ライフサイエンスコーパス: nerve terminal

1 s (DCVs) as they circulate in and out of the nerve terminal.

2 minode and in regulating excitability of the nerve terminal.

3 egulates the presynaptic excitability of the nerve terminal.

4 minode and in regulating excitability of the nerve terminal.

5 y and compared them to the mechanisms in the nerve terminal.

6 t anterograde, transport in the axon and the nerve terminal.

7 -endocytic sorting steps likely occur in the nerve terminal.

8 ing anterograde DCV transport in the axon or nerve terminal.

9 ynaptic release sites within the presynaptic nerve terminal.

10 results in approximately 10(6) free ATPs per nerve terminal.

11 naptic action potential (AP) waveform at the nerve terminal.

12 nly) complex, as might be found in a central nerve terminal.

13 to cannabinoid type 1 receptors on the motor nerve terminal.

14 ocytosis at the active zone of a presynaptic nerve terminal.

15 udy assembly and function of the presynaptic nerve terminal.

16 ynaptic myofiber surface and phagocytosis of nerve terminals.

17 at triggers neurotransmission at presynaptic nerve terminals.

18 oxins (BoNTs) possess unique specificity for nerve terminals.

19 S) contained the densest accumulation of MCH nerve terminals.

20 interacting with polarity-specific afferent nerve terminals.

21 ich inhibit neurotransmission at cholinergic nerve terminals.

22 exocytic machinery component SNAP25 in motor nerve terminals.

23 of synaptic vesicles and degeneration of the nerve terminals.

24 of continuous NET uptake and release at the nerve terminals.

25 degeneration and regeneration of peripheral nerve terminals.

26 of tubulovesicular structures at presynaptic nerve terminals.

27 at develop progressive degeneration of motor nerve terminals.

28 eristics of calcium currents recorded at the nerve terminals.

29 ly represents specific uptake in sympathetic nerve terminals.

30 ransmitter release at human peripheral motor nerve terminals.

31 ght (NF-L) protein in distal axons and motor nerve terminals.

32 studies to quantify presynaptic cholinergic nerve terminals.

33 regulator of SV replenishment in presynaptic nerve terminals.

34 vestibular hair cells to postsynaptic calyx nerve terminals.

35 ated protein 25 (SNAP-25) within presynaptic nerve terminals.

36 d an endocytic deficit specific to aminergic nerve terminals.

37 enhance glutamate release at cerebrocortical nerve terminals.

38 during high-frequency stimulation in central nerve terminals.

39 o a role in vesicle-related processes within nerve terminals.

40 ing showed that both proteins are present at nerve terminals.

41 ock neuro-muscular transmission by poisoning nerve terminals.

42 encodes a probable vesicular transporter in nerve terminals.

43 through non-Orai mechanisms but is absent at nerve terminals.

44 n of action potentials (APs) in auditory CNS nerve terminals.

45 e action potential (AP)-driven exocytosis at nerve terminals.

46 tic transmission and the normal structure of nerve terminals.

47 y controlled synaptic vesicle numbers within nerve terminals.

48 KR and its physiological modulation in small nerve terminals.

49 as a sign of acute activation of nociceptive nerve terminals.

50 ial cells decipher the strength of competing nerve terminals.

51 ges the proportion of presynaptically silent nerve terminals.

52 still formed in the absence of glutamatergic nerve terminals.

53 s level is modulated by neuronal activity in nerve terminals.

54 roteolytic conversion of proBDNF to mBDNF at nerve terminals.

55 probability for more mature calyces of Held nerve terminals.

56 tion sites, S76 and T181, of syndapin I from nerve terminals.

57 e differentiation and stabilization of motor nerve terminals.

58 monstrate that RyR1 plays a role in VICaR in nerve terminals.

59 rine/threonine protein phosphatase 2A in the nerve terminals.

60 ivity-driven Ca(2+) influx and exocytosis at nerve terminals.

61 s such as TMEM16a in GPCR-activation of itch nerve terminals.

62 y transient Ca(2+) elevations in presynaptic nerve terminals.

63 orrelates directly with the levels of Htt at nerve terminals.

64 al activity and pH regulation in presynaptic nerve terminals.

65 cytosis) to efficiently retrieve membrane at nerve terminals.

66 , vesicles are retrieved and recycled within nerve terminals.

67 y regulator of synaptic vesicle recycling at nerve terminals.

68 e-induced action potential discharge in itch nerve terminals.

69 ation of BoNT/C1 ad with diaphragmatic motor nerve terminals.

70 re and are characterized by poorly arborized nerve terminals.

71 deficits in transporter export to axons and nerve terminals.

72 n, the influx of Ca(2+) into the presynaptic nerve terminal activates a Ca(2+) sensor for vesicle fus

73 release of glutamate from the calyx of Held nerve terminal activates CP-AMPARs in the principal cell

74 in triggering the regeneration of peripheral nerve terminals affected by other forms of neurodegenera

75 nent of glutamate release in cerebrocortical nerve terminals after blocking Na(+) channels with tetro

76 The increase in FDG6P in nerve terminals agreed well with the increase in cortica

77 pathogenic role remains unclear, in healthy nerve terminals alpha-synuclein undergoes a cycle of mem

78 In normal nerve terminals, alpha-synuclein is present in an equili

79 raction were similar for axosomatic auditory nerve terminals, although rostral auditory nerve termina

80 2A (SV2A) can be used to index the number of nerve terminals, an indirect estimate of synaptic densit

81 icle, we review the role of synuclein at the nerve terminal and in membrane remodeling.

82 d pathway stabilizes AZ specification at the nerve terminal and that such a novel function is indepen

83 ects the synaptic strength of each competing nerve terminal and the state of synaptic competition.

84 Q-induced action potential discharge at itch nerve terminals and bouts of scratching by about 50%.

85 M) are closely associated with enteric motor nerve terminals and electrically coupled to smooth muscl

86 Parkinson's disease, is distributed both at nerve terminals and in the cell nucleus.

87 nin gene-related peptide (CGRP) from sensory nerve terminals and insulin from isolated pancreatic isl

88 e mutant form of SYT1 correctly localizes to nerve terminals and is expressed at levels that are appr

89 an vesicles just being exocytosed, occurs at nerve terminals and non-neuronal secretory cells.

90 lomeruli, releasing GABA and DA onto sensory nerve terminals and postsynaptic neurons.

91 rds a relationship between its generation at nerve terminals and structural synaptic pathology.

92 ave shown that silencing is achieved both at nerve terminals and the soma and is independent of membr

93 Immune cells at peripheral nerve terminals and within the spinal cord release media

94 s critical for targeting mitochondria to the nerve terminal, and a disruption in mitochondrial fissio

95 ) RyR1 plays a role in VICaR in hypothalamic nerve terminals; and (ii) a neuronal alteration accompan

96 nd propagation through this long presynaptic nerve terminal are unknown.

97 ogenous, nonvesicular glycine/GABA levels in nerve terminals are 5-7 mm, and that vesicular transport

98 Nerve terminals are a locus of this vulnerability, but h

99 -dependent mechanisms.SIGNIFICANCE STATEMENT Nerve terminals are highly specialized regions of a neur

100 We found that a fraction of nerve terminals are kept in a presynaptically silent sta

101 pinephrine released locally from sympathetic nerve terminals are significantly increased in the acute

102 ol, as well as on SV distribution within the nerve terminal, are virtually abolished in mouse SynI kn

103 to sustain cellular function and identifies nerve terminals as critical sites of proper metabolic co

104 cal defects were largely restricted to motor nerve terminals, as the ultrastructure of motoneuron som

105 elease and recycling of synaptic vesicles at nerve terminals, as well as with the architecture of the

106 howed abnormalities of striatal dopaminergic nerve terminals at an earlier stage than SJ1(RQ)KI mice.

107 ism for axons to independently functionalize nerve terminals at great distances from cellular somata.

108 the Drosophila brain, LRP4 localizes to the nerve terminals at or near active zones.

109 ecific effects were found on the presynaptic nerve terminals at the neuromuscular junction level, but

110 raction-induced injury occurs at or near the nerve terminal axon.

111 duration, and an end region near the tip of nerve terminal branches where the AP is briefer.

112 ted endocytosis and synaptic transmission at nerve terminals, but its potential role in synaptic deve

113 otoxicity has been characterized in cochlear nerve terminals, but much less is known about whether ex

114 ulinum neurotoxin type B (BoNT/B) recognizes nerve terminals by binding to 2 receptor components: a p

115 to profoundly impact information transfer at nerve terminals by controlling both vesicle priming and

116 eveal new mechanisms by which neuroendocrine nerve terminal Ca(2+) can be controlled in the brain.

117 rsts last seconds; however, the increases in nerve terminal Ca(2+) driven by neuropeptides can persis

118 e both capable of evoking large increases in nerve terminal Ca(2+) Increases in Ca(2+) driven by spik

119 xert powerful and long-lasting regulation of nerve terminal Ca(2+) independently from actions at the

120 ing in brain slices from mice to address how nerve terminal Ca(2+) is controlled in gonadotropin-rele

121 Using extracellular recording of CCSNs nerve terminals combined with in vivo confocal tracking

122 es, in particular when different presynaptic nerve terminals compete for the control of the same syna

123 ential-triggered Ca(2+) influx in inhibitory nerve terminals, consistent with the deficits in synapti

124 SCs phagocytose nerve terminals contacting the muscle fiber.

125 cles in gamma-aminobutyric acid (GABA)-ergic nerve terminals contain labeling for both VGLUT3 and the

126 Nerve terminals contain multiple sites specialized for t

127 y nerve terminals, although rostral auditory nerve terminals contained a greater concentration of syn

128 (tens of seconds) endocytosis in calyx-type nerve terminals containing conventional active zones and

129 ing that glutamate is enriched in inhibitory nerve terminals containing VGLUT3 compared to those lack

130 a very brief AP waveform and that the motor nerve terminal contains three distinct electrical region

131 tures, and auditory brainstem, glutamatergic nerve terminals corelease zinc to modulate excitatory ne

132 We determined the resting pH of the nerve terminal cytosol to be 7.30 +/- 0.02, and observed

133 ted dopaminergic neuronal loss, dopaminergic nerve terminal damage and behavioral deficits caused by

134 red to be normal at the stages when synaptic nerve terminals degenerated.

135 ular and molecular mechanisms of presynaptic nerve terminal degeneration.

136 ments leads to elevated BMP signaling within nerve terminals, driving excessive synaptic growth.

137 calcium (Ca(2+)) accumulating in presynaptic nerve terminals during repetitive action potentials.

138 hydrolase that degrades 2-AG in presynaptic nerve terminals-elevates 2-AG levels and suppresses the

139 rate, which is actively transported into the nerve terminal, eliciting vesicular depletion and revers

140 We show that neurotrophin stimulation of nerve terminals elicits new bclw transcripts that are im

141 ctive anterograde transport of the tracer to nerve terminal endings in bone, the periosteum (whole-mo

142 is approach to selective labeling of sensory nerve terminal endings will help to better identify how

143 ons of sensory neurons, and their peripheral nerve terminal endings, interact with bone.

144 ng presynaptic Ca(2+) rises and increases in nerve terminal excitability.

145 We have previously shown that nerve terminals exposed to spider or snake presynaptic n

146 ynaptic vesicles (SVs) from live hippocampal nerve terminals expressing vesicle-associated membrane p

147 itions at the basolateral pole, and auditory-nerve terminals extend towards the hair cell's apical en

148 tent reduction of the labeled chorda tympani nerve terminal field volume and density in the NTS follo

149 se surprising results suggest that gustatory nerve terminal fields remain plastic well into adulthood

150 rda tympani and greater superficial petrosal nerve terminal fields were 1.4x and 1.6x larger than age

151 ns that rely on hyperactivity of cholinergic nerve terminals for 25 years.

152 organizes the differentiation of excitatory nerve terminals formed onto them.

153 The nerve terminals found in the body wall of Drosophila mel

154 during elimination: their processes separate nerve terminals from each other and from the muscle fibe

155 dings suggest a more severe loss of striatal nerve terminal function compared with neuronal cell bodi

156 ion of subcellular components of sympathetic nerve terminal function does not occur simultaneously.

157 Thus, GnRH nerve terminal function is controlled over disparate tim

158 gy efficiency can be viewed as one aspect of nerve terminal function, in balance with others, because

159 ed, immediate rescue of deficits in dopamine nerve-terminal function in animals with a history of hig

160 he brain to counteract and regulate aberrant nerve terminal growth.

161 ular mechanisms of catecholamine handling in nerve terminals has not been investigated.

162 and Protein-kinase C (PKC) signaling in the nerve terminal have been widely implicated in the short-

163 rried by the vagus nerve, and vagal afferent nerve terminals have been well defined in animals.

164 these metabolic responses in mitochondria in nerve terminals have not been determined.

165 known neuronal metabolites, were compared in nerve terminals, homogenate, and cortex of anesthetized

166 We report, for the first time, a nerve terminal impairment in SV trafficking selectively

167 dependence of exocytosis on Ca(2+) entry at nerve terminals implies that voltage control of both Ca(

168 o-sensitive terminals and lower frequency of nerve terminal impulse discharges under mechanical stimu

169 igated the excitability of the calyx of Held nerve terminal in dysmyelinated auditory brainstems usin

170 estion using the calyx of Held (CH), a large nerve terminal in the auditory brainstem in mice.

171 Using the calyx of Held, a giant nerve terminal in the mouse brainstem, we evaluated the

172 Hence, we investigated isolated nerve terminals in brain slices by transecting hippocamp

173 s of metabolism in excitatory and inhibitory nerve terminals in mammalian systems.

174 ed Sox2 expression and formation of afferent nerve terminals in mouse utricles between postnatal days

175 in (aS) is a protein abundant in presynaptic nerve terminals in Parkinson disease (PD) and is a major

176 to the cytosol and function, for example, in nerve terminals in short-term synaptic plasticity.

177 3 receptors, increased glutamate release at nerve terminals in some LHb neurons.

178 tonin and norepinephrine, respectively, into nerve terminals in the brain.

179 P2X2 -IR identifies probable vagal nerve terminals in the central (Ce) subnucleus in the in

180 These findings demonstrate that nerve terminals in the corneal epithelium of mice and gu

181 explore the structure and neurochemistry of nerve terminals in the corneal epithelium of mice and gu

182 ordings of mechano- and polymodal-nociceptor nerve terminals in the corneal surface of Piezo2 conditi

183 s released from synaptic vesicles of certain nerve terminals in the hippocampus during neuronal activ

184 marker for dopamine production, in GABAergic nerve terminals in the median eminence suggested that ra

185 absence of tyrosine hydroxylase in GABAergic nerve terminals in the median eminence suggests that onl

186 to presynaptic gamma-aminobutyric acidergic nerve terminals in the NAcSh originating from the dorsal

187 ia, increase in tyrosine hydroxylase in both nerve terminals in the SAT and sympathetic ganglia neuro

188 other GPCRs) leads to activation of the itch nerve terminals in the skin, but previous studies have f

189 nt in synaptic vesicles in acetylcholinergic nerve terminals in the striatum.

190 le body and found degeneration of peripheral nerve terminals in the torso.

191 The degeneration of nerve terminals in Ub(G76V)-GFP-Syb2 mice was preceded b

192 Activation of MCH nerve terminals in vitro reduced firing of hippocampal p

193 in clinical development for mapping cardiac nerve terminals in vivo using PET.

194 Nerve terminals in which dynamin 1 and 3 have been repla

195 euronal activity when ATP consumption within nerve terminals increases drastically.

196 Voltage-gated Ca(2+) channels in presynaptic nerve terminals initiate neurotransmitter release in res

197 specially prominent for cholinergic C-bouton nerve terminal input onto motor neurons in affected C1q-

198 output processes: olfactory receptor neuron nerve terminals (input) and mitral/tufted cell apical de

199 rs of bouton-like swellings on stalks of the nerve terminals inversely correlate with release probabi

200 anes with high endocytic activity, including nerve terminals involved in neurotransmitter recycling,

201 data support the hypothesis that the sensory nerve terminal is able to release vesicles to fine-tune

202 ents show that the buffering capacity of the nerve terminal is markedly lower for Sr(2+) than for Ca(

203 of these toxins to target and bind to motor nerve terminals is a key factor determining their potenc

204 ervous system development, axon branching at nerve terminals is an essential step in the formation of

205 ired integrity of dopaminergic nigrostriatal nerve terminals is associated with nigrostriatal axonal

206 lation of acetylcholine receptors (AChRs) at nerve terminals is critical for signal transmission at t

207 The control of neurotransmitter release at nerve terminals is of profound importance for neurologic

208 numerous neurological diseases, its role at nerve terminals is poorly understood.

209 at direct uptake and oxidation of glucose in nerve terminals is substantial under resting and activat

210 gest that the overshoot pool exists at every nerve terminal, is of limited size arising from vesicles

211 the uptake and phosphorylation of glucose in nerve terminals isolated from rats infused with the gluc

212 esynaptic proteins in resting and stimulated nerve terminals isolated from the brains of Wistar rats.

213 iated primary neurons, we show that at small nerve terminals K(+) channels constrain the peak voltage

214 equency stimulation (HFS) of the presynaptic nerve terminal leads to a PcTx1-sensitive increase in in

215 Abnormal accumulation of Abeta at nerve terminals leads to synaptic pathology and ultimate

216 at many terminals, including the calyx-type nerve terminal, led to a well accepted "principle" that

217 ulation of Kv1.2 potassium channel in the IN nerve terminals likely augmented their excitability and

218 ow and rapid forms of vesicle endocytosis at nerve terminals, likely by functioning downstream of Ca(

219 The remaining two mutants displayed a nerve terminal localization but did not support efficien

220 %, respectively; (2) after correcting for DA nerve terminal loss, DA uptake per VMAT2 transport site

221 ns can perturb either axonal arborization or nerve terminal maturation, depending on the stage of del

222 he AP waveform along the length of the motor nerve terminal may explain the proximal-distal gradient

223 Nerve terminals may use all available vesicles to maximi

224 clearance of anti-ganglioside antibodies by nerve terminals might also be of sufficient magnitude to

225 peroxidation, we investigated the effect of nerve terminal mitochondrial dysfunction on airway senso

226 TMEM184b is necessary for normal peripheral nerve terminal morphology and maintenance.

227 e being enveloped in a single large afferent nerve terminal, named the calyx, and by the expression o

228 increases the rate of exocytosis in isolated nerve terminals, neuromuscular junctions, neuroendocrine

229 Degeneration of motor nerve terminals occurs in amyotrophic lateral sclerosis

230 leus, as well as to additional expression in nerve terminals of cortical projections to RA from the l

231 only in the soma but also in the presynaptic nerve terminals of GABAergic neurons.

232 we have performed live Ca(2+) imaging in the nerve terminals of gonadotropin-releasing hormone neuron

233 ELKS is required for normal Ca(2+) influx at nerve terminals of inhibitory hippocampal neurons.

234 component of the clearance occurred at motor nerve terminals of neuromuscular junctions, from where a

235 ed in neurons, such as motoneurons and motor nerve terminals of the neuromuscular junction (NMJ).

236 al accumulation of intermediate filaments in nerve terminals of the neuromuscular synapse and improve

237 iatum, the location of nigrostriatal pathway nerve terminals, of 3-month-old DJ-1 KO rats.

238 Consistent with previous reports, olfactory nerve terminals onto both cell types had a high release

239 ransmitter concentrations inside presynaptic nerve terminals, or the dynamics of vesicle refilling af

240 sine hydroxylase-immunolabeled (sympathetic) nerve terminals originating from the superior cervical g

241 s ranged in distribution from 3 to 111 motor nerve terminals per unit.

242 a tripartite synapse that is formed by motor nerve terminals, postjunctional muscle membranes, and te

243 OSCC tumors sensitize peripheral trigeminal nerve terminals, providing a unique opportunity to study

244 king of reinnervation, extracellular corneal nerve terminal recordings, tearing measurements in vivo,

245 ce that during action potential (AP) firing, nerve terminals rely on the glucose transporter GLUT4 as

246 neurotrophins affect synapses, particularly nerve terminals, remains unclear.

247 clear presence of the protein in inhibitory nerve terminals revealed by immunohistochemistry.

248 s of a tripartite synapse with a presynaptic nerve terminal, Schwann cells that ensheathe the termina

249 cytosis kinetics at hippocampal and cortical nerve terminals show a bi-phasic dependence on electrica

250 ctivity and the density of calyceal afferent nerve terminals (specific to Type I hair cells) increase

251 erable NMJs often fail to guide compensatory nerve terminal sprouts and to adopt a phagocytic phenoty

252 ervated NMJs and failed to initiate or guide nerve terminal sprouts at disease-vulnerable NMJs, a phe

253 mportant function for TMEM184b in peripheral nerve terminal structure, function, and the axon degener

254 Localization to the nerve terminal suggests a role in neurotransmitter relea

255 cate that alpha-SYN, present in dopaminergic nerve terminals supplying the subependymal zone, acts as

256 n's vast number of synapses, the presynaptic nerve terminal, synaptic cleft, and postsynaptic special

257 In a presynaptic nerve terminal, synaptic strength is determined by the p

258 In a nerve terminal, synaptic vesicle docking and release are

259 In a presynaptic nerve terminal, synaptic vesicle exocytosis is restricte

260 bles of cortical and hippocampal presynaptic nerve terminals (synaptosomes) from commonly used mouse

261 tripartite motor synapse consisting of motor nerve terminal, terminal Schwann cells (tSCs) and postsy

262 The calyx of Held is a giant nerve terminal that forms a glutamatergic synapse in the

263 n in this study reveals defects in the motor nerve terminal that may compensate for the muscle hypere

264 synaptogenesis at the calyx of Held, a large nerve terminal that selectively innervates the cell body

265 clearance mechanisms are present in central nerve terminals that regulate intracellular free calcium

266 ase neuropeptides and neurotransmitters from nerve terminals that regulate vascular, innate, and adap

267 addressed this apparent conflict at a large nerve terminal, the calyx of Held in rat brainstem, in w

268 depolarization at a large mammalian central nerve terminal, the rat calyx of Held, we report for the

269 As BoNTs act in the cytosol of nerve terminals, the entry into an appropriate compartme

270 t neuroblastoma cell line and isolated mouse nerve terminals, the N-terminal beta-amyloid fragment pr

271 yperexcitability near axon branch points and nerve terminals, thereby leading to uncontrolled movemen

272 ral neuropathy, such as depletion of sensory nerve terminals, thermal hypoalgesia, and nerve conducti

273 cryptin, promotes the assembly of inhibitory nerve terminals through integrin receptors.

274 in density or morphology of intra-epidermal nerve terminals throughout the course of vincristine tre

275 What causes a motor nerve terminal to degenerate remains unknown.

276 indicate that pathogenic Htt acts locally at nerve terminals to alter trafficking between endosomal c

277 e that pathogenic Htt can act locally within nerve terminals to disrupt synaptic endosomal signaling

278 Complexin functions at presynaptic nerve terminals to inhibit spontaneous SNARE-mediated sy

279 We show that SCs in mice lead nerve terminals to prepatterned AChRs.

280 functional properties of ion channels at the nerve terminals, using electrophysiology, dynamic Na(+)

281 Neuronal transmitters are released from nerve terminals via the fusion of synaptic vesicles with

282 tabotropic glutamate receptors on inhibitory nerve terminals was attenuated, allowing modulation of G

283 The percentage of primary auditory nerve terminals was larger in caudal AVCN, whereas non-p

284 at different regions along the length of the nerve terminal, we show that the terminal is divided int

285 ence or presence of transmitter glutamate in nerve terminals, we developed a new method to count func

286 Three morphologies for these nerve terminals were identified.

287 Properties of presumed optic nerve terminals were investigated in the optic tectum us

288 is is unlikely to be due to an effect at the nerve terminals, where chloride channels may play a more

289 s, neurites, axons, and dendrites but not at nerve terminals, where peptidergic neurotransmission occ

290 ion of potassium ion channels at presynaptic nerve terminals, where they modulate excitability and th

291 rogressive adult-onset degeneration of motor nerve terminals, whereas GFP-Syb2 and Ub(G76V)-GFP-Synta

292 cularly at the last axon heminode before the nerve terminal, which regulates the presynaptic excitabi

293 We tested this in calyx of Held nerve terminals, which allow simultaneous recording of p

294 ry transduction in cutaneous primary sensory nerve terminals, which converts thermal stimuli into dep

295 LC3-positive autophagosomes generated in the nerve terminals, which then underwent retrograde transpo

296 ddressed this issue at the rat calyx of Held nerve terminal with capacitance measurements.

297 23)I-MIBG demonstrated stable storage at the nerve terminal with resistance to a NET inhibitor chase,

298 phology and neurochemistry, and suggest that nerve terminals with different sensory modalities can be

299 GRP- and IB4-immunoreactive primary afferent nerve terminals without noticeable expression on glial c

300 number of available vesicles for release and nerve terminals would have to distinguish the recycling