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PubMed1991

In situ hybridization analysis of c-fos and c-jun expression in the rat brain following transient forebrain ischemia.

Early induction of the mRNAs encoding the c-Fos and c-Jun nuclear proteins was examined in rat brain by in situ hybridization at various timepoints following global forebrain ischemia by the method of four-vessel occlusion. All animals were subjected to 20 min of transient ischemia. This produced a pattern of proto-oncogene activation that was most intense in the granule cells of the dentate gyrus 30 min after ischemia, while the hilar cells in the dentate and the pyramidal cells of the CA3 region in the hippocampus showed a more delayed but robust expression of these immediate early genes at 1 h. The neurons of the CA1 region exhibited a more moderate hybridization signal at 1-2 h postischemia. Very little hybridization signal for either immediate early gene could be detected in animals perfused with fixative immediately following ischemia, suggesting that cellular energy levels may have to be restored to a certain level before efficient de novo mRNA synthesis can occur. In the cerebellum, a similar temporal pattern was observed: the granule cells exhibited a prompt but patchy expression of c-fos and c-jun that was followed by a delayed signal in the Purkinje cells. Without exception c-fos and c-jun appeared to be expressed in unison, although the time course of c-fos and c-jun mRNA accumulation and decay was different in various brain regions: invariably the cerebellum returned rapidly to its baseline with virtually no remaining signal at 3 h postischemia, while c-fos and c-jun activation in the hippocampus remained high at 3 h and returned to baseline by 6 h. Several other brain regions showed early production of c-fos and c-jun mRNAs, such as the medial habenula, piriform cortex, the amygdala, the centromedian, lateral posterior, paracentral, intermediodorsal and reuniens nuclei of the thalamus and the ventromedial and dorsal nuclei of the hypothalamus; in the brainstem, the trapezoid body and the noradrenergic neurons of the locus ceruleus as well as the adrenergic neurons in the ventrolateral medulla (C1 group) and nucleus tractus solitarius (C2 group) regions displayed slightly less intense hybridization signals. In addition, the ependyma of the lateral ventricles and the third ventricle showed a prompt albeit short-lived production of c-fos and c-jun mRNAs. Sham-operated animals as well as animals that had survived to one week postischemia showed either no or only trace levels of hybridization signal.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Characterization and anatomical distribution of selective long-term potentiation in the olfactory forebrain.

High-frequency stimulation of the granule cell layer of the olfactory bulb (OB) has previously been shown to result in a form of long-term potentiation in the piriform cortex (PC) that is selective to late components of the potential evoked in the PC58. This phenomenon was explored in male Long-Evans rats with chronically implanted electrodes by recording potentials evoked in the OB and in various sites in the ipsilateral and contralateral PC before and after repeated high-frequency stimulation of the OB. Recordings at all sites exhibited a gradually developing potentiation that was selective to late components of the evoked potential. In the OB and ipsilateral PC this potentiation had an overt long-term component that lasted for days, and all sites exhibited a latent potentiation that enabled the reestablishment of substantial levels of potentiation by mild patterns of stimulation that had no effect in control animals. No potentiation of the population EPSP representing input from the lateral olfactory tract to the PC was seen. Available evidence concerning the neuronal elements activated by the stimulation and the neuronal events likely to underlie the potentiated components of the evoked potentials suggests that this potentiation may represent an enhancement of inhibitory interactions within the PC and between the PC and OB.

Animals↗
PubMed1991

An ultrastructural study of neurotensin-like immunoreactive terminals in the mediodorsal thalamic nucleus of the rat.

Neurotensin-like immunoreactive (NTir) axon terminals in the mediodorsal nucleus of the thalamus (MD) in the adult rat were demonstrated by electron microscopic immunohistochemistry. Most NTir terminals were large (greater than 2 microns in diameter) with round synaptic vesicles and asymmetrical synaptic contacts although smaller (less than 1.5 microns in diameter) axon terminals were also labeled. Both types of terminals were found in the medial and central parts of MD with the greatest density in the medial part. These NTir boutons have similar ultrastructural features as anterogradely labeled terminals from the piriform cortex and the preoptic area, which have previously been identified as sources of NTir axons in MD. A few NTir boutons were also found in the medial part of MD with pleomorphic vesicles and symmetrical synaptic contacts.

Animals↗
PubMed1991

Sexual behavior increases c-fos expression in the forebrain of the male rat.

The ability of a wide variety of pharmacological and physiological stimuli to increase neuronal expression of Fos has led to the suggestion that it might serve as a marker of neuronal activation. Psychomotor stimulants increase the release of dopamine from the terminals of nigrostriatal and mesolimbic neurons and enhance Fos immunoreactivity in the striatum and nucleus accumbens (NAc). Because sexual behavior also increases dopamine release in these and other forebrain regions, the present study examined the effect of copulation on Fos immunoreactivity in the forebrain of intact, sexually active male rats. Sexual behavior produced a striking increase in Fos immunoreactivity in the medial preoptic area (MPOA), NAc, bed nucleus of the stria terminalis and piriform cortex. However, no increase in Fos immunoreactivity was observed in the striatum. These results are consistent with neurochemical, physiological, and behavioral data suggesting that the MPOA and NAc are important substrates of sexual behavior.

Animals↗
PubMed1992

Binding sites for pituitary adenylate cyclase activating polypeptide (PACAP): comparison with vasoactive intestinal polypeptide (VIP) binding site localization in rat brain sections.

Pituitary adenylate cyclase activating polypeptide (PACAP) is structurally similar to vasoactive intestinal polypeptide (VIP). We investigated the characteristics and topographical distribution of [125I]PACAP binding sites compared with those of [125I]VIP binding sites in the rat brain. Radiolabeled PACAP and VIP showed highly specific binding to sections at the level of the dorsal hippocampus. The specific binding of [125I]PACAP was 10 times higher than that of [125I]VIP in hippocampal sections. [125I]PACAP binding was scarcely displaced by unlabeled VIP, while [125I]VIP binding was effectively displaced by unlabeled PACAP. Therefore, PACAP binding sites may reflect both PACAP specific binding sites and VIP/PACAP binding sites. However, the amount of VIP/PACAP binding sites was negligibly low. Autoradiography revealed that [125I]PACAP binding sites were dense in the piriform cortex, diagonal band, accumbens nucleus, anterior part of the striatum, hippocampal formation, habenular nucleus, lateral hypothalamic area, superior colliculus and dorsal raphe nucleus. Moderate to high labeling was observed in the medial septal nucleus, olfactory tubercle, caudal part of the striatum, most parts of the thalamus, supraoptic and periventricular hypothalamic nuclei, central gray, substantia nigra pars compacta, locus coeruleus, pontine reticular nucleus and cerebellum. Distribution pattern was remarkably different from that of [125I]VIP binding sites in the hippocampal formation, lateral hypothalamic area, substantia nigra pars compacta, pontine reticular nucleus and cerebellum. The present results suggest that PACAP may have a physiological role in the regulation of the central nervous system.

Animals↗
PubMed1992

Decreased [3H]hemicholinium binding to high-affinity choline uptake sites in aged rat brain.

The binding of [3H]hemicholinium ([3H]HCh-3) to sodium-dependent high-affinity choline uptake sites provides a useful neuroanatomical and functional marker of the cholinergic system. We examined the autoradiographic distribution of [3H]HCh-3 binding sites in the forebrain of young (4-6 months) and old (32 months) rats. There was a widespread reduction of [3H]HCh-3 binding site density in the aged rat brain. This loss presented regional differences with maximal reduction in the medial and posterior striatum (55%) and in the dentate gyrus (47%), in limbic areas such as basolateral amygdala, tubercle olfactorium and piriform cortex the autoradiographic signal was about 25-30% lower. In aged hippocampus and cerebral cortex the density of [3H]HCh-3 binding sites was about 40% lower, the difference between young and senescent animals being less evident in the medial septum and basal nucleus. No significant alterations were observed in interpeduncular nucleus from old rats. These data are in agreement with the functional results obtained by measuring other cholinergic parameters in the aged rat and confirm the vulnerability of cholinergic system during aging.

Aging↗
PubMed1992

Angiotensin II binding sites in the hamster brain: localization and subtype distribution.

This study was designed to characterize the distribution of angiotensin II (AII) binding sites in the hamster brain. Brain sections were incubated with [125I][sar1,ile8]-angiotensin II in the absence and presence of angiotensin II receptor subtype selective compounds, losartan (AT1 subtype) and PD123177 (AT2 subtype). Binding was quantified by densitometric analysis of autoradiograms and localized by comparison with adjacent thionein stained sections. The distribution of AII binding sites was similar to that found in the rat, with some exceptions. [125I][sar1,ile8]-angiotensin II binding was not evident in the subthalamic nucleus and thalamic regions, inferior olive, suprachiasmatic nucleus, and piriform cortex of the hamster, regions of prominent binding in the rat brain. However, intense binding was observed in the interpeduncular nucleus and the medial habenula of the hamster, nuclei void of binding in the rat brain. Competition with receptor subtype selective compounds revealed a similar AII receptor subtype profile in brain regions where binding is evident in both species. One notable exception is the medial geniculate nucleus, predominately AT1 binding sites in the hamster but AT2 in the rat. Generally, the AII binding site distribution in the hamster brain parallels that of the other species studied, particularly in brain regions associated with cardiovascular and dipsogenic functions. Functional correlates for AII binding sites have not been elucidated in the majority of brain regions and species mismatches might provide clues in this regard.

Angiotensin II↗
PubMed1993

Cortical refractoriness to N-methyl-D,L-aspartic acid (NMA) stimulation in the lactating rat: recovery after pup removal and blockade of progesterone receptors.

We have previously reported that lactating rats, unlike cycling rats, are refractory to N-methyl-D,L-aspartic acid (NMA), but not kainate, in terms of behavioral responses and activation of cFos expression in the neocortex and hippocampus. To study the factors involved in the suppression of cortical activation in lactating rats in response to NMA, we examined the effects of removing either the suckling stimulus and/or progesterone. The degree of cFos expression was used as a marker for cortical activation. Whereas control suckled animals exhibited little or no cFos activation in the piriform cortex in response to NMA, cycling rats showed a high degree of activation. Blockade of the effects of progesterone or removal of the pups for 24 h, resulted in a moderate level of cFos intensity in response to NMA. Total recovery was observed only in animals who had their pups removed for 24 h and the effects of progesterone were blocked. In general, similar results were obtained in the hippocampus except that the total recovery of hippocampal activation took longer than the cortex. Thus, the deficits in cortical activation depend on the presence of both the suckling stimulus and progesterone. However, progesterone alone cannot induce these cortical deficits since pregnant rats showed no deficits in cortical activation in response to NMA when compared to cycling rats. Therefore, the suckling stimulus is required for the inhibition of NMDA-receptor mediated activation of the cortex and hippocampus. The effects of progesterone appear to act synergistically with the effects of suckling.

Animals↗
PubMed1993

Intracellular filling in fixed brain slices using Miniruby, a fluorescent biocytin compound.

Biocytin is useful for intracellular filling in living slices because it is soluble, has high electrophoretic mobility and a high affinity for avidin. In fixed slices, however, membrane potential cannot be used to signify that a cell is impaled. Thus, it is necessary to inject a fluorescent molecule so that impalement and filling can be visually monitored. As biocytin does not fluoresce, it cannot be used by itself in fixed slices. Here, we report that a biocytin-dextran (MW 10 kDa and 40 kDa) compound, Miniruby (MR), is a useful intracellular marker for injecting neurons in fixed slices. Fixed slices (200-400 microns) of adult rat olfactory bulb, piriform cortex, midbrain periaqueductal gray and locus coeruleus were used. Slices were stained by 0.001% ethidium bromide so that cell bodies could be visualized. The slices were imaged and filled using a specially designed hinged, epi-fluorescent microscope. A cell was impaled with a pipette containing 1-5% MR; positive pulsed constant current (1-5 nA; 300-400 ms on and 600-700 ms off; approximately 10 min) was applied until the fine dendrites were brightly fluorescent. Slices were post-fixed for 6-12 h, then reacted by a conventional ABC-DAB protocol. Miniruby has several advantages: (1) it is easy to visualize the electrode in relation to the cell bodies; (2) the staining procedure is very sensitive, does not require immunohistochemistry, and the reaction product is light stable; (3) injected neurons, dendrites and initial part of axons are well visualized by bright-field microscopy. It should be possible to analyze MR filled cells at the EM level.

Animals↗
PubMed1993

Variation in the expression of c-fos after intoxication by soman. Comparative study using in situ hybridization and immunohistochemistry.

A massive and transitory increase in c-fos mRNA and Fos protein occurred in rats intoxicated by a single dose of soman (organophosphate compound and irreversible cholinesterase inhibitor) only in animals that had seizures. Comparison of immunohistochemistry that localizes Fos protein and of in situ hybridization that localizes its mRNA showed that there was an early and explosive expression of mRNA in many cerebral regions followed by transitory immunoreactivity in only some regions (piriform cortex, entorhinal area, hippocampus). The levels of mRNA and c-fos-like immunoreactivity decreased slowly and returned to basal level 24 h after soman administration.

Animals↗
PubMed1993

Long-term changes in regional brain cytochrome oxidase activity induced by electroconvulsive treatment in rats.

Quantitative cytochrome oxidase (CO) histochemistry was used to examine brain regional metabolic effects of electroconvulsive shock-induced seizures (ECS). Rats receive a course of either eight ECS or control treatments and were sacrificed either 24 h or 28 days after the last session. Regional CO activity (mumol/gT/min) was quantitated throughout the brain using internally calibrated standards. Twenty-four hours after the last ECS session there was no significant difference between ECS- and sham-treated brains in any of the 99 brain regions examined. In contrast, 28 days after the last session, ECS brains showed significant increases in CO activity in the interpeduncular nucleus (+20%), bed nucleus of the stria terminalis (+25%), dorsomedial hypothalamus (+20%), ventromedial hypothalamus (+12%), mammillary nucleus (+14%), pontine nucleus (+16%), basolateral amygdala (+14%), medial amygdala (+12%), piriform cortex (+12%) and ventromedial thalamus (+9%). These results suggest that ECS induces localized increases in brain CO activity which are long-lasting and may develop independently of additional stimulation. The fact that CO changes were predominantly in limbic areas suggests that they may be relevant to the antidepressant effects of ECS.

Animals↗
PubMed1994

Decreased muscarinic receptor binding in rat brain after paradoxical sleep deprivation: an autoradiographic study.

Previous work demonstrated that paradoxical sleep deprivation (PSD) leads to a decrease in yawning behavior elicited by cholinergic agonists, suggesting that a downregulation of cholinergic muscarinic receptors may occur after PSD. More recent work using intracerebral injections of muscarinic agonists has suggested a critical role for M2 receptors in paradoxical sleep. In this study [3H]AF-DX 384 was used to investigate the effects of PSD on M2-type cholinergic receptors throughout the brain using quantitative autoradiography. After 96 h of paradoxical sleep deprivation, [3H]AF-DX 384 binding was generally reduced throughout the brain, and significantly so in the olfactory tubercle (-20%), n. accumbens (-23%), frontal caudate-putamen (-16%), islands of Callejas (-20%), piriform cortex (-24%), lateral (-26%) and medial (-24%) septum, anteromedial (-19%), ventrolateral (-22%), and lateral geniculate (-15%) nuclei of thalamus, deep layers of the superior colliculus (-15%), entorhinal cortex (-12%) and subiculum (-23%). [3H]AF-DX 384 binding was reduced in pontine structures, but not to a higher degree than in other brain areas. The observed downregulation of M2-type muscarinic receptors after PSD may be causally related to the previously reported decrease in cholinergically induced behaviors after PSD.

Animals↗
PubMed1995

NMDA and non-NMDA receptors on rat supraoptic nucleus neurons activated monosynaptically by olfactory afferents.

The recently discovered efferent projections from the main and accessory olfactory bulbs to the supraoptic nucleus (SON) were further investigated. Intracellular electrophysiological methods were used to determine (a) if these projections are monosynaptic, (b) which excitatory amino acid (EAA) receptor subtypes mediate responses to activation of these pathways and (c) whether the same receptor subtypes mediate responses of phasically firing (vasopressin) and continuously firing (putative oxytocin) neurons. Recordings were made from SON neurons in large explants and 500 microns thick horizontal slices, containing 2-6 mm of the piriform cortex and lateral olfactory tract (LOT). This allowed recording of synaptic responses to selective stimulation of the LOT. EPSPs in SON neurons faithfully followed stimulus frequencies of 50-100 Hz, indicating that these inputs were monosynaptic. Stimulus-evoked EPSPs were blocked by the non-specific EAA antagonist, kynurenate. Perifusion of the slice with Mg(2+)-free medium revealed the presence of NMDA receptors in addition to the non-NMDA receptors on both phasically and continuously firing cells, indeed, on all cells tested. Partial blockade of these EPSPs in Mg(2+)-free medium could be achieved with either the NMDA antagonist, AP5, or the non-NMDA antagonist, CNQX or NBQX. Full blockade of the stimulus-evoked EPSPs was effected by adding both types of antagonists to the medium, although spontaneous EPSPs were still observed in several cells. These results are consistent with prior studies showing both receptor subtypes in the SON. This is the first demonstration that afferent stimulation activates both subtypes in the same SON neuron regardless of its peptide content.

2-Amino-5-phosphonovalerate↗
PubMed1995

NBQX, a selective antagonist of the AMPA receptor, affects neither field potentials nor long-term potentiation in vivo.

NBQX (2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline), a selective antagonist of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) receptors, at an anticonvulsant dose of 40 mg/kg (i.p.), was shown in vivo to have no effects on either the field potentials in the piriform cortex or those in the dentate gyrus of the hippocampus. The same dose of NBQX also exerted no significant effects on long-term potentiation in the hippocampus. These results suggest that the mechanism underlying the anticonvulsant action of NBQX in vivo does not involve a suppressive action on physiological synaptic transmission. The possible clinical usefulness of AMPA receptor antagonists as antiepileptic drugs is suggested.

Animals↗
PubMed1995

Distribution of Fos-positive neurons in cortical and subcortical structures after picrotoxin-induced convulsions varies with seizure type.

The distribution of Fos protein was mapped in rat brain following a single non-focal convulsive seizure. Single seizures were induced with intravenous picrotoxin in unhandled animals housed in isolation. Different convulsive behaviours occurred unpredictably. The least severe seizures were predominantly localised to the face, head and forelimbs, without loss of posture control (restricted seizures). The most extensive seizures affected all limbs and trunk, sometimes with falling (generalised seizures). There was a correlation between seizure behaviour and distribution of Fos induction. After restricted seizures, Fos was induced at highest levels in neocortex and piriform cortex and was prominent in entorhinal cortex, caudal-ventral caudate-putamen and amygdala. Regions of thalamus were consistently and lightly labelled, but Fos induction did not occur in hippocampus. After generalised seizures, there was Fos induction in cortex but less than after restricted seizures and, in three of four animals, also in dentate gyrus, hippocampus and subiculum. There was occasional or variable labelling of thalamus, basolateral amygdala and caudate-putamen. One animal with generalised seizures showed no hippocampal Fos induction. The findings indicate that picrotoxin induces seizures with at least two different patterns of neuronal involvement. The cortex, part of the caudate-putamen, amygdala and thalamus are involved in restricted seizures while the hippocampus, cortex and thalamus are involved in generalised seizures. The results do not support the view that generalised seizures are a progression from restricted forms. Cortical Fos involvement is entirely consistent with the participation of cortex in non-focal epilepsy. In these non-focal seizures, the dentate-hippocampus may be a source of excitation to cortex in the generalised group while the cortex appears to be the predominant site of excitation in the restricted group.

Animals↗
PubMed1995

Expression of non-angiotensin II -125I-CGP 42112 binding sites on activated microglia after kainic acid induced neurodegeneration.

[125I]CGP 42112, first developed to identify angiotensin II receptor subtype 2 (AT2), was recently shown to bind to a novel non-angiotensin binding site in injured rat brain tissue. We addressed the question whether non-angiotensin [125I]CGP 42112 binding appears after kainic acid induced hippocampal neurodegeneration, a process of neuronal cell death at a distance from the toxin injection site. After intraventricular kainic acid injection, we found non-angiotensin [125I]CGP 42112 binding in the hippocampal areas CA3 (4 and 14 days after injection), CA1 and CA4 and the subiculum (14 days after injection). In addition, 14 days after kainic acid injection, [125I]CGP 42112 binding was found in 50% of the animals, in the thalamus, amygdala and piriform cortex, areas receiving projections from the hippocampus and suffering kainic acid induced delayed neurodegeneration. The loss of neurons in these regions was accompanied by an accumulation of activated microglia as demonstrated by immunostaining with the specific antibodies OX-42 and ED1. The time course and regional pattern of OX-42/ED1 positive immunostaining was identical with the appearance and distribution of the non-angiotensin [125I]CGP 42112 binding site. The non-angiotensin [125I]CGP 42112 binding was not detected in brain regions unaffected by kainic acid injection. Our findings indicate the expression of a novel [125I]CGP 42112 binding site on activated microglia. This site appears at a distance from the lesion and may be of importance in the process of neuronal death and brain tissue repair.

Angiotensin II↗
PubMed1996

Regional distribution and time-course of calpain activation following kainate-induced seizure activity in adult rat brain.

Systemic injection of kainic acid (KA) in adult rat elicits a pattern of neuronal pathology which exhibits several features of human temporal lobe epilepsy. KA-induced seizure activity is accompanied by the activation of the calcium-dependent protease calpain in limbic structures. In the present study, we evaluated the spatio-temporal activation of calpain after the onset of seizure activity by immunohistochemistry using an antibody for the spectrin breakdown product (sbdp) generated by calpain-mediated spectrin proteolysis. In addition, we compared the changes in sbdp immunoreactivity with those in immunoreactivity to subunits of the Glu/AMPA receptors (GluR1 and GluR2/3). One hour after seizure onset, sbdp accumulation was observed in selected interneurons in stratum oriens and in the hilus of the dentate gyrus. By 4 h, sbdp immunoreactivity was prominent in dendritic fields of the hippocampus as well as in neurons in thalamus and piriform cortex. By 8 h, sbdp immunoreactivity had disappeared from interneurons but was localized in pyramidal cell bodies in hippocampus. Intense labeling of cell bodies and dendritic fields persisted until 5 days following KA treatment. Changes in GluR subunit immunoreactivity were mirror images of those seen for sbdp. In general, increased sbdp immunoreactivity in dendritic fields was associated with decreased GluR1 immunoreactivity. However, increased sbdp immunoreactivity in neuronal perikarya was also associated with increased GluR immunoreactivity. These results indicate that calpain activation following seizure onset exhibits a specific spatio-temporal pattern, with activation in restricted interneurons preceding widespread activation in pyramidal neurons. Calpain activation also precedes neuronal pathology and could thus represent an initial trigger for neuronal pathology. Finally, the results suggest that calpain activation produces rapid alterations in GluR subunit properties which could be involved in the hyperexcitability observed following seizure activity.

Animals↗
PubMed1996

Distribution of AT4 receptors in the Macaca fascicularis brain.

Angiotensin IV (Val Tyr Ile His Pro Phe), administered centrally, increases memory retrieval and induces c-fos expression in the hippocampus and piriform cortex. Angiotensin IV binds to a high affinity site that is quite distinct in pharmacology and distribution from the angiotensin II AT1 and AT2 receptors and is known as the AT4 receptor. These observations suggest that the AT4 receptor may have multiple central effects. The present study uses in vitro receptor autoradiography, and employs [125I]angiotensin IV to map AT4 receptors in the macaca fascicularis brain. The distribution of the AT4 receptor is remarkable in that its distribution extends throughout several neural systems. Most striking is its localization in motor nuclei and motor associated regions. These include the ventral horn spinal motor neurons, all cranial motor nuclei including the oculomotor, abducens, facial and hypoglossal nuclei, and the dorsal motor nucleus of the vagus. Receptors are also present in the vestibular, reticular and inferior olivary nuclei, the granular layer of the cerebellum, and the Betz cells of the motor cortex. Moderate AT4 receptor density is seen in all cerebellar nuclei, ventral thalamic nuclei and the substantia nigra pars compacta, with lower receptor density observed in the caudate nucleus and putamen. Abundant AT4 receptors are also found in areas associated with cholinergic nuclei and their projections, including the nucleus basalis of Meynert, ventral limb of the diagonal band and the hippocampus, somatic motor nuclei and autonomic preganglionic motor nuclei. AT4 receptors are also observed in sensory regions, with moderate levels in spinal trigeminal, gracile, cuneate and thalamic ventral posterior nuclei, and the somatosensory cortex. The abundance of the AT4 receptor in motor and cholinergic neurons, and to a lesser extent, in sensory neurons, suggests multiple roles for the AT4 receptor in the primate brain.

Acetylcholinesterase↗