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PubMed1998

Differential expression of c-fos mRNA and Fos protein in the rat brain after restraint stress or pentylenetetrazol-induced seizures.

1. c-fos mRNA expression and Fos protein expression were investigated by in situ hybridization and immunohistochemistry after 30 min of forced restraint stress or pentylenetetrazol (PTZ; 64 mg/kg, i.p.)-induced seizures. 2. Forced restraint stress and PTZ-induced seizures generated c-fos mRNA expression of distinct intensities, but in similar brain regions, including the hippocampus, the amygdala, the piriform cortex, the paraventricular hypothalamic nucleus, the habenula, and parts of the cerebral cortex. 3. The distribution of Fos-like immunoreactivity induced by stress or seizures only partially overlap. No Fos-like expression was found in the hippocampus or the habenula after restraint stress. Nevertheless, both areas presented Fos-like expression after PTZ-induced seizures. 4. Our results support the suggestion that immediate early gene expression in vivo may exhibit both region- and stimulus-specific expression.

Animals↗
PubMed1994

Differential expression of Fos protein in the brain of female mice dependent on pup sensory cues and maternal experience.

Immunoreactivity for Fos protein following 30 min of sensory and behavioral experience with foster pups was measured in different brain areas of nulliparous female Balb/c mice who were intact, ovariectomized, or selectively depleted of olfactory bulb noradrenaline. Fos expression was also investigated in intact nulliparous female mice undergoing distal exposure to pup sensory cues. Behavioral interaction with pups increased Fos immunoreactivity in the olfactory areas (anterior olfactory nucleus, piriform cortex, corticomedial amygdala, and entorhinal cortex) as well as in the medial preoptic area, and this occurred regardless of whether females were intact or ovariectomized. Noradrenaline depletion of the olfactory bulb prevented Fos induction in primary olfactory areas, but not in the medial preoptic area, whereas distal exposure to pup cues enhanced Fos expression in the olfactory areas but not in the medial preoptic area.

Amygdala↗
PubMed1996

The effects of olfactory and somatosensory desensitization on Fos-like immunoreactivity in the brains of pup-exposed postpartum rats.

Fos-like immunoreactivity (fos-lir) was examined in sites within the "maternal circuit" in postpartum female rats that received various sensory desensitizations and were exposed to pups for 1 or 2 hr. Neither olfactory bulbectomy nor thelectomy (nipple removal) significantly reduced the fos-lir in the anterior medial preoptic area (MPOA), although reductions following bulbectomy in medial amygdala did occur. Peripherally induced hyposmia by ZnSo4 reduced fos-lir in the olfactory structures (olfactory bulbs, piriform cortex, and olfactory tubercle), in medial and cortical nuclei of the amygdala, but not in anterior MPOA. Application of the topical anesthetic Emla to the ventrum only reduced fos-lir in the somatosensory cortex. Combined olfactory and ventral desensitizations produced marginal reductions in posterior MPOA. It is suggested that the MPOA is primarily involved as part of the effector system in the expression of the behavior. In contrast, the amygdala is involved in processing sensory cues received from pups during dam-litter interactions.

Afferent Pathways↗
PubMed1999

The role of cognitive and affective processing in a transgenic mouse model of cortical-limbic neuropotentiated compulsive behavior.

Obsessive compulsive disorder (OCD) may involve abnormal cortical-limbic processing or responsiveness. Mice with behaviors resembling the symptoms of OCD and related disorders were made by expression of a neuropotentiating cholera toxin (CT) transgene in cortical-limbic D1 receptor-expressing neurons. Because these D1CT mice express CT in the piriform cortex and amygdala (major cognitive and affective olfactory processing areas) it was tested whether abnormal odor perception, discrimination, or responsiveness facilitates their compulsion-like behavior. The mice exhibited normal olfactory discriminative capability. An anxiogenic odor potentiated their abnormal repetitive leaping, but novel or familiar nonthreatening odors did not. These data suggest that compulsions can be triggered not by impaired cortical-limbic processing but by increased cortical-limbic responsiveness, particularly to sensory or cognitive stimuli with affective properties.

Animals↗
PubMed1975

Functional organization of the rat amygdala with respect to avoidance behavior.

Bilateral electrolytic lesions in the periamygdaloid piriform cortex of female albino rats produced marked disruptive effects on the acquisition of active avoidance responses in a 1-way as well as a 2-way test situation, significantly impaired passive avoidance behavior, and inhibited feeding in a novel environment. Lesions in each of the 6 major subdivisions of the amygdala (cortical, medial, central, intercalated, lateral, and basolateral nuclei) consistently produced facilitatory effects on active avoidance behavior in 1-way as 2-way situations. Passive avoidance behavior was impaired in animals with lesions in the central, intercalated, and basolateral nuclei. Damage to the anterior amygdaloid area or the the nuclei of the lateral olfactory tract did not reliably affect active or passive avoidance behavior.

Agonistic Behavior↗
PubMed1994

N-acetylaspartate as an in vivo marker of neuronal viability in kainate-induced status epilepticus: 1H magnetic resonance spectroscopic imaging.

N-acetylaspartate (NAA) has been proposed as a marker of neuronal density. Therefore, regional measurement of NAA by magnetic resonance spectroscopic imaging (MRSI) may provide a sensitive method for detection of selective neuronal loss, in contrast to conventional imaging techniques such as magnetic resonance imaging (MRI). To test this hypothesis, we produced selective neuronal injury by kainate-induced status epilepticus. Three days later three-dimensional 1H-MRSI was obtained and compared with conventional T2-weighted MRI and histological findings in normal and kainate-treated rats. Reduction of NAA determined by MRSI in piriform cortex, amygdala, and hippocampus correlated well with neuronal injury determined from histology. Changes of NAA, without any MRI changes in hippocampus, indicated greater sensitivity of MRSI for detection of neuronal injury. These results are consistent with the hypothesis that reduction of NAA measured by MRSI may be a sensitive marker of neuronal injury in vivo in a variety of disease states.

Animals↗
PubMed1995

The influence of acidosis on hypoglycemic brain damage.

The objective of the study was to explore whether hypoglycemic brain damage is affected by super-imposed acidosis. To that end, animals with insulin-induced hypoglycemic coma, defined in terms of a negative DC potential shift, massive release of K+, or cellular uptake of Ca2+, were exposed to excessive hypercapnia (PaCO2 approximately 200 or approximately 300 mm Hg) during the last 25 min of the 30-min coma period. Animals were allowed to survive for 7 days before their brains were fixed by perfusion, and the cell damage was assessed by light microscopy. Other animals were analyzed with respect to changes in extracellular pH (pHe) or extracellular K+ or Ca2+ concentrations (K+e and Ca2+e, respectively). The total CO2 content (TCO2) was also measured to allow derivation of intracellular pH (pHi). The increase in PaCO2 to 190 +/- 15 and 312 +/- 23 mm Hg (means +/- SD) reduced the pHe from a predepolarization value of approximately 7.4 and a postdepolarization value (after the first 5 min of coma) of approximately 7.3 to 6.8 and 6.7, respectively. The corresponding mean pHi values were 6.7 and 6.5. The hypercapnia did not alter the K+e, which rose to 50-60 mM at the onset of hypoglycemic coma, but it increased the Ca2+e from approximately 0.05 to 0.10-0.16 mM. Normocapnic animals with induced hypoglycemic coma of 30-min duration showed the expected neuronal lesions in the neocortex, hippocampus, and caudoputamen. Hypercapnia clearly aggravated this damage, particularly in the caudoputamen, subiculum, and CA1 region of the hippocampus, and caused additional damage to cells in the CA3 region and piriform cortex. A rise in CO2 tension from approximately 200 to 300 mm Hg did not further aggravate the damage. The results thus demonstrate that relative moderate acidosis aggravates damage that is believed to be mostly neuronal, sparing glia cells and vascular tissue.

Acidosis↗
PubMed2001

Telencephalic cells take a tangent: non-radial migration in the mammalian forebrain.

During development of the mammalian telencephalon, cells migrate via diverse pathways to reach their final destinations. In the developing neocortex, projection neurons are generated from cells that migrate radially from the underlying ventricular zone. In contrast, subsets of cells that populate the ventral piriform cortex and olfactory bulb reach these sites by migrating long distances. Additionally, it has been recently established that cells migrate tangentially from the ventral ganglionic eminences to the developing cortex. These tangentially migrating cells are a significant source of cortical interneurons and possibly other cell types such as oligodendrocytes. Here we summarize the known routes of migration in the developing telencephalon, with a particular focus on tangential migration. We also review recent genetic and transplantation studies that have given greater insight into the understanding of these processes and the molecular cues that may guide these migrating cells.

Animals↗
PubMed1997

Localization of Fos-like immunoreactivity induced by the NK3 tachykinin receptor agonist, senktide, in the guinea-pig brain.

1. The effects of intracerebroventricular (i.c.v.) administration of the NK3 tachykinin receptor agonist, senktide (10 nmol each side), in guinea-pigs pretreated with the selective NK3 tachykinin receptor antagonist, SR142801 (3 mg kg(-1) subcutaneous, s.c., 30 min before senktide), or its less active enantiomer, SR142806 (3 mg kg(-1) s.c. 30 min before senktide), on behaviour and on the distribution of Fos-like immunoreactivity (Fos-LI) in central neurones were investigated. Guinea-pigs were chosen for the study since they possess NK3 tachykinin receptors with pharmacological characteristics similar to those in man. 2. Wet-dog shakes, but not locomotor activity, elicited by senktide i.c.v. were significantly reduced by SR142801 but not by SR142806, confirming the involvement of NK3 tachykinin receptors in wet-dog shake behaviour. 3. Senktide induced increased numbers of Fos-LI neurones in the following brain areas: frontal, parietal and piriform cortex, the lateral septum, the CA1, CA2, subiculum and dentate gyrus of the hippocampus, most areas in the amygdala, thalamus and hypothalamus, medial geniculate nucleus and the ventral cochlear nucleus. Pretreatment with SR142801, but not with SR142806, before administration of senktide inhibited Fos-LI expression in the cingulate cortex, dentate gyrus of the hippocampus, some regions of the thalamus, hypothalamus and amygdala and the ventral cochlear nucleus. 4. The present results are the first demonstration that senktide induces Fos-LI in widespread areas of the guinea-pig brain. It is proposed that NK3 tachykinin receptors may play a more extensive role in the control of diverse brain functions, including cortical processing, learning and memory, neuroendocrine and behavioural regulation, than is currently recognized.

Animals↗
PubMed2002

Behavioural and biochemical evidence for interactions between Delta 9-tetrahydrocannabinol and nicotine.

Behavioural and pharmacological effects of Delta9-tetrahydrocannabinol (THC) and nicotine are well known. However, the possible interactions between these two drugs of abuse remain unclear in spite of the current association of cannabis and tobacco in humans. The present study was designed to analyse the consequences of nicotine administration on THC-induced acute behavioural and biochemical responses, tolerance and physical dependence. Nicotine strongly facilitated hypothermia, antinociception and hypolocomotion induced by the acute administration of THC. Furthermore, the co-administration of sub-threshold doses of THC and nicotine produced an anxiolytic-like response in the light - dark box and in the open-field test as well as a significant conditioned place preference. Animals co-treated with nicotine and THC displayed an attenuation in THC tolerance and an enhancement in the somatic expression of cannabinoid antagonist-precipitated THC withdrawal. THC and nicotine administration induced c-Fos expression in several brain structures. Co-administration of both compounds enhanced c-Fos expression in the shell of the nucleus accumbens, central and basolateral nucleus of the amygdala, dorso-lateral bed nucleus of the stria terminalis, cingular and piriform cortex, and paraventricular nucleus of the hypothalamus. These results clearly demonstrate the existence of a functional interaction between THC and nicotine. The facilitation of THC-induced acute pharmacological and biochemical responses, tolerance and physical dependence by nicotine could play an important role in the development of addictive processes.

Animals↗
PubMed2004

Bv8, the amphibian homologue of the mammalian prokineticins, modulates ingestive behaviour in rats.

1. The small protein Bv8, secreted by the skin of the frog Bombina variegata, belongs to a novel family of secreted proteins whose mammalian orthologues have been identified and named prokineticins (PK-1 and PK-2). 2. Bv8 (from 2.5 to 60 pmol) injected into the lateral ventricles of rat brain suppressed diurnal, nocturnal, deprivation-induced and neuropeptide Y-stimulated feeding and stimulated diurnal drinking. Nocturnal drinking was increased only in fasted rats. 3. PK-2 mRNA is expressed in discrete areas of the rat brain, including the suprachiasmatic nucleus (SCN), medial preoptic area (MPA) and nucleus of the solitary tract (NTS). In the SCN neurons, PK-2 mRNA is highest during the light phase of the circadian cycle and undetectable during the dark phase. 4. The G-protein-coupled receptor prokineticin receptor 2 (PKR-2), which binds Bv8 and PK-2 with high affinity, is mainly expressed in the piriform cortex, paraventricular thalamic nucleus, parataenial nucleus (PT), SCN, hypothalamic paraventricular (PVH) and dorsomedial (DMH) nuclei, arcuate nucleus (ARC) and subfornical organ (SFO) of the rat brain. 5. Bv8 microinjected into the ARC, at doses from 0.02 to 2.0 pmol during night-time or from 0.2 to 5 pmol in 24-h-fasted rats, selectively suppressed feeding without affecting drinking. When injected into the SFO, Bv8 (from 0.2 to 2 pmol) stimulated drinking but did not affect feeding. Bv8 injections into other brain areas left rat ingestive behaviours unchanged. 6. We hypothesize that PK-2-rich projections from SCN neurons to PKR-expressing ARC neurons could transmit the circadian rhythm of feeding, whereas inputs from the PK-2-expressing NTS neurons to the PKR-2-expressing SFO neurons could transmit visceral information on the water-electrolyte balance and osmotic regulation.

Amphibian Proteins↗
PubMed2006

Matrix metalloproteinase-mediated disruption of tight junction proteins in cerebral vessels is reversed by synthetic matrix metalloproteinase inhibitor in focal ischemia in rat.

Matrix metalloproteinases (MMPs) disrupt the blood-brain barrier (BBB) during reperfusion. Occludin and claudins are recently described tight junction proteins (TJPs) that form the BBB. We hypothesized that the opening of the BBB was because of the degradation of TJPs by the MMPs. Spontaneously hypertensive rats had a 90 mins middle cerebral artery occlusion with reperfusion for 2, 3, or 24 h. Matrix metalloproteinases were measured by immunohistochemistry and in situ and gel zymography. Real-time polymerase chain reaction (PCR) measured mRNAs of MMP-2 and -9, furin, membrane-type MMP (MT1-MMP), occludin, and claudin-5. There was opening of the BBB in the piriform cortex after 3 h of reperfusion, and an MMP inhibitor, BB-1101 (30 mg/kg), prevented the opening. At 3 h, in situ zymograms showed gelatinase activity. Zymography and PCR showed greater increases in MMP-2 than in MMP-9. There were increased mRNA and immunohistochemistry for MT1-MMP and furin, which activate MMP-2. Claudin-5 and occludin mRNA expression decreased at 2 h in both hemispheres with fragments of both proteins seen on Western blot by 3 h on the ischemic side; treatment with BB-1101 reversed the degradation of the TJPs. Immunohistochemistry at 3 h showed fragmented TJPs within the endothelial cell clefts. By 24 h, in situ zymography showed gelatinase activity and gel zymography showed elevated levels of MMP-9. Disrupted TJPs previously seen in endothelial cells appeared in the surrounding astrocytes. Our results provide direct evidence that MMPs open the BBB by degrading TJPs and that an MMP inhibitor prevents degradation of the TJPs by MMPs.

Animals↗
PubMed2003

Cloning of murine TReP-132, a novel transcription factor expressed in brain regions involved in behavioral and psychiatric disorders.

In recent studies that addressed the transcriptional control of steroid synthesis, a transcriptional regulating protein of 132 kDa (TReP-132) was cloned and demonstrated to regulate expression of the human P450 side chain cleavage (P450scc) gene. In the present study, we describe the cloning and characterization of the mouse orthologue of the human factor, mouse transcriptional regulating protein (mTReP-132). mTReP-132 encodes a 1216-residue protein that is 85.5% homologous to the human protein. Both factors contain characteristic motifs, namely glutamine-, proline- and acidic-rich regions. The primary structure also exhibits two zinc fingers of the C(2)H(2) subtype, suggesting that this protein has the ability to act as a DNA binding transcription factor. mTReP-132 may also be a co-regulator of nuclear receptors because of two nuclear box motifs in this protein. Northern blot analysis demonstrated the expression of two transcripts of 4.4 and 7.5 kb in several tissues, but expression was clearly highest in the brain, thymus and testis of mice. In the brain, the hybridization signal was quite localized and strong in the basal ganglia, hippocampus, piriform cortex, cerebral cortex, ventromedial nucleus of the hypothalamus, and the dorsal and superior central nuclei of the raphe. Although classical steroidogenesis pathways have yet to be firmly established in the brain, expression of both mTReP-132 and P450scc provides anatomical evidence that mTReP-132 may regulate this key steroidogenic enzyme within specific regions involved in behavioral and psychiatric disorders. Moreover, the presence of both mTReP-132 and steroidogenic factor 1 (SF-1) transcripts in the ventromedial nucleus of the hypothalamus suggests a role for mTReP-132 in brain development and function. The molecular cloning and the highly specific expression of mTReP-132 across the brain further consolidate the hypothesis that this tissue is able to synthesize de novo steroids in a region-specific manner.

Adrenal Glands↗
PubMed1968

Excitatory acidic amino acids and the cation content and sodium ion flux of isolated tissues from the brain.

1. Sample from the neocortex and piriform cortex of guinea pigs and rats were incubated in inulin-containing glucose-saline. Their intracellular (non-inulin) space contained 19-27muequiv. of Na(+)/g. of original tissue. These values were stable between 30 and 100min. after incubation commenced, but addition of (22)NaCl to the neocortical samples showed them to be associated with a flux of 400muequiv. of Na(+)/g. of tissue/hr. 2. Addition of 0.5-10mm-l-glutamic acid or 0.1mm-N-methyl-dl-aspartic acid rapidly increased the tissue's Na(+) content; N-acetyl-dl-aspartic acid was without action. 3. During the first 1-1.5min. after the addition of l-glutamic acid to neocortical samples their Na(+) content increased at 600muequiv./g. of tissue/hr., and the rate of (22)Na(+) influx corresponded to 1230muequiv. of Na(+)/g./hr. These rates were calculated to be sufficiently rapid to account for loss of the tissue's normal membrane potential within 1-2sec. of the addition of the acid. 4. In addition, a rapid but more limited loss of K(+) took place after the addition of l-glutamic acid or the methylaspartic acid; on continued incubation tissue K(+) content increased, as also did the intracellular volume of the tissue, from its original 670mul./g. to 1100mul./g. 5. Interpretation of these and of associated changes is offered in terms that involve a cation pump and the permeability changes associated with the nerve impulse.

Amino Acids↗
PubMed2001

Discharge threshold is enhanced for several seconds after a single interictal spike in a model of focal epileptogenesis.

Interictal spikes (ISs) are typically observed between seizures in focal epilepsies. Whether ISs are causally involved or represent protective elements in the transition toward an ictal discharge is an open question. Previous studies suggested that inhibition or disfacilitation occurs during the period elapsing between two ISs induced by local application of either bicuculline or penicillin in the piriform cortex of the in vitro isolated guinea pig brain preparation. We further investigated this issue by studying responses to afferent stimulation during the interspike period (6.3 +/- 2.5 s; mean +/- SD). Properly set stimulation intensity of the lateral olfactory tract resets ISs exclusively (and not before) 4-10 s (5.6 +/- 2.0 s; mean +/- SD) after a preceding spontaneous spike. This finding demonstrates the existence of a period of enhanced threshold to stimulus-evoked activation that coincides with the interspike interval in the absence of stimulation. Current source density analysis of depth laminar profiles demonstrated that both stimulus-evoked and spontaneous ISs were generated by the activation of an identical cortical circuit. Our study suggests that interictal spiking could play a protective role or at least provide an effective restraint against the onset of a focal ictal discharge.

Action Potentials↗
PubMed2001

Control elements between -9.5 and -3.0 kb in the human tissue-type plasminogen activator gene promoter direct spatial and inducible expression to the murine brain.

Tissue-type plasminogen activator (t-PA) participates in the control of synaptic plasticity and memory formation in the central nervous system (CNS). Transgenic mice harbouring either 9.5, 3.0 or 1.4 kb of the human t-PA promoter fused to the LacZ reporter gene were used to assess t-PA promoter-directed expression in vivo. The 9.5 kb t-PA promoter directed expression to the brain, most notably to the dentate gyrus, superior colliculus, hippocampus, thalamus and piriform cortex. Staining was also observed in the retrosplenial and somatosensory cortex. The 3.0 kb t-PA promoter directed generalized and poorly defined expression to the cortex and hippocampus, while the 1.4 kb t-PA promoter directed expression selectively to the medial habenula. Intravenous administration of lipopolysaccharide into mice harbouring the 9.5 kb t-PA promoter resulted in an increase in reporter gene activity in the lateral orbital cortex and thalamus. Results of in vitro transfection experiments of NT2 cells with a series of t-PA promoter deletion constructs confirmed the presence of regulatory elements throughout the 9.5 kb promoter region. Finally, we describe a cis-acting element related to the NFAT recognition site that provides a protein-binding site and which may play a role in the selective expression of the 1.4 t-PA promoter in the medial habenula. These results indicate that elements between -3.0 and -9.5 kb of the t-PA promoter confer constitutive and inducible expression to specific regions of the CNS.

Animals↗
PubMed1997

Castration decreases single cell levels of mRNA encoding glutamic acid decarboxylase in the diagonal band of broca and the sexually dimorphic nucleus of the preoptic area.

Using quantitative in situ hybridization histochemistry (ISHH), we determined the effect of castration on single cell levels of glutamic acid decarboxylase (GAD) mRNA in discrete hypothalamic regions of the male rat brain associated with the control of gonadotropin secretion. A 48-base oligodeoxynucleotide probe was used to detect with equal affinity the two isoforms of GAD message, GAD65 and GAD67. GAD message also was quantitated in a number of selected areas of the brain to contrast GAD gene expression amongst several populations of GABAergic neurons. Comparison of 11 brain regions demonstrated a 9.3-fold range in the quantity of single cell GAD mRNA with levels being highest in the amygdala and the diagonal band of Broca, moderate in the piriform cortex, caudate nucleus, substantia innominata, globus pallidus, cingulate cortex and medial septal nucleus, and lowest in the lateral septal nucleus and the medial preoptic nucleus (MPN). Castration markedly reduced single cell GAD mRNA levels in the DBB and the MPN, two discrete hypothalamic structures known to contain dendritic fields, cell bodies, and axons of GnRH neurons projecting to the median eminence. A striking finding was a dense core of steroid-sensitive GABAergic neurons within the MPN comprising the sexually dimorphic nucleus of the preoptic area (SDN-POA). Similar to the MPN as a whole, the amount of GAD mRNA expressed by cells in the SDN-POA of sham operated control rats was greater than in castrated animals. GAD mRNA levels were inversely related to serum LH titers, suggesting a role for these neurons in the mechanism controlling gonadal steroid negative feedback on LH secretion. This report provides the basis for future work to determine if GAD65, GAD67 or whether both isoforms are affected by gonadal steroid input.

Animals↗
PubMed1998

Region-specific expression of thyrotrophin-releasing hormone-degrading ectoenzyme in the rat central nervous system and pituitary gland.

Thyrotrophin-releasing hormone (TRH), a hypothalamic neuropeptide hormone and a putative neuromodulator/ neurotransmitter in the central nervous system is inactivated by the TRH-degrading ectoenzyme (TRH-DE), a TRH-specific metallopeptidase localized on the surface of neuronal brain cells in culture and on lactotrophic cells of the pituitary. After succeeding in cloning the cDNA of TRH-DE we now report on the cellular distribution pattern of this enzyme in rat brain, spinal cord and pituitary gland using in situ hybridization histochemistry. In the pituitary, TRH-DE mRNA was found both in the anterior and the neural lobe but not in the intermediate lobe. After treatment with triiodothyronine (T3) a dramatic increase in the mRNA levels of the TRH-DE and a decrease in the intensity of the TRH receptor could be observed in the anterior lobe of the pituitary. In brain, TRH-DE transcripts were predominantly found in neo- and allocortical regions with strongest signals in the olfactory bulb, the piriform cortex, the cerebral cortex, the granular layer of the cerebellar cortex and the pyramidal cells of the Ammon's horn. In the diencephalon, the highest TRH-DE mRNA levels were observed in the medial habenulae followed by several hypothalamic subregions. In the mesencephalon and brainstem, moderate signals were present in the superior colliculi, substantia nigra, dorsal raphe and in the periolivar region. In the spinal cord, TRH-DE mRNA positive neurons were present in all layers. The very distinct distribution of TRH-DE in the brain and the hormonal regulation of the adenohypophyseal enzyme support the concept that this peptidase serves very specialized functions.

Aminopeptidases↗