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PubMed1996

Estimation of in-vivo neurotransmitter release by brain microdialysis: the issue of validity.

Although microdialysis is commonly understood as a method of sampling low molecular weight compounds in the extracellular compartment of tissues, this definition appears insufficient to specifically describe brain microdialysis of neurotransmitters. In fact, transmitter overflow from the brain into dialysates is critically dependent upon the composition of the perfusing Ringer. Therefore, the dialysing Ringer not only recovers the transmitter from the extracellular brain fluid but is a main determinant of its in-vivo release. Two types of brain microdialysis are distinguished: quantitative micro-dialysis and conventional microdialysis. Quantitative microdialysis provides an estimate of neurotransmitter concentrations in the extracellular fluid in contact with the probe. However, this information might poorly reflect the kinetics of neurotransmitter release in vivo. Conventional microdialysis involves perfusion at a constant rate with a transmitter-free Ringer, resulting in the formation of a steep neurotransmitter concentration gradient extending from the Ringer into the extracellular fluid. This artificial gradient might be critical for the ability of conventional microdialysis to detect and resolve phasic changes in neurotransmitter release taking place in the implanted area. On the basis of these characteristics, conventional microdialysis of neurotransmitters can be conceptualized as a model of the in-vivo release of neurotransmitters in the brain. As such, the criteria of face-validity, construct-validity and predictive-validity should be applied to select the most appropriate experimental conditions for estimating neurotransmitter release in specific brain areas in relation to behaviour.

Journal Article↗
PubMed1991

Differential modulation of spontaneous and evoked neurotransmitter release from hair cells: some novel hypotheses.

It has been generally accepted that even in the absence of mechanical stimulation of the transductional elements, a resting depolarizing current exists which is ultimately responsible for the spontaneous release of neurotransmitter. Movement of the transductional elements modulates this resting current and thereby the evoked release of neurotransmitter occurs. Recent data from our laboratory and others have led us to question whether the relationship between spontaneous and evoked neurotransmitter release is as simple as stated. Indeed, a variety of experimental manipulations appear to influence the two modes of release differently. Examination of our results and the results of others has led us to four hypotheses: 1. the two modes of neurotransmitter release are processed differently by the hair cells; 2. cyclic AMP is involved in spontaneous but not evoked neurotransmitter release; 3. there is a positive feedback step involving an excitatory amino acid and its receptor on the hair cell in evoked neurotransmitter release and; 4. different pools of calcium are involved according to the mode of release. Accordingly, there may be several biochemical steps between the transductional movement of the stereocilia at the apex of the hair cells and the ultimate release of the neurotransmitter at the base of these cells. Some of these biochemical steps are different depending on whether the mode of release is spontaneous or evoked. These biochemical steps may amplify or at least interact with the biophysical processes previously described in the hair cells.

Acetylcholine↗
PubMed1987

Is taurine a hypothalamic neurotransmitter?: A model of the differential uptake and compartmentalization of taurine by neuronal and glial cell particles from the rat hypothalamus.

Although taurine has been postulated to be a neurotransmitter or neuromodulator in the mammalian CNS, little is known concerning its role in brain function. Evidence suggesting that taurine may influence endocrine and homeostatic mechanisms via the hypothalamus resulted in our investigations into its function in this brain region. The main objectives of the research were to characterize the specific binding, uptake, and release of taurine in the hypothalamus. A specific aim was to examine the proposed neurotransmitter role for taurine in the hypothalamus. This was accomplished by comparing the characteristics and properties of the binding, uptake, and release of taurine with those for the classical neurotransmitters which satisfy the criteria for a neurotransmitter. On such a comparative basis, the characteristics of taurine uptake satisfy the neurotransmitter criterion of inactivation of taurine in the hypothalamus. However, the observed characteristics of taurine binding and release in the hypothalamus do not satisfy the respective neurotransmitter criteria of specific receptors and Ca2+-dependent evoked release. Therefore, solely on the basis of the experimental observations reported herein, we must conclude that taurine apparently does not function as a neurotransmitter in the hypothalamus. Two uptake systems were found in the P2 fraction, a high affinity uptake system and a low affinity uptake system. Uptake systems for taurine have previously been reported in glial and nerve cell homogenates, and therefore, because of the known contamination of crude synaptosomal preparations with glial particles, we sought to determine the cellular origin of the two taurine uptake systems in our crude preparation. Using a variety of diverse biochemical techniques such as hypo-osmotic shock, release experiments and Arrhenius plots, we determined that physical changes of the media or depolarizing stimuli which would influence neuronal and glial cell particles differently, also had differing effects on high and low affinity taurine uptake or its release from the respective uptake compartments. We conclude that the high affinity taurine uptake system/compartment is located on/in neuronal membranes/particles/particles and that the low affinity taurine uptake system/compartment is located on/in neuronal membranes/particles and that model for the differential cellular transport and compartmentalization of taurine into neuronal and glial cells has important implications concerning its possible role in the CNS.

Animals↗
PubMed1993

Neurotransmitter properties of guinea-pig sympathetic neurons grown in dissociated cell culture--I. Adult neurons.

The autonomic nervous system of mammals displays extensive neurotransmitter diversity. The guinea-pig sympathetic nervous system has served as a model for in vivo studies of neurotransmitter co-expression. We have developed methods for the dissociation and long-term culture of adult guinea-pig prevertebral sympathetic ganglia. The neurotransmitter properties of cultured adult guinea-pig sympathetic neurons from the celiac and superior mesenteric ganglia were examined. Cultured principal neurons were found to display many of their in vivo neurotransmitter characteristics, including catecholamine-specific histofluorescence and immunoreactivity for tyrosine hydroxylase and the neuropeptides, neuropeptide Y, somatostatin and vasoactive intestinal polypeptide. In addition, the cultures of both ganglia displayed the various neurotransmitter characteristics in approximately the same percentage of the cultured neurons as reported in in vivo studies. A small percentage of principal neurons and many small, intensely fluorescent-like cells labeled with antibodies against 5-hydroxytryptamine. Many of the principal neurons were found to bear 5-hydroxytryptamine3 receptors, suggesting a possible role for this neurotransmitter in neuron-neuron and small, intensely fluorescent cell-neuron transmission. We conclude that adult guinea-pig sympathetic neurons retain their neurotransmitter phenotypes when grown in dissociated cell culture. These properties include the co-expression of the classical transmitters, norepinephrine, 5-hydroxytryptamine and neuropeptides. This culture preparation will prove to be valuable in future studies on the functional properties of these neurons and their development.

Animals↗
PubMed2005

Effects of tissue trauma on the characteristics of microdialysis zero-net-flux method sampling neurotransmitters.

Microdialysis has been used for studying neurochemistry in brain regions that respond to afferent inputs or administered drugs. As the knowledge derived from and concerning microdialysis grows, so do the concerns over its invasiveness and, hence, the credibility of resulting data. Recent experimental and theoretical studies impugned the validity of the microdialysis zero-net-flux (ZNF) method in measuring brain extracellular neurotransmitters, suggesting that the tissue trauma resulting from probe implantation seriously compromises its worth. This paper developed a theoretical model to study the influences of two categories of tissue trauma on microdialysis ZNF operation: (1) morphological alterations in tissue extracellular structure and (2) physiological impairment of neurotransmitter release and uptake processes. Model results show that alterations of tissue extracellular structure negligibly affect the accuracy of the ZNF method in determining the basal level of extracellular neurotransmitter but do affect the fundamental characteristics of microdialysis: the extraction efficiency and relative recovery. An inhibited or damaged neurotransmitter uptake process always decreases the efficiency of microdialysis extraction, but rise of the relative recovery of neurotransmitters with the same uptake inhibition/damage occurs only when there is far more damage to the neurotransmitter release than to the uptake process in the tissue. A criterion for this rising trend of microdialysis relative recovery is discussed in terms of trauma parameters and neurotransmitter uptake inhibition.

Brain Injuries↗
PubMed1996

Immunoregulatory role of neurotransmitters.

The nervous and endocrine systems modulate the immune system functions through releasing neurotransmitters, neuropeptides and endocrine hormones as they regulate the other physiological functions. The immune system in turn communicates with the nervous and endocrine systems through secreting immunocompetent substances. In this report we review our concepts and evidence concerning the immunoregulatory role of acetylcholine (ACh) and monoamine neurotransmitters which include noradrenaline (NA), 5-hydroxytryptamine (5-HT) and dopamine (DA). The immunoregulatory role comprises two aspects, the modulation of immune functions by neurotransmitters and the effect of the immune system on nervous system functions. The inhibition of ACh biosynthesis in the central nervous system (CNS) caused the enhancement of the humoral immune response of rats to sheep red blood cells (SRBC); by contrast, the inhibition of acetyl-cholinesterase (AChE) activity in the CNS resulted in the suppression of the immune response. It seems that ACh in the brain plays an immunoinhibitory role. The role can be blocked by atropine, a muscarinic antagonist, but not by hexamethonium, a nicotinic antagonist. During the humoral immune response (days 3-6 after SRBC injection), activity of AChE in the hypothalamus and hippocampus was strikingly lower. It is suggested that a functional connection is present in the ACh of the brain and the immune system. In vitro, ACh at 10(-9) to 10(-4) mol/l dose range significantly strengthened the spleen cell proliferation induced by concanavalin (Con A). The action of ACh only occurred either before or just after T lymphocytes were activated through muscarinic cholinergic receptors. In vivo, the depletion of monoamine neurotransmitters or only NA in the CNS caused the impairment of the anti-SRBC response of rats. During the phases of days 2-7 post-immunization, the metabolic alterations of NA, 5-HT and DA emerged in the CNS and the lymphoid organs of rats, which mainly exhibited that in the peak periods of the antibody response, the metabolism of the monoamine neurotransmitters in the hypothalamus and hippocampus was markedly increased, but NA content in the spleen and thymus was significantly decreased. These results provide evidence for the bidirectional information exchange network between the monoamine neurotransmitters and the immune system. Exposure to NA (at 10(-8)-10(-5) mol/l concentration range) in vitro was shown to inhibit the Con A-induced proliferation of the rat spleen cells. This effect of NA was related to the early events involved in the initiation of T cell proliferation and was mediated by either alpha- or beta-adrenergic receptors. The evidence that altering 5-HT level in the central or peripheral nervous systems through various ways of administering the drugs to regulate 5-HT biosynthesis led to the variations of the antibody response, and that cyproheptadine, an antagonist of serotoninergic receptors, can block the action of 5-HT show that 5-HT may exert an immunoinhibitory effect, which appears to be mediated via the peripheral mechanism to relate to the 5-HT receptors. However, the antibody response can cause changes in 5-HT metabolism in the CNS. The possible reasons for these results are discussed. Collectively, the antibody response arouses the metabolic variations of ACh, NA, 5-HT and DA in the central and peripheral nervous systems and then, these alterations can in turn influence immune function through neurotransmitter relevant receptors present on the immunocytes. The purpose of this interaction is most likely to maintain the homeostasis of the immune and other physiological functions.

Adjuvants, Immunologic↗
PubMed1999

Development of peripheral autonomic synapses: neurotransmitter receptors, neuroeffector associations and neural influences.

1. The functional innervation of autonomic target tissues occurs early during development, at a time when both the nerves and post-synaptic target tissues are still differentiating. 2. Physiological responses appear soon after the arrival of the first fibres when uptake and release mechanisms within the nerves are already functional. Initial responses differ from those in the mature animal, both in the form and, frequently, in the subtypes of receptors involved. 3. Results of a number of studies suggest that the initial expression of neurotransmitter receptors during development is largely independent of neural influences. Changes recorded in neurotransmitter receptor expression during development appear to be similarly independent of neural influences. 4. While signal transduction pathways coupling adrenergic neurotransmitter receptors to effector responses appear to develop independently of the nerves, the efficient coupling of muscarinic receptors often requires the action of the neurotransmitter, acetylcholine. 5. During the period of synapse formation, the neural plexus continues to expand. While developing varicosities can release the neurotransmitter, the capacity for neurotransmitter retention appears to be restricted. Developmental changes in the neurotransmitters that produce functional responses, while well known in the sweat glands, may also be seen in more subtle forms in other target tissues. 6. Ultrastructural studies suggest that close physical associations between the membranes of the release sites of the developing nerves and the target cells may form early during development when physiological responses are still immature. These close associations could enable more specific reciprocal interactions between nerves and target cells involving known and novel growth factors, neuropeptides and cytokines important in shaping the mature synaptic characteristics.

Animals↗
PubMedDate not supplied

The impact of stressors on immune and central neurotransmitter activity: bidirectional communication.

Antigenic challenge may have broad ranging effects which include not only immunological changes, but also endocrine and central neurotransmitter repercussions, and may thus elicit profound behavioral sequelae. Commensurate with the notion that bidirectional communication exists between the immune and central nervous systems it has been demonstrated that manipulations which influence central neurotransmitter or endocrine activity provoke alterations of immune functioning, and conversely immunological alterations will affect central neurotransmitter and endocrine activity. It seems, as well, that environmental stressors may provoke marked alterations of the activity of each of these systems. Indeed, in several respects the variables that influence vulnerability to stressor-provoked neurotransmitter changes, likewise affect the immunological alterations engendered by stressors. Moreover, immunological challenges will affect central neurotransmitter functioning in much the same way as stressors provoke such effects. It is thought that immune derived products (including cytokines as well as peptide hormones) may act directly or indirectly to moderate neurotransmitter functioning, and centrally derived neurotransmitters and hormones may affect receptors present on lymphocytes. In accordance with earlier suggestions, it is maintained that the immune system may be acting as a sensory organ informing the brain of the presence of antigenic challenges, and the brain may interpret such challenge as a stressor, hence leading to behavioral alterations.

Animals↗
PubMed1989

[Neurotransmitters and neurologic disorders].

Neurotransmitters should fulfil the following main three criteria; 1) they should be localized in synaptic terminals, 2) they should have certain actions on neurons, 3) they should be released from the terminals after nerve stimulation. In addition to the above three, recent studies have revealed that neurotransmitters should have their own receptors. Moreover, recent immunohistochemical studies have revealed certain neurons to have two or more neurotransmitter candidates; one classic and the other non-classic neurotransmitter candidate. These progresses in the field of neurotransmitter science were briefly reviewed. As an extension of the basic studies mentioned above, clinical studies of measurements of neurotransmitter markers in brains of neurodegenerative disorders are now actively performed. Based on my own studies in the same line, it is possible to summarize the fundamental patterns of neurotransmitter alterations in neurodegenerative disorders as follows: 1) they decrease as a result of degeneration of neuron groups (the most popular pattern); 2) they decrease in spite of the morphologically normal appearance of neurons ("biochemical non-functioning"); 3) they increase in the projecting regions of certain neurons which escaped degeneration. This may be a result of simple condensation of normal nerve terminals or real increase based on the compensatory mechanisms.

Brain↗
PubMed1996

Neurotransmitter transporters: new insights into structure, function and pharmacology.

Neurotransmitter transporters on neurons and glial cells catalyze the uptake of neurotransmitter, and may serve to limit the activation of receptors during synaptic signaling. Over the past few years significant progress has been made toward a molecular understanding of neurotransmitter transporters in the CNS. The plasma membrane neurotransmitter carriers are comprised of two structurally- and mechanistically-distinct gene families, the Na+ and Cl(-)-dependent transporters that include the carriers for most of the classical CNS neurotransmitters and several additional carriers for amino acids and other substrates outside the nervous system. A second structurally distinct family of Na(+)-dependent carriers encompasses the excitatory amino acid transporters. For both carrier families the transport of substrate is coupled to the cotransport of sodium ions down a concentration gradient. Electrophysiological studies of neurotransmitter transporters indicate that many of the carriers are electrogenic and may operate in some ways similar to ion channels. In addition, emerging data indicate that these carriers not only function in the uptake of neurotransmitter, but also that as a consequence of their ability to alter the membrane potential they may have a broader role in regulating neuronal excitability and signaling mechanisms.

Antidepressive Agents↗
PubMed2006

Neurotransmitters of the suprachiasmatic nuclei.

There has been extensive research in the recent past looking into the molecular basis and mechanisms of the biological clock, situated in the suprachiasmatic nuclei (SCN) of the anterior hypothalamus. Neurotransmitters are a very important component of SCN function. Thorough knowledge of neurotransmitters is not only essential for the understanding of the clock but also for the successful manipulation of the clock with experimental chemicals and therapeutical drugs. This article reviews the current knowledge about neurotransmitters in the SCN, including neurotransmitters that have been identified only recently. An attempt was made to describe the neurotransmitters and hormonal/diffusible signals of the SCN efference, which are necessary for the master clock to exert its overt function. The expression of robust circadian rhythms depends on the integrity of the biological clock and on the integration of thousands of individual cellular clocks found in the clock. Neurotransmitters are required at all levels, at the input, in the clock itself, and in its efferent output for the normal function of the clock. The relationship between neurotransmitter function and gene expression is also discussed because clock gene transcription forms the molecular basis of the clock and its working.

Journal Article↗
PubMed2002

In vivo properties of the Drosophila inebriated-encoded neurotransmitter transporter.

Altering neurotransmitter levels within the nervous system can cause profound changes in behavior and neuronal function. Neurotransmitter transporters play important roles in regulating neurotransmitter levels by performing neurotransmitter reuptake. It was previously shown that mutations in the Drosophila inebriated (ine)-encoded neurotransmitter transporter cause increased neuronal excitability. Here we report a further functional characterization of Ine. First we show that Ine functions in the short-term (time scale of minutes to a few hours) to regulate neuronal excitability. Second, we show that Ine is able to control excitability from either neurons or glia cells. Third, we show that overexpression of Ine reduces neuronal excitability. Overexpression phenotypes of ine include: delayed onset of long-term facilitation and increased failure rate of transmitter release at the larval neuromuscular junction, reduced amplitude of larval nerve compound action potentials, suppression of the leg-shaking behavior of mutants defective in the Shaker-encoded potassium channel, and temperature-sensitive paralysis. Each of these overexpression phenotypes closely resembles those of loss of function mutants in the para-encoded sodium channel. These data raise the possibility that Ine negatively regulates neuronal sodium channels, and thus that the substrate neurotransmitter of Ine positively regulates sodium channels.

Action Potentials↗
PubMed1996

Immunohistochemical localization of neurotransmitters utilized by neurons in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) that project to the oculomotor and trochlear nuclei in the cat.

The rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF) contains excitatory and inhibitory burst neurons that are related to the control of vertical and torsional eye movements. In the present study, light microscopic examination of the immunohistochemical localization of amino acid neurotransmitters demonstrated that the riMLF in the cat contains overlapping populations of neurons that are immunoreactive to the putative inhibitory neurotransmitter gamma-aminobutyric acid (GABA) and the excitatory neurotransmitters glutamate and aspartate. By using a double-labelling paradigm, GABA-, glutamate-, and aspartate-immunoreactive neurons in the riMLF were retrogradely labelled by transport of horseradish peroxidase (HRP) from the oculomotor and trochlear nuclei. Electron microscopy showed that the oculomotor and trochlear nuclei contain synaptic endings that are immunoreactive to GABA, glutamate, or aspartate. Each neurotransmitter-specific population of synaptic endings has distinctive ultrastructural and synaptic features. Synaptic endings in the oculomotor and trochlear nuclei that are anterogradely labelled by transport of biocytin from the riMLF are immunoreactive to GABA, glutamate, or aspartate. Taken together, the findings from these complimentary retrograde and anterograde double-labelling studies provide rather conclusive evidence that GABA is the inhibitory neurotransmitter, and glutamate and aspartate are the excitatory neurotransmitters, utilized by premotor neurons in the riMLF that are related to the control of vertical saccadic eye movements.

Animals↗
PubMed1991

Appearance of putative amino acid neurotransmitters during differentiation of neurons in embryonic turtle cerebral cortex.

Pyramidal and nonpyramidal neurons can be recognized early in the development of the cerebral cortex in both reptiles and mammals, and the neurotransmitters likely utilized by these cells, glutamate and gamma-aminobutyric acid, or GABA, have been suggested to play critical developmental roles. Information concerning the timing and topography of neurotransmitter synthesis by specific classes of cortical neurons is important for understanding developmental roles of neurotransmitters and for identifying potential zones of neurotransmitter action in the developing brain. We therefore analyzed the appearance of GABA and glutamate in the cerebral cortex of embryonic turtles using polyclonal antisera raised against GABA and glutamate. Neuronal subtypes become immunoreactive for the putative amino acid neurotransmitters GABA and glutamate early in the embryonic development of turtle cerebral cortex, with nonpyramidal cells immunoreactive for GABA and pyramidal cells immunoreactive for glutamate. The results of controls strongly suggest that the immunocytochemical staining in tissue sections by the GABA and glutamate antisera corresponds to fixed endogenous GABA and glutamate. Horizontally oriented cells in the early marginal zone (stages 15-16) that are GABA-immunoreactive (GABA-IR) resemble nonpyramidal cells in morphology and distribution. GABA-IR neurons exhibit increasingly diverse morphologies and become distributed in all cortical layers as the cortex matures. Glutamate-immunoreactive (Glu-IR) cells dominate the cellular layer throughout development and are also common in the subcellular layer at early stages, a distribution like that of pyramidal neurons and distinct from that of GABA-IR nonpyramidal cells. The early organization of embryonic turtle cortex in reptiles resembles that of embryonic mammalian cortex, and the immunocytochemical results underline several shared as well as distinguishing features. Early GABA-IR nonpyramidal cells flank the developing cortical plate, composed primarily of pyramidal cells, shown here to be Glu-IR. The earliest GABA-IR cells in turtles likely correspond to Cajal-Retzius cells, a ubiquitous and precocious cell type in vertebrate cortex. Glutamate-IR projection neurons in vertebrates may also be related. The distinctly different topographies of GABA and glutamate containing cells in reptiles and mammals indicate that even if the basic amino acid transmitter-containing cell types are conserved in higher vertebrates, the local interactions mediated by these transmitters may differ. The potential role of GABA and glutamate in nonsynaptic interactions early in cortical development is reinforced by the precocious expression of these neurotransmitters in turtles, well before they are required for synaptic transmission.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Immunoelectron microscopic localization of neurotransmitters in the cochlea.

This paper presents the works and methods of our respective laboratories using electron microscopic immunocytochemistry to identify and localize cochlear neurotransmitters. Antibodies to various prospective neurotransmitters and associated enzymes have been used to study the ultrastructural localization of several candidates for olivocochlear efferent neurotransmitters previously suggested by light microscopic immunocytochemistry. Antibodies against enkephalins label lateral olivocochlear efferent fibers. Antibodies against choline acetyltransferase (ChAT) (an enzyme marker for acetylcholine) label a major population of both lateral and medial efferent fibers and terminals, whereas antibodies to gamma-aminobutyric acid (GABA) label what might be a small subpopulation of both the lateral and medial efferent systems. The GABA-like immunostained medial efferent fibers are preferentially located in the upper turns of the guinea pig cochlea, particularly the third turn. Immunoelectron microscopy shows that neither GABA nor ChAT immunolabels all medial efferent terminals, regardless of cochlear turn. All the different types of immunolabeled efferent terminals have been observed to make characteristic synaptic contacts; lateral efferent terminals on afferent dendrites and medial efferent terminals on outer hair cells and occasionally on type II afferent dendrites. Other types of contacts involving GABA-like, and sometimes met-enkephalin-like, immunostained fibers are occasionally seen particularly in the upper turns of the cochlea. Immunoelectron microscopic results suggest that both medial and lateral efferent systems might be further subdivided on the basis of differences in neurotransmitters. Future trends of immunocytochemical research on cochlear neurotransmitters are proposed, particularly colocalization studies, which show a complex pattern of coexistence of neurotransmitters in the lateral efferent system.

Animals↗
PubMed2001

Molecular mechanisms of neurotransmitter release.

The release of neurotransmitter from neurons represents one of the pivotal events in synaptic transmission. Neurotransmitters are released from synaptic vesicles in presynaptic neurons in response to neural activity, diffuse across the synaptic cleft, and bind specific receptors in order to bring about changes in postsynaptic neurons. Some of the molecular processes that govern neurotransmitter release are now becoming better understood. The steps involved can be broken down into two partially overlapping presynaptic cycles, the neurotransmitter cycle and the synaptic vesicle cycle. The neurotransmitter cycle involves transmitter biosynthesis, storage, reuptake, and degradation. The synaptic vesicle cycle involves targeting to the nerve terminal, docking, fusion, endocytosis, and recycling. Biochemical and structural studies have yielded important insight into our understanding of each of these two cycles. Further, both pharmacological and genetic interference with either of these cycles results in profound alterations in synaptic transmission and behavior, demonstrating the crucial role of neurotransmitter release.

Animals↗
PubMed1994

On the molecular mechanism of adrenocorticotrophic hormone in the CNS: neurotransmitters and receptors.

A neural mechanism for the clinical efficacy of adrenocorticotrophic hormone (ACTH) independent of steroid effects in neurological disorders such as infantile spasms, myoclonic seizures in infants, and the opsoclonus-myoclonus syndrome remains controversial. This article reviews evidence that ACTH is a neurotransmitter, neuromodulator, and growth factor. It summarizes studies of anticonvulsant, antimyoclonic, and neurophysiologic effects of ACTH and ACTH fragments, the binding of ACTH in vitro to neurotransmitter receptors in brain, the chronic effects of ACTH on central neurotransmitter receptors and metabolism, effects of neurotransmitters on ACTH secretion, effects of ACTH on growth of cultured neurons, anatomic evidence for interactions of ACTH with neurotransmitters, behavioral effects and interactions of ACTH with neurotransmitter systems in vivo, and other neurochemical properties which may alter neurotransmission.

Adrenocorticotropic Hormone↗
PubMed1979

Neurotransmitters and neuromodulators and their mediation by cyclic nucleotides.

An effort has been made here to devise criteria allowing discrimination between neurotransmitters, modulators and mediators. However, after consideration of several technical pitfalls in studies of these criteria, and examination of the properties of two examples of neuroactive agents (norepinephrine and endorphins) often referred to as "modulators", it is still difficult to classify these agents in all cases. Thus, in most central targets where NE-fibers are known to terminate, the synaptic actions of NE appear to have properties of both a neuromodulator and a neurotransmitter. Although much more research needs to be pursued, the opioid peptides may be neuromodulators for some neurons (spinal cord neurons) and neurotransmitters for others (myenteric plexus and spinal cord neurons). It may be that classification of such peptide agonists will need to be done on a cell-by-cell basis, with the endogenous peptides subserving a multi-faceted role in central and peripheral neuronal communication. As more and more endogenous ligands and transmitter-like substances are extracted from brain, it begins to appear that the language of neuronal communication is much richer than originally imagined from responses of spinal neurons to the fast-acting classical neurotransmitters. Indeed, it may evolve that the "deviant" forms of communication or transmission are more the rule than the exception. In the final analysis, each neurotransmitter may possess its own "fingerprint" of holistic actions attesting to the unique individuality of neuron types and their neurotransmitters. Such individualities might be expected to accomplish more sophisticated integrative operations, and hence behaviors, than could simple rapid "yes" or "no" messages.

Acetylcholine↗