatment suggests that the transmitter acetylcholine may inhibit the release of the coexisting peptide--i.e., VIP--via muscarinic autoreceptors.

Evidence for and significance of the projection of VIP neurons from the myenteric plexus to the taenia coli in the guinea pig

Immunohistochemical studies of the distribution of vasoactive intestinal polypeptide were made in the cecum from normal guinea pigs and from guinea pigs after lesions of the cecal wall had been made. These experiments were designed to determine the origin of the vasoactive intestinal polypeptide axons which supply the taenia of the cecum in order to ascertain whether the projections of the vasoactive intestinal polypeptide neurons were consistent with VIP being contained in enteric inhibitory neurons. Vasoactive intestinal peptide was found in nerve cell bodies of both the myenteric and submucous plexuses. After severing connections between the taenia and the myenteric plexus the vasoactive intestinal polypeptide fibers in the taenia disappeared, but there was no effect on these fibers if the taenia was separated from the submucous plexus or surrounding muscle while leaving connections with the myenteric plexus intact. Retrograde degenerative signs were seen in VIP fibers and nerve cell bodies of the myenteric plexus after removal of the taenia. In conclusion, VIP is contained in neurons that have the same projections as the enteric inhibitory neurons from the myenteric plexus to the taenia of the cecum.

VIP (vasoactive intestinal polypeptide)-immunoreactive neurons in the retina of the rat.

Immunoreactive vasoactive intestinal polypeptide (VIP) was detected in a population of amacrine cells in the retina of the rat. Processes of these cells reach both the inner and outer half of the inner plexiform layer where they form sublayers. The VIP neurons are different from previously known amacrine cell types.

Distribution of VIP neurons in the peripheral and central nervous system.

Vasoactive intestinal polypeptide (VIP) was isolated from porcine intestine in 1970 by Said & Mutt (1970). Characterization showed that it consists of 28 amino acids (Mutt & Said, 1974). Antibodies were raised against the peptide (Said & Faloona, 1975) and radioimmunological determinations revealed high concentrations of VIP in the gastro-intestinal tract (Polak et al., 1974 ; Said, 1975), in neural cell lines (Said & Rosenberg, 1976) and in the central nervous system (Bryant et al., 1976 ; Larsson et al., 1976b ; Said & Rosenberg, 1976). Immunohistochemical studies located the VIP-like immunoreactivity to gastro-intestinal neurons (Bryant et al., 1976; Larsson et al., 1976b ; Fuxe et al., 1977), cerebrovascular nerves (Larsson et al., 1976a) and central neurons (Fuxe et al., 1977 ; Larsson et al., 1976b).The present paper gives a brief account of the distribution of VIP immunoreactive neurons in the central and peripheral nervous system as revealed by immunohistochemistry.